++
The complications of epidural, spinal, or caudal anesthetics range from the bothersome to the crippling and life-threatening (Table 45-6). Broadly, the complications can be thought of as those resulting from excessive effects of an appropriately injected drug, placement of the needle (or catheter), and systemic drug toxicity.
++
A very large survey of regional anesthesia from France provides an indication of the relatively low incidence of serious complications from spinal and epidural anesthesia (Table 45-7). The American Society of Anesthesiologists (ASA) Closed Claims Project helps to identify the most common causes of liability claims involving regional anesthesia in the operating room setting. In a 20-year period (1980-1999), regional anesthesia accounted for 18% of all liability claims. In the majority of these claims, the injuries were judged as temporary or nondisabling (64%). Serious injuries in the remaining claims included death (13%), permanent nerve injury (10%), permanent brain damage (8%), and other permanent injuries (4%). The majority of regional anesthesia claims involved either lumbar epidural anesthesia (42%) or spinal anesthesia (34%) and tended to occur mostly in obstetric patients. The latter may at least partly reflect the relatively higher use of neuraxial anesthesia compared with other regional techniques and its relatively very high utilization in obstetric patients. Of note is that caudal anesthesia was utilized in only 2% of claims.
+++
Complications Associated with Excessive Responses to Appropriately Placed Drug
++
Exaggerated dermatomal spread of neural blockade can occur readily with either spinal or epidural anesthesia. Administration of an excessive dose, failure to reduce standard doses in selected patients (eg, the elderly, pregnant, obese, or very short), or unusual sensitivity or spread of local anesthetic may be responsible. Patients may complain of dyspnea and have numbness or weakness in the upper extremities. Nausea often precedes hypotension. Once exaggerated spread of anesthesia is recognized, patients should be reassured, oxygen supplementation may be required, and bradycardia and hypotension should be treated.
++
Spinal anesthesia ascending into the cervical levels causes severe hypotension, bradycardia, and respiratory insufficiency. Unconsciousness, apnea, and hypotension resulting from high levels of spinal anesthesia are referred to as a “high spinal,” or when the block extends to cranial nerves, as a “total spinal.” These conditions can also occur following attempted epidural/caudal anesthesia if there is accidental intrathecal injection (see below). Apnea is more often the result of severe sustained hypotension and medullary hypoperfusion than a response to phrenic nerve paralysis from anesthesia of C3-C5 roots. Anterior spinal artery syndrome has been reported following neuraxial anesthesia, presumably due to prolonged severe hypotension together with an increase in intraspinal pressure.
++
Treatment of an excessively high neuraxial block involves maintaining an adequate airway and ventilation and supporting the circulation. When respiratory insufficiency becomes evident, in addition to supplemental oxygen, assisted ventilation, intubation, and mechanical ventilation may be necessary. Hypotension can be treated with rapid administration of intravenous fluids, a head-down position, and intravenous vasopressors. Bradycardia can be treated early with atropine. Ephedrine or epinephrine can also increase heart rate and arterial blood pressure. If respiratory and hemodynamic control can be readily achieved and maintained after high or total spinal anesthesia, surgery may proceed.
+++
Cardiac Arrest during Spinal Anesthesia
++
Examination of data from the ASA Closed Claim Project identified several cases of cardiac arrest during spinal anesthesia. Because many of the reported cases predated the routine use of pulse oximetry, many physicians believed oversedation and unrecognized hypoventilation and hypoxia were the causes. However, large prospective studies continue to report a relatively high incidence (perhaps as high as 1:1500) of cardiac arrest in patients having received a spinal anesthetic, Many of the cardiac arrests were preceded by bradycardia, and many occurred in young healthy patients. Examination of this problem identified vagal responses and decreased preload as key factors and suggests that patients with high baseline vagal tone are at risk. To prevent this from occurring, hypovolemia should be corrected. Prompt drug treatment of hypotension and bradycardia are recommended. Many clinicians will not allow the heart rate to fall below 50 beats per minute during spinal anesthetic blockade.
