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Regional Anesthesia Complications 

Regional Anesthesia Complications
Regional Anesthesia Complications

Nikhil Bhatnagar

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date: 24 October 2020

Complete Spinal Anesthesia


Inadvertent spread of local anesthetic to cervical and brain stem regions after a regional block resulting in loss of consciousness, cardiovascular instability, and respiratory failure.


  • Initial symptoms are consistent with a high spinal and include nausea and vomiting, hypotension, and bradycardia.

  • Symptoms then progress to upper extremity anesthesia and respiratory distress.

  • Eventually the patient may lose consciousness.

  • All of these symptoms may occur simultaneously or in rapid succession.


A complete spinal anesthetic causes significant venous and arterial dilation, decreasing preload and afterload, and resulting in hypotension. Bradycardia is caused by blockade of the T1 to T4 spinal roots, which contain the cardiac accelerator fibers. Blockade of the C3 to C5 nerve roots results in phrenic nerve paralysis and respiratory arrest. When the local anesthetic reaches the brain stem, further hemodynamic and respiratory compromise occurs because many of the respiratory and vasomotor centers are located in the brain stem.

Differential Diagnosis

  • Local anesthetic systemic toxicity (LAST)

  • Vasovagal reaction

  • High spinal anesthesia

  • Excessive sedation

  • Anaphylactic reaction

Immediate Management

  • Stop injecting local anesthetic.

  • Place patient in reverse Trendelenberg position to prevent a further increase in block height. If a total spinal anesthetic is already present, position the patient with his or her head down to increase venous return to the heart.

  • Increase FiO2 to 100%.

  • If necessary, intubate the trachea and initiate mechanical ventilation.

  • If the patient is conscious but requires general anesthesia for airway management, etomidate or ketamine should be used to minimize hemodynamic instability.

  • Support the blood pressure with fluid and vasoconstrictors (e.g., epinephrine 10- to 20-mcg bolus or 0.1–0.2 mcg/kg/min, ephedrine 5-mg bolus, and phenylephrine 100-mcg bolus or 1 mcg/kg/min) Note: Phenylephrine may exacerbate bradycardia.

  • Immediately begin advanced cardiac life support if cardiac arrest occurs!

Diagnostic Studies

  • This is a clinical diagnosis based on the symptoms occurring after a spinal anesthetic.

  • A computed tomography (CT) or magnetic resonance image (MRI) of the brain and spinal cord only if symptoms persist after several hours or the patient is not arousable.

Subsequent Management

  • If patient has persistent hypotension and respiratory depression, cancel the surgical procedure and transfer the patient to the intensive care unit (ICU) for further monitoring.

  • Symptoms of total spinal usually resolve in 90–120 minutes if bupivicaine is injected. Shorter-acting anesthetics will have quicker resolution.

  • If the total spinal anesthetic may have been caused by a malpositioned epidural catheter, aspirate the catheter. If cerebrospinal fluid (CSF) is drawn into the syringe, remove the catheter.

Risk Factors

  • High volume or total dose of local anesthetic used for spinal or epidural anesthesia.

  • Placing a patient into the supine or head-down position too rapidly after initiating an epidural or spinal anesthetic.

  • Using a high lumbar or low thoracic site for an epidural or spinal anesthetic.

  • Increased intraabdominal pressure: Epidural vein engorgement decreases epidural volume. Pregnant and obese patients are at higher risk for this complication.

  • Elderly patients are at higher risk because of decreased compliance of the epidural space.


Minimize total dose and volume of local anesthetic during spinal and epidural anesthesia. Aspirate an epidural catheter to prevent local anesthetic from being injected into the intrathecal space. A test dose of 3 cc of 1.5% lidocaine with 1:200,000 epinephrine should be injected before dosing an epidural catheter. Local anesthetic should be administered through an epidural catheter slowly and in divided doses. After initiating an epidural or spinal anesthetic, the patient should remain sitting for at least 30 seconds to avoid cephalad spread.

Special Considerations

  • Spinals and epidural anesthetics are not the only regional techniques that can result in a total spinal anesthetic. This complication has been reported after interscalene, retrobulbar, peribulbar, paravertebral, intercostal, and lumbar plexus blocks.

