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Side Effects and Complications of the Injection Procedures

The injection procedures described here are associated with various side effects, although the risk for significant complications is very low. The physician who performs injection procedures should have the training and education to recognize and treat a wide range of potential complications (Table 67-4). Advanced cardiac life support (ACLS) protocols are used in airway management and cardiorespiratory resuscitation (27).

Side Effects and Complications of the Injection Procedures

aSympathetic block above T-4 adds cardioaccelerator nerve blockade to the vasodilatation seen with blockade below T-4; total spinal block may have rapid onset.
From Covino BG. Clinical pharmacology of local anesthetic agents. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and Management of Pain. 2nd ed. Philadelphia, PA: JB Lippincott; 1988:134, with permission.

Systemic Toxic Reaction

Various toxic reactions have been reported after use of local anesthetics, but with very low incidence. Local anesthetic agents are relatively lipid-soluble, low-molecular-weight compounds that readily cross the blood-brain barrier. As toxic levels are reached, disturbances of CNS function are observed initially, producing signs of CNS excitation. Early symptoms of overdose include headache, ringing in the ears, numbness in the tongue and mouth, twitching of facial muscles, and restlessness. As blood levels increase, generalized tonic-clonic seizures may occur. If sufficiently high blood levels are reached, the initial excitation is followed by generalized CNS depression. Respiratory depression and ultimately respiratory arrest may occur secondary to the toxic effect of the local anesthetic agent on the respiratory center in the medulla. Occasionally, the excitatory phase may not occur, and toxicity presents as CNS depression.

Cardiovascular system (CVS) effects either result indirectly from inhibition of autonomic pathways during regional anesthesia (as in high spinal or epidural block) or are directly due to depressant actions on the CVS. The CVS is generally more resistant to toxicity than the CNS. The CVS-to-CNS toxicity ratio is lower for bupivacaine and etidocaine than for lidocaine. Convulsive activity may initially be associated with an increase in heart rate, blood pressure, and cardiac output. As the blood concentration of a local anesthetic agent increases further, CVS depression occurs, resulting in a decrease in blood pressure secondary to myocardial depression, impaired cardiac conduction, and eventual peripheral vasodilation. Ultimately, circulatory collapse and cardiac arrest may result. In addition, certain agents such as bupivacaine may cause ventricular arrhythmias and fatal ventricular fibrillation. The onset of CVS depression with bupivacaine may occur relatively early and be resistant to usual therapeutic modalities. The pregnant patient is more sensitive to the cardiotoxic effects of bupivacaine. Systemic toxicity may be due to unintentional intravascular injection or drug overdose. Intravascular injection produces signs of toxicity (usually seizures) during the injection itself, especially if injected directly into blood vessels supplying to the brain (e.g., vertebral arteries). A relative overdose results in toxic reactions when peak blood levels are reached, about 20 to 30 minutes after the injection. Factors that affect the blood concentration (site of injection, drug, dosage, addition of vasoconstrictor, speed of injection) influence the potential for systemic toxic reactions to develop.

To minimize systemic reactions to local anesthetic agents, intravascular injection (the most common cause of seizures) should be avoided. Careful, intermittent aspiration should be used while injecting large quantities of local anesthetic agents. Patient complaints of metallic taste, numbness around the mouth, and ringing in the ears are suggestive of intravascular needle placement. Patients may be premedicated with midazolam or diazepam to raise the seizure threshold if necessary.

Systemic toxicity is treated with general supportive measures. If early signs of toxicity occur, constant verbal contact should be maintained, oxygen administered, breathing encouraged, and CVS function monitored. If seizure activity occurs, a clear airway should be maintained and oxygen administered by assisted or controlled ventilation. If seizures continue, thiopental (50 to 100 mg) or diazepam (5 to 10 mg) should be administered intravenously, avoiding large doses of thiopental, which may produce additional CVS or CNS depression. If airway maintenance is jeopardized, succinylcholine should be used to facilitate endotracheal intubation. Muscular convulsive activity is terminated with succinylcholine, but the seizure activity in the brain is not affected. If CVS depression occurs, hypotension should be treated by increasing intravenous fluids, positioning the patient properly (elevate the legs), and using vasopressors such as ephedrine or epinephrine (Table 67-5).

Side Effects and Complications of the Injection Procedures

CNS, central nervous system; CVS, cardiovascular system; IV, intravenous.
From Covino BG. Clinical pharmacology of local anesthetic agents. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and Management of Pain. 2nd ed. Philadelphia, PA: JB Lippincott; 1988:135, with permission.

Epinephrine Reaction

Reaction to epinephrine may sometimes be confused with local anesthetic overdose. Systemic absorption of epinephrine produces palpitations and restlessness about 1 to 2 minutes after completion of the injection. Avoiding epinephrine should be considered in patients who are sensitivity prone (e.g., hypertensive, or hyperthyroid, arrhythmic patients). Epinephrine should not be used for blocks of the fingers, toes, or penis, owing to the possibility of localized vasoconstriction. An epinephrine reaction is treated with a small dose of fast-acting barbiturate to reduce blood pressure to within normal limits. If hypertension persists, a vasodilator may be required.

Vasovagal Reaction

Vasovagal reaction is a frequent response to injection procedures that is attributable to physiologic and psychological factors. This response may result in bradycardia, hypotension, and loss of consciousness. This usually occurs in the initial portion of the procedure when skin is penetrated before any medication is injected. Vasovagal reaction is often mislabeled as an allergic reaction to the medication. This response is often preceded by dizziness, faintness, sweating, and pallor. Vasovagal reaction is rapidly reversible by removing painful stimuli and placing the patient in a head down and legs up position to improve venous blood return to the heart. If this fails to relieve the symptoms, then treatment with general supportive measures is indicated, including airway maintenance, oxygen, intravenous fluids, anticholinergics such as atropine, and vasopressors such as ephedrine (see Table 67-5).

