20 Complications and General Contraindications of Peripheral Blocks
20.1 Complications of Peripheral Nerve Blocks
Besides the specific complications described for the individual techniques, the following complications of peripheral nerve blocks are possible:
Toxic reactions caused by the local anesthetic (LAST: Local Anesthetic Systemic Toxicity)
Neurological injuries (neuropathy)
20.1.1 Toxic Reactions Caused by the Local Anesthetic
Toxic reactions can be due to overdose at a correct initial injection site. The symptoms do not occur immediately at the time the injection is made, but can be expected to develop later, at the time of maximum blood levels depending on the rate of absorption.
Accidental intravascular injection.
In the event of accidental intravascular injection of the local anesthetic, small amounts may be enough to cause a toxic reaction (see above). For this reason, the maximum doses for many local anesthetics recommended by the manufacturer should be regarded with a degree of skepticism, since much smaller doses can lead to major incidents in the event of accidental intravascular injection, while much higher doses may be tolerated with correct injection.
Systemic intoxication by local anesthetics is expressed in cerebral and cardiac effects; the cerebral effects usually precede the cardiac effects (Fig. 20.1). Early symptoms are a metallic taste on the tongue, tinnitus, dizziness, and acoustic phenomena, followed by muscle twitching, confusion, unconsciousness, seizure, and coma. The cardiac changes occur in parallel with correspondingly higher blood levels. First there is tachycardia and hypertension, followed by bradycardia and hypotension possibly progressing to asystole.
When injecting the local anesthetic it is important to watch for early symptoms of intoxication in order to stop administration immediately in case of accidental intravascular injection. For this reason, in addition to repeated aspiration to rule out intravascular injection, the local anesthetic must be given slowly with constant verbal communication with the patient (“verbal monitoring”) to ensure that the patient still responds lucidly and has no symptoms (Mulroy and Hejtmanek 2010).
Intoxication symptoms are enhanced by hypoxia and acidosis, so prophylactic oxygen administration is recommended.
In case of cerebral intoxication, oxygen must be given immediately and if there is a seizure, the patient must also be ventilated adequately (if necessary with intubation and mechanical ventilation) and benzodiazepines (midazolam, diazepam) or barbiturates should be administered.
The cardiac effects are differentiated between indirect effects (tachycardia, hypertension) that can be explained by the central inhibition of the “inhibitory effects” and the direct cardiotoxic effect, which occurs in the form of bradycardia up to complete cardiopulmonary arrest associated with impairment of contractility.
With regard to the cardiac effects, the first rule is to avoid hypoxia and acidosis. Naturally, injection of the local anesthetic must stop immediately and, in addition to administration of positive inotropic and chronotropic medications (atropine, catecholamines) and volume replacement, prolonged mechanical cardiac massage may be required. This may be the case in particular with bupivacaine, as bupivacaine may block the effect of an external electrical pacemaker.
After successful ventilation and oxygenation, a lipid infusion should be considered at the first sign of intoxication (Fig. 20.2; Weinberg 2010). Propofol is not a substitute for administering a 20% lipid solution.
Treatment of Systemic Intoxication with Local Anesthetics (LAST)
Recommendation for the treatment of systemic intoxication with local anesthetics (dosages for adults; Weinberg 2010):
Secure airways: Avoid hypoxia and acidosis (sufficient ventilation, administration of 100% O2).
Treatment of a seizure: Benzodiazepines, if necessary propofol or thiopental (fractionated), lipid infusion (see below).
Treatment of circulatory arrest: Resuscitation according to standard protocol: epinephrine fractionated (10–100 µg). Avoid: calcium channel blockers, beta receptor blockers. If the patient has ventricular arrhythmia: amiodarone.
Treatment with a 20% lipid emulsion:
Initial bolus: 1.5 mL/kg body weight within 1 minute (equivalent to about 100 mL); continuous: 0.25 mL/kg body weight per minute (equivalent to 400 mL in 20 min).