Further Reading

Caplan R, Ward R, Posner K, Cheyney F. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology. 1988; 68(1): 5–11.Find this resource:

Carpenter R, Caplan R, Brown D, Stephenson C, Wu R. Incidence and risk factors for sid effects of spinal anesthesia. Anesthesiology. 1992; 76(6): 906–916.Find this resource:

Epidural Abscess


A collection of purulent matter (neutrophils, bacteria, and necrotic cells) within the epidural space that causes compression of the spinal cord, leading to subsequent neurologic sequella and possibly meningitis or sepsis.


  • Radicular back pain is the most common presenting symptom.

  • Erythema and fluctuance at insertion site.

  • Fever (only occurs in one-third of patients but is usually the initial symptom)

  • Leukocytosis

  • Meningitis (nuchal rigidity and stiffness). This is relatively uncommon but can occur with cervical epidurals.

  • Neurologic symptoms (sensory, motor, and bladder/bowel incontinence). This is a relatively late symptom.

  • Symptoms usually occur 4–7 days after needle insertion, but this is highly variable.

  • Classic triad of fever, back pain, and neurologic signs only occurs 11% of the time.

  • Sepsis is a late and ominous finding of an untreated epidural abscess.


The most common mechanism is direct inoculation of the epidural space with skin or respiratory flora (S. Aureus, S. epidermidis, and P. aeruginosa). The infection causes an inflammatory reaction and creation of purulent matter in the posterior epidural space causing a mass effect that produces neurologic sequellae. If the infection spreads to the blood stream, signs of systemic infection will occur with eventual progression to sepsis.

Differential Diagnosis

  • Epidural hematoma

  • Direct needle insertion and injection of local anesthetic into the spinal cord

  • Transient neurologic symptoms

  • Meningitis

  • Spinal headache

Immediate Management

  • Obtain immediate MRI or CT imaging of the spine if signs or symptoms of an epidural abscess are present.

  • If imaging studies demonstrate an epidural abscess, transfer the patient to the ICU.

  • Request emergency neurosurgical and infectious disease consultations.

  • If neither neurologic symptoms nor signs of sepsis are present, surgery may be delayed and the patient can be managed on antibiotics. Blood cultures and CT-guided cultures guide management.

  • Initial broad spectrum antibiotic coverage includes vancomycin, a third-generation cephalosporin, and gram-negative coverage (e.g., gentamicin) and is narrowed after a diagnosis is made.

  • If the patient shows signs of neurologic deterioration, request an emergency neurosurgical consultation for posterior decompression.

Diagnostic Studies

  • Magnetic resonance image of spine

  • Computed tomography of spine

  • Complete blood count with differential

  • Blood and epidural cultures

Subsequent Management

  • Antibiotic therapy is managed by an infectious disease specialist, and is usually 3–4 weeks in duration.

  • If the diagnosis made early enough, there may be no neurologic sequelae. Late diagnosis may lead to sepsis and permanent neurologic impairment.

  • The amount of time from symptom onset to surgical decompression determines neurologic outcome.

Risk Factors

  • Immunocompromised patients, including diabetics, patients on chemotherapy and radiation, patients who are treated with immunosuppressive drugs, and patients with human immunodeficiency virus (HIV).

  • Patients who are septic or who have an active infection.

  • Patients who require an epidural catheter for long period of time, usually >3 days.

  • Lack of aseptic technique during insertion of an epidural catheter or injection of medications.


The best prophylaxis is strict aseptic technique, including hand washing and wearing a hat, a mask, and sterile gloves during insertion. The insertion site should be prepped with either chlorhexadine or a betadine solution and a sterile drape applied. Immunocompromised patients and those with signs of active infection warrant consideration of the infection risk before a neuraxial technique is performed. If an indwelling catheter is in place, it should be examined every day for signs of infection. Limit the duration of indwelling catheters to the minimum amount necessary.

Special Considerations

  • Unlike epidural hematomas, which occur in the hospital and usually within the first 48 hours, an epidural abscess often occurs a week or more after needle insertion. Therefore, all patients who have neuraxial anesthesia should be given information about symptoms of epidural abscess before discharge.