++
Local anesthetic block of S2-S4 root fibers decreases urinary bladder tone and inhibits the voiding reflex. Epidural opioids can also interfere with normal voiding. These effects are most pronounced in male patients. Urinary bladder catheterization should be used for all but the shortest acting blocks. If a catheter is not present postoperatively, close observation for voiding is necessary. Persistent bladder dysfunction can also be a manifestation of serious neural injury, as discussed below.
+++
Complications Associated with Needle or Catheter Insertion
+++
Inadequate Anesthesia or Analgesia
++
As with other regional anesthesia techniques, neuraxial blocks are associated with a small, but measureable, failure rate that is usually inversely proportional to the clinician’s experience. Failure may still occur, even when CSF is obtained during spinal anesthesia. Movement of the needle during injection, incomplete entry of the needle opening into the subarachnoid space, subdural injection, or loss of potency of the local anesthetic solution may be responsible. Causes for failed epidural blocks were discussed above (see “Failed Epidural Blocks”).
+++
Intravascular Injection
++
Accidental intravascular injection of the local anesthetic for epidural and caudal anesthesia can produce very high serum levels. Extremely high levels of local anesthetics affect the central nervous system (seizure and unconsciousness) and the cardiovascular system (hypotension, arrhythmias, and depressed contractility). Because the dosage of medication for spinal anesthesia is relatively small, this complication is seen after epidural and caudal (but not spinal) blocks. Local anesthetic may be injected directly into a vessel through a needle or later through a catheter that has entered a blood vessel (vein). The incidence of intravascular injection can be minimized by carefully aspirating the needle (or catheter) before every injection, using a test dose, always injecting local anesthetic in incremental doses, and close observation for early signs of intravascular injection (tinnitus, lingual sensations). Treatment is resuscitative, and lipid rescue should be employed.
++
The local anesthetics vary in their propensity to produce severe cardiac toxicity. The rank order of local anesthetic potency at producing seizures and cardiac toxicity is the same as the rank order for potency at nerve blocks. Chloroprocaine has relatively low potency and also is metabolized very rapidly; lidocaine and mepivacaine are intermediate in potency and toxicity; and levobupivacaine, ropivacaine, bupivacaine, and tetracaine are most potent and toxic.
+++
Total Spinal Anesthesia
++
Total spinal anesthesia can occur following attempted epidural/caudal anesthesia if there is accidental intrathecal injection. Onset is usually rapid, because the amount of anesthetic required for epidural and caudal anesthesia is 5-10 times that required for spinal anesthesia. Careful aspiration, use of a test dose, and incremental injection techniques during epidural and caudal anesthesia can help avoid this complication.
++
As with accidental intravascular injection, and because of the larger amount of local anesthetic administered, accidental subdural injection of local anesthetic during attempted epidural anesthesia is much more serious than during attempted spinal anesthesia. A subdural injection of epidural doses of local anesthetic produces a clinical presentation similar to that of high spinal anesthesia, with the exception that the onset may be delayed for 15-30 min and the block may be “patchy”. The spinal subdural space is a potential space between the dura and the arachnoid containing a small amount of serous fluid. Unlike the epidural space, the subdural space extends intracranially, so that anesthetic injected into the spinal subdural space can ascend to higher levels than epidural medications. As with high spinal anesthesia, treatment is supportive and may require intubation, mechanical ventilation, and cardiovascular support. The effects generally last from one to several hours.
++
As a needle passes through skin, subcutaneous tissues, muscle, and ligaments it causes varying degrees of tissue trauma. Bruising and a localized inflammatory response with or without reflex muscle spasm may be responsible for postoperative backache. One should remember that up to 25% to 30% of patients receiving general anesthesia also complain of backache postoperatively, and a significant percentage of the general population has chronic back pain. Postoperative back soreness or ache is usually mild and self-limited, although it may last for a number of weeks. If treatment is sought, acetaminophen, NSAIDs, and warm or cold compresses should suffice. Although backache is usually benign, it may be an important clinical sign of much more serious complications, such as epidural hematoma and abscess (see below).