If adequate circulation cannot be restored:
2 repetitions of the bolus at 5-minute intervals (equivalent to 2 further boli of 100 mL)
If necessary, double the infusion rate (0.5 mL/kg/min, 400 mL within 10 min)
Continue infusion until stable circulation is restored.
Important: Cardiopulmonary resuscitation must be continued during these measures.
If there is no response: cardiopulmonary bypass (if available).
The American Society of Regional Anesthesia and Pain Therapy (ASRA) published a checklist for the treatment of systemic intoxication with local anesthetics (Neal et al 2012).
Selecting the Local Anesthetic
When selecting the local anesthetic, consideration must be given to its potential toxicity, especially in the event of accidental intravascular injection.
Medium-acting local anesthetics are less toxic than the long-acting drugs; prilocaine compares positively to the other medium-acting local anesthetics mainly due to its high spread volume. The formation of methemoglobin by prilocaine is a disadvantage. For this reason, doses higher than 600 mg should be avoided. Repeated doses of prilocaine should not be given.
Of the currently employed long-acting local anesthetics—namely, racemic bupivacaine, levobupivacaine, S(–) isomer of bupivacaine, and the S(–) isomer ropivacaine—the least cardiotoxic is ropivacaine. With regard to intracellular energy metabolism also, it has clear advantages compared to levobupivacaine.
In contrast to ropivacaine and the medium-acting local anesthetics, levobupivacaine and bupivacaine may lead to a complete block of ATP synthesis in the myocardium at toxic concentrations (Sztark et al 1998, 2000).
Allergic reactions are extremely rare with the amide local anesthetics that are used almost exclusively today.
20.1.2 Neurological Injuries (Neuropathy)
Neurological injuries (Fig. 20.3) after peripheral nerve blocks are reported with an incidence between 0.019% (Auroy et al 1997), 0.04% (Barrington et al 2009), 1.7% (Fanelli et al 1999), and 3% (Brull et al 2007).
Not all postoperative nerve lesions are due to a nerve block; other causes such as position-induced injury or injury caused by the operation must be considered (Cheney et al 1999, Fanelli et al 1999, Barrington et al 2009).
Permanent or severe nerve damage in connection with peripheral blocks is considered to be extremely rare (Brull et al 2007, Neal 2008).
The incidence is reported to be 0.019% (Auroy et al 1997) and 0.04% (Barrington et al 2009).
A subfascial hematoma can lead to mechanical nerve compression (Jöhr 1987). Occasionally brachial plexus neuropathy or “idiopathic neuritis” or “idiopathic plexitis” occurs in association with an interscalene brachial plexus block (Tetzlaff et al 1997, Horlocker et al 2000, Hebl et al 2001). This is associated with severe nerve pain, numbness, and motor weakness. Characteristically, this complication will become manifest only after complete disappearance of the block in the meantime. An immediate injury due to the injection has not taken place here; accordingly, the neurological picture cannot be attributed to injury of individual cords or nerves. The syndrome is due to an inflammatory immunological process. Postoperative plexus neuropathy can also occur spontaneously independently of the anesthesia procedure performed. This makes it difficult to make a causal distinction from regional anesthesia (Malamut et al 1994).
Classification of Nerve Injuries.
Nerve injuries are classified into one of three groups: neurapraxia, axonotmesis, and neurotmesis (Sawyer et al 2000):
Neurapraxia is a functional paralysis without any evident anatomical lesion.
In axonotmesis the axons are disrupted while the myelin sheath is still intact.
In neurotmesis there is complete (mechanical) disruption of both axon and myelin sheath.
Usually, neurapraxia and axonotmesis have a good prognosis (Stan et al 1995, Fanelli et al 1999). After weeks to months, complete or extensive resolution of the paresis and pain can be expected (Stöhr 1996). However, in individual cases (neurotmesis), residual paresis interfering with function—sometimes associated with causalgiform pain syndromes—can persist.
Very little data is available on which measures are best for avoiding nerve damage (Neal 2008).