Further Reading

Grewal S, Hocking G, Wildsmith JMW. Epidural abscesses: review article. Br J Anaesthes. 2006; 96 (3): 292–302.Find this resource:

Wang L, Hauerberg J, Schmidt J. Incidence of spinal epidural abscess after epidural analgesia: a national 1-year survey. Anesthesiology. 1999; 91(6): 1928–1936.Find this resource:

Mackenzie AR, Laing RBS, Smith CC, Kaar GF, Smith FW. Spinal epidural abscess: the importance of early diagnostics and treatment. J Neurol Neurosurg Psychiatry. 1998; 65(2): 209–212.Find this resource:

Epidural Hematoma


Penetration or injury of the epidural vessels resulting in a collection of blood that leads to compression of the spinal cord and subsequent neurologic sequelae.


  • Radicular back pain

  • Bladder dysfunction

  • Sensory dysfunction that outlasts the expected duration of the block or increases in intensity when no additional anesthetic has been injected.

  • Motor dysfunction that outlasts the local block or increases in intensity when no additional local anesthetic has been injected.

  • There is no specific sequence of events that makes the diagnosis. Any of these symptoms can occur in isolation, simultaneously, or at different times.


Spinal hematoma is most commonly caused by disruption of the epidural venous plexus. The expanding hematoma creates a mass effect because the cross-sectional area of the spinal canal is fixed. Continued expansion displaces the CSF and causes further compression of the arteries, veins, and eventually the spinal cord, ultimately causing progressive spinal cord ischemia. Injury can be either transient or permanent.

Differential Diagnosis

  • Epidural or spinal abscess

  • Needle insertion and local anesthetic injection into the spinal cord

  • Transient neurologic symptoms

Immediate Management

  • Discontinue local anesthetic infusions through the epidural catheter.

  • Symptoms of cord compression mandate an immediate MRI or CT of the spine.

  • Request an emergency neurosurgical consultation if radiographic evidence of a hematoma is observed.

  • If patient is at high risk for a spinal hematoma, neurologic checks should occur every 2 hours, preferably in an ICU.

  • Symptom progression from radicular back pain to paralysis can occur very rapidly, usually only 14 hours after initial onset of symptoms. Any delay in surgical decompression will worsen the prognosis, so rapid diagnosis and intervention are imperative.

Diagnostic Studies

  • Computed tomography of spine (fast but less optimal)

  • Magnetic resonance image of spine (slower but gold standard)

Subsequent Management

  • A rapidly deteriorating patient should be evaluated immediately by the neurosurgical service for surgical decompression.

  • No more than 8 hours should elapse from symptom onset to neurosurgical decompression.

  • If the patient is not rapidly deteriorating or the hematoma is small, a conservative course of close observation, serial neurologic exams, and MRIs may be appropriate.

Risk Factors

  • Coagulopathy, including patients with kidney failure, liver failure, pre-eclamptic patients, or patients who have disseminated intravascular coagulation. As a general rule, international normalized ratio (INR) should be <1.5 or platelets >100,000.

  • Treatment with anticoagulant, antiplatelet, or fibrinolytic drugs. Examples include heparin, platelet inhibitors (e.g., clopidogrel), thrombin inhibitors (e.g., dabigatran), and others.

  • Multiple attempts at regional or a bloody puncture.

  • Epidural catheter placement and removal is associated with higher probability of epidural hematoma than is a single shot epidural or spinal anesthetic.

  • Patients with spinal stenosis, spinal tumors, or other space occupying lesions have higher chances of having clinically significant epidural hematomas because of smaller spinal canal diameters.


The most important preventive measure is a focused history and physical, especially in high-risk patients. A careful history of antithrombotic medication use should be elicited, with special attention to when these drugs were stopped. Laboratory studies should include a platelet count and INR. Note: Some drugs, such as low-molecular weight heparin, cannot be monitored with conventional laboratory studies. Newer laboratory studies (e.g., functional platelet levels, factor X assays, and thromboelastogram) provide more comprehensive information about coagulation status, especially in patients treated with newer anticoagulants.