+++
Postdural Puncture Headache
++
Any breach of the dura may result in a postdural puncture headache (PDPH). This may follow a diagnostic lumbar puncture, a myelogram, a spinal anesthetic, or an epidural “wet tap” in which the epidural needle passed through the epidural space and entered the subarachnoid space. Similarly, an epidural catheter might puncture the dura at any time and result in PDPH. An epidural wet tap is usually immediately recognized as CSF pouring from the epidural needle or aspirated from an epidural catheter. However, PDPH can follow a seemingly uncomplicated epidural anesthetic and may be the result of just the tip of the needle scratching through the dura. Typically, PDPH is bilateral, frontal or retroorbital, or occipital and extends into the neck. It may be throbbing or constant and associated with photophobia and nausea. The hallmark of PDPH is its association with body position. The pain is aggravated by sitting or standing and relieved or decreased by lying down flat. The onset of headache is usually 12-72 hr following the procedure; however, it may be seen almost immediately. Untreated, the pain may last weeks, and in rare instances, has required surgical repair.
++
PDPH is believed to result from leakage of CSF from a dural defect and intracranial hypotension. Loss of CSF at a rate faster than it can be produced causes traction on structures supporting the brain, particularly the meninges, dura, and tentorium. Increased traction on blood vessels and cranial nerves may also contribute to the pain. Traction on the cranial nerves may occasionally cause diplopia (usually the sixth cranial nerve) and tinnitus. The incidence of PDPH is strongly related to needle size, needle type, and patient population. The larger the needle, the greater the likelihood of PDPH. Cutting-point needles are associated with a higher incidence of PDPH than pencil-point needles of the same gauge. Factors that increase the risk of PDPH include young age, female sex, and pregnancy. The greatest risk, then, would be expected following an accidental wet tap with a large epidural needle in a young woman (perhaps as high as 20% to 50%). The lowest incidence would be expected in an elderly male using a 27-gauge pencil-point needle (<1%). Studies of obstetric patients undergoing spinal anesthesia for cesarean section with small-gauge pencil-point needles have shown rates as low as 3% or 4%.
++
Conservative treatment involves recumbent positioning, analgesics, intravenous or oral fluid administration, and caffeine. Keeping the patient supine will decrease the hydrostatic pressure driving fluid out of the dural hole and minimize the headache. Analgesic medication may range from acetaminophen to NSAIDs and opioids. Hydration and caffeine work to stimulate production of CSF. Caffeine further helps by vasoconstricting intracranial vessels. Stool softeners and soft diet are used to minimize Valsalva straining. Headache may persist for days, despite conservative therapy.
++
An epidural blood patch is an effective treatment for PDPH. It involves injecting 15-20 mL of autologous blood into the epidural space at, or one interspace below, the level of the dural puncture. It is believed to stop further leakage of CSF by either mass effect or coagulation. The effect is usually immediate but may take some hours as CSF production slowly builds intracranial pressure. Approximately 90% of patients will respond to a single blood patch, and 90% of initial nonresponders will obtain relief from a second injection. We do not recommend prophylactic blood patching through an epidural catheter that was placed after a wet tap. Not all patients will develop PDPH, and the tip of the catheter may be many levels away from the dural defect. Most practitioners either offer the epidural blood patch when PDPH becomes apparent or allow conservative therapy a trial of 12-24 hr.
++
When evaluating patients with presumed PDPH, other sources of headache, including meningeal infection and subarachnoid hemorrhage, should be considered in the differential diagnosis.