Allergic Reaction

An allergic reaction to local anesthetic agents rarely occurs and in some instances may be confused with a vasovagal reaction or a reaction to epinephrine. Ester anesthetic agents (e.g., procaine, tetracaine) are more frequently associated with allergic reactions than amide anesthetic agents (e.g., lidocaine, ropivacaine), because esters are derivatives of paraaminobenzoic acid (PABA). However, the use of amides from multiple-dose vials may result in an allergic reaction secondary to the preservative methylparaben. Allergic reaction is treated with general supportive measures and the administration of fluids, antihistamine, steroids, and epinephrine (if warranted), as well as removal of any additional offending agent. The patient should be closely monitored for a clear airway.

Although this is a rare event, if there is a question of patient hypersensitivity to anesthetic agents, intradermal skin tests (injection with diluted [1:1,000] followed by undiluted local anesthetic) can be used successfully to diagnose adverse responses. However, false-positive results may occur. Anaphylactic shock is treated as systemic toxic reaction with attention to maintaining cardiovascular and ventilatory function (see Table 67-5).

Accidental Spinal Block

Inadvertent subarachnoid or epidural blockade can occur with any injection that is performed close to the spine. These injections include intercostal nerve blocks, sympathetic blocks, and nerve root injections. Proper equipment and staff should always be available to treat any possible complication. This includes the ability to administer fluids and vasopressors if the patient develops hypotension from sympathetic blockade and to maintain ventilation with oxygen if the patient has impaired respiratory function.

Concurrent Medical Episode

Concurrent medical problems may be exacerbated by injection procedures. Hypotension will reduce myocardial profusion and may be a major factor for reinfarction in patients with ischemic heart disease. Patients with poorly treated hypertension risk developing hypertensive crisis, myocardial infarction, or stroke triggered by the stress of the procedure. Patients with chronic renal failure are more susceptible to toxicity from local anesthetics. Diabetic patients have an increased sensitivity to the effects of corticosteroid injection. Patients with liver disease may have reduced metabolism of local anesthetic medications resulting in an increased possibility of toxicity at standard doses. Other medical illnesses may decompensate clinically, owing to mild toxicity and changes in fluid and electrolyte balance. These risks are minimized with appropriate monitoring and optimal medication regimes. Patients should be medically stable before undergoing elective injection procedures.


Although infectious complications rarely occur, cutaneous and joint infection, epidural abscess, bacterial meningitis, and adhesive arachnoiditis have been associated with injection procedures. Epidural abscess may cause spinal cord compression. Signs and symptoms of epidural abscess are severe back pain, localized tenderness, fever, leukocytosis, cervical rigidity, increased protein and leukocytes in the cerebral spinal fluid, progressive neurologic symptoms, and abnormal imaging studies of the spine. Early diagnosis and prompt treatment are essential to avoid catastrophic complications. Meningitis and adhesive arachnoiditis are the result of the introduction of bacterial or irritating contaminants into the spinal fluid as well as trauma during the procedure.


Injections into the thoracic region have the potential to cause a pneumothorax. In procedures that put the patient at risk for needle penetration of the lung, less than 1% develop a pneumothorax (32,33). Most of these patients can be easily treated with administration of 100% oxygen, close monitoring (e.g., O2 saturation, vital signs) of the patient, and, when necessary, needle aspiration of air. Only those pneumothoraces that result in significant dyspnea or those under tension require chest tube thoracostomy and vacuum drainage. Bilateral thoracic procedures should be undertaken with caution due to potential risk of bilateral pneumothorax.

Nerve Injury

Three major factors contribute to nerve injury during injections: trauma, toxicity, and ischemia, with all three contributing to most nerve injuries. Nerve blocks are the result of infiltration of anesthetic agents around the nerve, not directly into the neural tissue. Intraneural injections directly injure nerve fibers and cause a breakdown in the blood-nerve barrier. The use of short, beveled needles has significantly reduced nerve injuries from injections. Intense pain in the nerve distribution and high resistance upon injection are often the result of intraneural needle placement and necessitate immediate cessation of the injection and repositioning of the needle.

Other Complications

Local anesthetic agents used in recommended clinical concentrations have minimal irritating effects on the nerves, skin, and subcutaneous tissue. Complete recovery of function occurs after regional blocks. The administration of large doses of prilocaine may lead to methemoglobinemia, owing to the accumulation of a metabolite (OH-toluidine) that can convert hemoglobin to methemoglobin. It may be treated with intravenous methylene blue.

Hypotension may result from sympathetic blockade. This commonly occurs in patients who are hypovolemic and receive a spinal or epidural block involving a large portion of the sympathetic chain ganglia. Hypotension is treated with general supportive measures, including administration of intravenous fluids, vasopressors such as epinephrine to maintain blood pressure within normal limits, and proper positioning (elevating the legs). Bradycardia from blockade of sympathetic outflow from T1-4 may require prompt treatment.

Bleeding at the site of injection occurs commonly at the surface. Hematoma at the site of injection is a possibility but usually not clinically significant. If arterial puncture occurs, prolonged direct pressure is usually adequate to prevent the development of a hematoma.


Source: Physical Medicine and Rehabilitation – Principles and Practice

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