Special Considerations

The sensory and motor deficits that occur during a local anesthetic block can mimic the symptoms of a spinal hematoma. Epidural infusions should be periodically discontinued in order to assess motor and sensory function. Heavy sedation may mask symptoms, and developmentally delayed patients may not be able to express symptoms or cooperate with an examination. If a patient develops a coagulopathy or is given an anticoagulant when an epidural catheter is in place, discontinue local anesthetic administration, discontinue anticoagulation, and follow serial coagulation studies. The patient should have frequent neurologic checks and the epidural catheter should be removed only when all values have normalized.

Patients treated with nonsteroidal anti-inflammatory drugs, aspirin, or subcutaneous heparin (<5000 U TID) may be considered for regional anesthesia. The American Society of Regional Anesthesia has published guidelines for the use of regional anesthetics in patients receiving antithrombotic therapy.

Further Reading

Neal J, Bernard C, Hadzik A, Hebl J, Hogan Q, Horlocker T, Lee L, Rathnell J, Sorenson E, Suresh S, Wedel D. ASRA practice advisory on neurologic complications in regional anesthesia and pain medicine. Regional Anesthes. Pain Med. 2008; 33(5): 404–415.Find this resource:

Vandermuelen E, Van Alen H, Vermylan J. Anticoagulants and spinal-epidural anesthesia. Anesthes Analges. 1994; 79: 1165–1177.Find this resource:

Wulf H. Epidural anaesthesia and spinal hematoma. Can J Anaesthes. 1996; 43(12): 1260–1271.Find this resource:

Globe Injury


Incidental globe penetration (entry) or globe perforation (entry and exit) can occur with accidental needle puncture during either retrobulbar or peribulbar block


  • Extreme intraocular pain on injection

  • Loss of visual acuity

  • Dark red reflex

  • Decrease in intraocular pressure


Introduction of needle into globe results in disruption of structures within the globe such as the retina and retinal vessels. Injection of local anesthetic can also lead to chemical injury. Ocular pressure is only rarely increased if local anesthetic solution is injected directly into the globe.

Differential Diagnosis

  • Retrobulbar hemorrhage

  • Injection into optic nerve

  • Retinal detachment

Immediate Management

  • Stop the injection immediately and withdraw the needle.

  • Request an emergency consultation from an ophthalmologist.

  • Cancel the surgical procedure.

Diagnostic Studies

  • Fundoscopic examination

  • Ultrasound examination. Note: This is especially helpful during the block procedure if globe penetration is suspected.

Subsequent Management

  • Cancel or defer the surgical procedure. Decreased intraocular pressure can further predispose the patient to retinal hemorrhage and retinal detachment.

  • Management is determined by the ophthalmologist and depends upon the extent of the injury. Therapy may include transscleral cyrotherapy, laser retinopexy, vitrectomy, silicone oil tamponade, and scleral buckling.

Risk Factors

  • Excessively sedated patients

  • Myopic patients with axial lengths >26 mm

  • Blunt needles tend to cause more trauma and that trauma is more difficult to treat as compared to sharp needles.


Retrobulbar techniques are associated with a much higher chance of globe perforation than are peribulbar techniques. Experienced practitioners are less likely to cause globe perforation while performing an ocular block. Avoid excessive sedation during ocular blocks.

Special Considerations

  • Anesthesiologists and ophthalmologists have identical complication rates. A fundoscopic examination always should be performed after this block in order to detect this complication more quickly and accurately. Delay in diagnosis can lead to irreparable vision loss.

Further Reading

Vohra SB, Good PA. Altered globe dimensions of axial myopia as risk factors for penetrating ocular injury during peribulbar anaesthesia. Br J Anaesthes. 2000; 85: 242–245.Find this resource:

Wong D. Regional anaesthesia for intraocular surgery. Can J Anaesthes. 1993; 40(7): 635–637.Find this resource:

Local Anesthetic Systemic Toxicity


Local anesthetic overdose that results in rapidly progressive central nervous system (CNS) and cardiac failure.


  • Central nervous system excitation: Prodromal symptoms such as agitation, confusion, metallic taste, and auditory changes only precede seizures 20% of the time. Seizures are usually the primary manifestation of LAST. Central nervous system depression and coma occur after seizures.