++
Perhaps no complication is more perplexing or distressing than persistent neurological deficits following an apparently routine neuraxial block. An epidural hematoma or abscess must be ruled out. Either nerve roots or spinal cord may be injured. The latter may be avoided if the neuraxial blockade is performed below the termination of the conus (L1 in adults and L3 in children). Postoperative peripheral neuropathies can be due to direct physical trauma to nerve roots. Although most resolve spontaneously, some are permanent. Some of these deficits have been associated with paresthesia from the needle or catheter or complaints of pain during injection. Some studies have suggested that multiple attempts during a technically difficult block are also a risk factor. Any sustained paresthesia should alert the clinician to redirect the needle. Injections should be immediately stopped and the needle withdrawn, if they are associated with pain. Direct injection into the spinal cord can cause paraplegia. Damage to the conus medullaris may cause isolated sacral nerve dysfunction, including paralysis of the biceps femoris muscles; anesthesia in the posterior thigh, saddle area, or great toes; and loss of bowel or bladder function. Not all neurological deficits occurring after a regional anesthetic are the result of the block. Surveys of complications have reported many instances of postoperative neurological deficits that were attributed to regional anesthesia when, in fact, only general anesthesia was used. Postpartum deficits, including lateral femoral cutaneous neuropathy, foot drop, and paraplegia, were recognized before the modern era of anesthesia and still occur in the absence of anesthetics. Less clear are the postanesthetic cases complicated by concurrent conditions such as atherosclerosis, diabetes mellitus, intervertebral disk disease, and spinal disorders.
+++
Spinal or Epidural Hematoma
++
Needle or catheter trauma to epidural veins often causes minor bleeding in the spinal canal, although this usually has no consequences. A clinically significant spinal hematoma can occur following spinal or epidural anesthesia, particularly in the presence of abnormal coagulation or a bleeding disorder. The incidence of such hematomas has been estimated to be about 1:150,000 for epidural blocks and 1:220,000 for spinal anesthetics. The vast majority of reported cases have occurred in patients with abnormal coagulation either secondary to disease or pharmacological therapies. Many hematomas have occurred immediately after removal of an epidural catheter. Thus, insertion and removal of an epidural catheter are risk factors.
++
The pathological insult to the spinal cord and nerves is due to the hematoma’s mass effect, compressing neural tissue and causing direct pressure injury and ischemia. The diagnosis and treatment must be accomplished promptly, if permanent neurological sequelae are to be avoided. The onset of symptoms is typically more sudden than with epidural abscess. Symptoms include sharp back and leg pain with a motor weakness and/or sphincter dysfunction. When hematoma is suspected, neurological imaging (magnetic resonance imaging [MRI] or computed tomography [CT]) and neurosurgical consultation must be obtained immediately. In many cases, good neurological recovery has occurred in patients who have undergone surgical decompression within 8-12 hr.
++
Neuraxial anesthesia should be avoided in patients with coagulopathy, significant thrombocytopenia, platelet dysfunction, or those who have received fibrinolytic/thrombolytic therapy. Practice guidelines should be reviewed when considering neuraxial anesthesia in such patients, and the risk versus benefit of these techniques should be weighed and delineated in the informed consent process.
+++
Meningitis and Arachnoiditis
++
Infection of the subarachnoid space can follow neuraxial blocks as the result of contamination of the equipment or injected solutions, or as a result of organisms tracked in from the skin. Indwelling catheters may become colonized with organisms that then track deep, causing infection. Fortunately, these are rare occurrences.
++
Arachnoiditis, another reported rare complication of neuraxial anesthesia, may be infectious or noninfectious. Clinically, it is marked by pain and other neurological symptoms, and, on radiographic imaging, is seen as a clumping of the nerve roots. Cases of arachnoiditis have been traced to detergent in a spinal procaine preparation. Lumbar arachnoiditis has been reported from subarachnoid steroid injection, but is more commonly seen following spinal surgery or trauma. Prior to of the wide availability of single-use disposable spinal anesthesia trays, caustic solutions used to clean reusable spinal needles caused chemical meningitis and severe neurological dysfunction. Strict sterile technique should be employed, and face masks should be worn by all individuals in the room where neuraxial blocks are to be placed. Careful attention is particularly warranted in the labor room where family members are often curious to see what is being done to mitigate the parturient’s pain. Such individuals should be advised to avoid contaminating the tray, if hospital policy permits their presence during epidural placement. If permitted, family members should also wear a mask to prevent contamination of the epidural tray with oral flora.
++
Spinal epidural abscess (EA) is a rare but potentially devastating complication of neuraxial anesthesia. The reported incidence varies widely, from 1:6500 to 1:500,000 epidurals. EA can occur in patients who did not receive regional anesthesia; risk factors in such cases include back trauma, injecting drug use, and neurosurgical procedures. Most reported anesthesia-related cases involve epidural catheters. In one reported series, there was a mean of 5 days from catheter insertion to the development of symptoms, although presentation can be delayed for weeks.
++
There are four classic clinical stages of EA, although progression and time course can vary. Initially, symptoms include back or vertebral pain that is intensified by percussion over the spine. Second, nerve root or radicular pain develops. The third stage is marked by motor and/or sensory deficits or sphincter dysfunction. Paraplegia or paralysis marks the fourth stage. Ideally, the diagnosis is made in the early stages. Prognosis has consistently been shown to correlate to the degree of neurological dysfunction at the time the diagnosis is made. Back pain and fever after epidural anesthesia should alert the clinician to consider EA. Radicular pain or neurological deficit heightens the urgency to investigate. Once EA is suspected, the catheter should be removed (if still present) and the tip cultured. The injection site is examined for evidence of infection; if pus is expressed, it is sent for culture. Blood cultures should be obtained. If suspicion is high and cultures have been obtained, anti-Staphylococcus coverage can be instituted, as the most common organisms causing EA are Staphylococcus aureus and Staphylococcus epidermidis. MRI or CT scanning should be performed to confirm or rule out the diagnosis. Early neurosurgical and infectious disease consultation is advisable. In addition to antibiotics, treatment of EA usually involves decompression (laminectomy), although percutaneous drainage with fluoroscopic or CT guidance has been reported. There are a few reports of patients with no neurological signs being treated with antibiotics alone.
++
Suggested strategies for guarding against the occurrence of EA include (1) minimizing catheter manipulations and maintaining a closed system when possible; (2) using a micropore (0.22-μm) bacterial filter; and (3) removing an epidural catheter or at least changing the catheter, filter, and solution after a defined time interval (eg, some clinicians replace or remove all epidurals after 4 days).
+++
Sheering of an Epidural Catheter
++
There is a risk of neuraxial catheters sheering and breaking off inside of tissues if they are withdrawn through the needle. If a catheter must be withdrawn while the needle remains in situ, both must be carefully withdrawn together. If a catheter breaks off within the epidural space, many experts suggest leaving it and observing the patient. If, however, the breakage occurs in superficial tissues, the catheter should be surgically removed.
+++
Complications Associated with Drug Toxicity
++
Absorption of excessive amounts of local anesthetics can produce toxic blood levels (see “Intravascular Injection”). Excessive absorption from epidural or caudal blocks is rare when appropriate doses of local anesthetic are used.
+++
Transient Neurological Symptoms
++
First described in 1993, transient neurological symptoms (TNS), also referred to as transient radicular irritation, are characterized by back pain radiating to the legs without sensory or motor deficits, occurring after the resolution of spinal anesthesia and resolving spontaneously within several days. It is most commonly associated with hyperbaric lidocaine (incidence up to 11.9%), but has also been reported with tetracaine (1.6%), bupivacaine (1.3%), mepivacaine, prilocaine, procaine, and subarachnoid ropivacaine. There are also case reports of TNS following epidural anesthesia. The incidence of this syndrome is greatest among outpatients, particularly males undergoing surgery in the lithotomy position, and least among inpatients undergoing surgery in positions other than lithotomy. The pathogenesis of TNS is believed to represent concentration-dependent neurotoxicity of local anesthetics.
++
CES was associated with the use of continuous spinal catheters (prior to their withdrawal) and 5% lidocaine (see “Spinal Catheters”). CES is characterized by bowel and bladder dysfunction together with evidence of multiple nerve root injury. There is lower motor neuron type injury with paresis of the legs. Sensory deficits may be patchy, typically occurring in a peripheral nerve pattern. Pain may be similar to that of nerve root compromise. Animal studies suggest that pooling or “maldistribution” of hyperbaric solutions of lidocaine can damage the nerve roots of the cauda equina. However, there are reports of CES occurring after uneventful single shot lidocaine spinals. CES has also been reported following epidural anesthesia.