Complications Associated with Needle or Catheter Insertion
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”).
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 ner-vous 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 injec-tion can be minimized by carefully aspirating the needle (or catheter) before every injection, using a test dose, always injecting local anesthetic in incre-mental doses, and close observation for early signs of intravascular injection (tinnitus, lingual sensa-tions). 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, ropi-vacaine, bupivacaine, and tetracaine are most potent and toxic.
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 tech-niques 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 presenta-tion 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 spi-nal subdural space is a potential space between the dura and the arachnoid containing a small amount of serous fluid. Unlike the epidural space, the sub-dural 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 tis-sues, muscle, and ligaments it causes varying degrees of tissue trauma. Bruising and a localized inflamma-tory 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 back-ache 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 suf-fice. Although backache is usually benign, it may be an important clinical sign of much more seri-ous complications, such as epidural hematoma and abscess .
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 epi-dural catheter. However, PDPH can follow a seem-ingly uncomplicated epidural anesthetic and may be the result of just the tip of the needle scratching through the dura. Typically, PDPH is bilateral, fron-tal or retroorbital, or occipital and extends into the neck. It may be throbbing or constant and associ-ated 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; how-ever, 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 driv-ing 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 intracra-nial 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 treat-ment 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 prophy-lactic 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 prac-titioners either offer the epidural blood patch when PDPH becomes apparent or allow conservative ther-apy a trial of 12–24 hr.
When evaluating patients with presumed PDPH, other sources of headache, including men-ingeal infection and subarachnoid hemorrhage, should be considered in the differential diagnosis.
Perhaps no complication is more perplexing or distressing than persistent neurological deficits fol-lowing 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 physi-cal 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 blad-der function. Not all neurological deficits occur-ring 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 defi-cits, 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 postanes-thetic cases complicated by concurrent conditions such as atherosclerosis, diabetes mellitus, interver-tebral disk disease, and spinal disorders.
Needle or catheter trauma to epidural veins often causes minor bleeding in the spinal canal, although this usually has no consequences. A clinically sig-nificant 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 coag-ulation either secondary to disease or pharmaco-logical 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, com-pressing neural tissue and causing direct pressure injury and ischemia. The diagnosis and treatment must be accomplished promptly, if permanent neu-rological sequelae are to be avoided. The onset of symptoms is typically more sudden than with epi-dural abscess. Symptoms include sharp back andleg pain with a motor weakness and/or sphincter dysfunction. When hematoma is suspected, neuro-logical 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 decompres-sion within 8–12 hr.
Neuraxial anesthesia should be avoided in patients with coagulopathy, significant thrombo-cytopenia, 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.
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 complica-tion of neuraxial anesthesia, may be infectious or non-infectious. Clinically, it is marked by pain and other neurological symptoms, and, on radiographic imag-ing, 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 chemi-cal 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 dur-ing 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 cath-eters. 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 diag-nosis is made in the early stages. Prognosis has con-sistently been shown to correlate to the degree of neurological dysfunction at the time the diagnosis is made. Back pain and fever after epidural anes-thesia 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 epidermi-dis. MRI or CT scanning should be performed toconfirm or rule out the diagnosis. Early neurosurgi-cal 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) bac-terial 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).
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 with-drawn 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.
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