  • Cardiac depression: Hypertension, tachycardia, and ventricular arrhythmia precede cardiovascular depression such as bradycardia, decreased ventricular conduction and contractility, and asystole.

  • CV symptoms usually occur after CNS symptoms. More potent local anesthetics have a low cardiovascular collapse (CC) to CNS ratio, which causes cardiac symptoms to occur simultaneously or even precede CNS symptoms. Bupivicaine is the classic local anesthetic with a low CC:CNS ratio.

  • Symptoms of LAST typically occur within the first minute after injection. This usually indicates intravascular injection. However, it is not uncommon for symptoms to occur several minutes or even hours later in cases in which there is a partial intravascular injection or a perineural/epidural catheter in place.


Local anesthetic’s primary mechanism of action is to bind to the intracellular side of the sodium channel, blocking the propagation of action potentials. Local anesthetics also block potassium channels and calcium channels at clinically relevant concentrations, which explains some of the side effects (e.g., decreased contractility and widening QRS complex). When the blood concentration of local anesthetic reaches the toxic range, to neurons in the CNS and cardiac nerve cells (bundle branch blocks and widening of QRS) are bound, inhibiting their function. At extremely high concentrations (lidocaine plasma concentration 5–10 mcg/mL and bupivacaine plasma concentration of 0.5–5 mcg/mL) local anesthetics will bind to sodium channels on the myocytes causing cardiac arrest.

Differential Diagnosis

  • Total spinal anesthesia

  • Vasovagal reaction

  • Severe hypotension

  • Anaphylactic reaction

Immediate Management

  • Immediately stop injecting local anesthetic.

  • Resuscitate the patient. Administer supplemental oxygen or intubate the trachea patient is unable to protect their airway.

  • If patient is having seizures consider administration of a benzodiazepine (lorazepam 1 mg or midazolam 2 mg in an adult). Avoid propofol because it may cause further myocardial depression and hypotension.

  • If patient is in cardiac arrest initiate advanced cardiovascular life support (ACLS). Do not administer lidocaine because this will exacerbate LAST. Administer epinephrine at much lower doses than the 1-mg dose typically given to adults (typically 1 mcg/kg) because high-dose epinephrine has been linked to worse outcomes in local anesthetic cardiac arrests. (The myocardium is especially susceptible to arrhythmias.)

  • Follow serial ABGs. Acidosis, hypoxemia, and hypercarbia all exacerbate the effects of LAST.

  • Administer lipids as early as possible. Administer a 1.5-mL/kg bolus of 20% lipid emulsion 1.5 mL/kg; continue as an infusion at 0.25 mL/kg/min over the next 30–60 minutes.

Diagnostic Studies

  • LAST is usually a clinical diagnosis.

  • Echocardiogram to look at structure and function of heart. Especially valuable when cardiac manifestations of LAST.

  • Serum local anesthetic levels. These are only really valuable if an epidural or nerve block catheter is placed and the patient is having vague prodromal LAST symptoms on the floor. These labs should not be drawn if there is an acute emergency.

  • Consider an EEG if seizures are intractable

Subsequent Management

  • Lipid emulsion therapy can be repeated after the initial bolus. Maximum dose is 12 mL/kg.

  • Myocardial depression may last for 80 to 90 minutes with LAST. Do not discontinue resuscitation efforts.

  • If lipid emulsion therapy fails, consider open cardiac massage or cardiopulmonary bypass.

Risk Factors

  • Potent local anesthetics with low CC:CNS ratios (e.g., bupivacaine). Avoid 0.75% bupivicaine because this has been associated with the most LAST complications.

  • Nerve blocks in areas that have inherently high rates of intravascular absorption. The rate of absorption from high to low are as follows intrapleural > intercostal > lumbar plexus > paravertebral > caudal > epidural > brachial plexus > femoral > sciatic > transverse abdominus plane block > subcutaneous > intra-articular > spinal.

  • Pregnant patients have engorged epidural veins and thus higher rate of absorption. Progesterone may also lower the threshold for LAST.

  • Patients with systemic diseases such as cardiac, hepatic, and renal failure because of decreased LA metabolism and lower cardiac reserve if LAST occurs.

  • Patients at extreme age ranges. The very young do not have fully developed renal and hepatic systems and are more prone to LA toxicity. The very old have decreased hepatic and renal function. By age 80, functioning nephrons have decreased by 50%.


Use the lowest volume and concentration (especially of bupivacaine) of local anesthetic that will achieve the desired result. Inject slowly and in divided doses and aspirate for blood frequently. Inject 5 mL of local anesthetic, waiting 30 seconds between doses. Epinephrine containing solutions (1:200,000) can be used as a marker for intravascular injection. Epinephrine also decreases systemic absorption of local anesthetic by 33%.

Special Considerations

  • Heavy sedation may mask the prodromal effects preceding LAST. The timing and sequence of LAST symptoms is highly variable, so one should have a low threshold for diagnosis. Although LAST typically occurs within a minute of injection, the patient should be monitored for at least half an hour. Lipid emulsion, along with intubating equipment and emergency drugs, always should be immediately available when performing a regional anesthetic. Lipid emulsions are thought to bind local anesthetics in the blood stream, mitigating their toxic effects.

Further Reading

Ciechanowicz S, Patil V. Lipid emulsion for local anesthetic systemic toxicity. Anesthesiol Res Pract. 2012; 131784: 11.Find this resource:

Neal J, Bernards C, Butterworth J, Di Gregorio G, Drasner K, Hejtmanek M, Mulray M, Rosenquist R, Weinberg G. ASRA practice advisory on local anesthetic systemic toxicity. Region Anesthes Pain Med. 2010; 35(2): 152–161.Find this resource:

Scholz A. Mechanisms of local anaesthetics on voltage-gated sodium and other ion channels. Br J Anaesthes. 2002; 89(1): 52–61.Find this resource:

Peripheral Nerve Injury


Mechanical, pharmacologic, or ischemic disruption of one or more structural components of a nerve, causing either a transient or permanent deficit.


  • Sensory changes include anesthesia, paresthesia, hyperalgesia, and allodynia along the nerve distribution.

  • Motor changes include paresis or paralysis along the nerve distribution.

  • Autonomic changes include sudomotor dysfunction (which may be indicated by increased or decreased sweating in the affected limb), swelling, and temperature changes along nerve distribution (complex regional pain syndrome).

  • Less severe nerve injury tends to be associated with sensory deficits; motor and autonomic changes are more likely with more severe injury.

  • Injury usually occurs immediately after needle insertion and injection. Injection pressure is higher than usual and patients usually, but not always, complain of paresthesias.


The most likely mechanisms of injury is mechanical injury, ischemia, or toxicity that occurs when the needle is inserted directly into the fascicle and local anesthetic is injected under high pressures. Needle insertion itself does not usually cause lasting injury.

Differential Diagnosis

  • Stroke

  • Position injury (much more common etiology than regional anesthesia)

  • Cervical or lumbar disc disease

  • Muscle or tendon injury

Immediate Management

  • If patient has a paresthesia during needle insertion, stop and evaluate the patient. If paresthesia is persistent, abandon the procedure and observe. If paresthesia abates, reposition the needle.

  • Do not inject local anesthetic if injection is painful or if high pressure is required to inject the anesthetic. Reposition the needle.

  • If patient has a complete or progressive motor and sensory deficit after local anesthetic has worn off, request an immediate surgical consultation.

Diagnostic Studies

  • This is a clinical diagnosis based upon the sequence of events during the procedure

  • Electromyography and nerve conduction study

  • Magnetic resonance imaging to rule out spinal injury

  • Computed tomography to rule out spinal injury

Subsequent Management

  • Incomplete or minor deficits after local anesthetic has worn off require observation and serial EMG and NCS.

  • A baseline EMG/NCS demonstrates only that nerve injury has occurred, and not the type of injury. It is not necessary to order a baseline EMG/NCS.

  • Wallerian degeneration will be complete after 10–14 days if there is axonal loss. Therefore, an NCS should be able to distinguish between neurapraxia with demyelination or actual axonal loss. This information is extremely valuable to determine the course of the injury because neurapraxia almost always resolves quickly, whereas axonal loss may be permanent or take significantly longer to resolve.

  • Electromyography has a more protracted time course. Fasciculations and spontaneous electrical activity indicate nerve injury that is 2–5 weeks old.

  • A follow-up EMG/NCS should be done at 3 and 6 months.

  • If the injury has not improved after 2–5 months, consider a neurosurgical evaluation. Spontaneous improvement in symptoms after 18–24 months is rare because Schwann cell tubes collapse.

  • Gabapentin and tricyclic antidepressants may ameliorate neuropathic pain.

Risk Factors

  • Patients with medical conditions that compromise the nerve (e.g., diabetes, Marie Charcot Tooth syndrome, or patients who have received chemotherapy).

  • Pre-existing nerve injury in the distribution being blocked. (Injured nerves are more susceptible to local anesthetic toxicity—the double crush phenomenon).

  • Prolonged tourniquet application.

  • Regional anesthetics performed on sedated or anesthetized patients. Consider risk/benefit in mentally challenged patients or pediatric patients, who may be unable to tolerate a nerve block while awake.

  • Injecting under high pressure

  • High-concentration local anesthetic

  • Use of vasoconstrictor such as epinephrine, which reduces perineural blood flow


  • Avoid injection of local anesthetic under high pressure.

  • Avoid performing blocks in oversedated or anesthetized patients. The patient should be able to complain of paresthesias or pain during the procedure.

  • Proceed with caution, and if possible, avoid regional anesthesia in patients with medical conditions that predispose to nerve injury or who have a pre-existing nerve injury.

  • Avoid performing a nerve block at the same level as the tourniquet. The tourniquet can cause significant perineural ischemia and increase the risk of a double crush injury.

  • A short beveled needle should always be used when doing a nerve block in order to reduce the risk of penetrating the nerve.

Special Considerations

  • Peripheral nerve injury is an exceedingly rare complication, with an incidence of 0.4 per 1000. Nerve injuries are more likely to occur as a result of malpositioning than from regional anesthesia. The vast majority of injuries are transient sensory injuries.

  • Ultrasound guidance and nerve stimulation are equally safe, but local anesthetic should not be injected if stimulation is occurring <0.2 mA.

  • The most benign type of injury is neurapraxia (focal demyelination with no disruption of nerve elements). Full recovery usually occurs within 2–12 weeks. In limited axonal loss, relatively few axons have been destroyed, and the fascicle and perineurium are intact. Full recovery usually occurs in between 2 and 4 months. Intermediate axonal loss involves the destruction of several axons and the interruption of a few fascicles. Patients usually recover within 4 to 6 months. Severe axonal loss involves interruption of the majority of fascicles with intact epineurium and stromal elements. There is significant sensorimotor loss and recovery, which is usually incomplete, takes between 6 and 18 months. Complete nerve discontinuity is the most severe injury; the nerve is effectively transected and the epineurium and all stromal elements are disrupted. Recovery will not occur without surgical intervention.

  • Symptom duration is highly variable and depends on the extent of neuronal injury. Minor injuries are self-limited and complete recovery usually takes place within weeks. Recovery from more severe injury may take as long as 18 months to 2 years and may only be partial. In the most severe cases, the nerve injury could progress to complex regional pain syndrome.

Further Reading

Barrington M, Watts S, Gledhill S, Thomas R, Said S, Synder G, Tay V, Jamrozik K. Preliminary results of the Australian Regional Anaesthesia Collaboration: a prospective audit of more than 7000 peripheral nerve and plexus blocks for neurologic and other complications. Region Anesthes Pain Med. 2009; 34(6): 534–541.Find this resource:

Cheney F, Domino K, Caplan R, Posner K. Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology. 1999; 90(4): 1062–1069.Find this resource:

Neal J, Bernard C, Hadzik A, Hebl J, Hogan Q, Horlocker T, Lee L, Rathnell J, Sorenson E, Suresh S, Wedel D. ASRA practice advisory on neurologic complications in regional anesthesia and pain medicine. Region Anesthes Pain Med. 2008; 33(5): 404–415.Find this resource: