#30874: Epidural Analgesia Update

In the category of drug advantages, the first benefit is the longer duration of analgesic effect. When administered into the epidural space, 5 mg of morphine has a duration of 6 to 24 hours, compared to three to four hours when given systemically [7]. As a result, patients receiving epidural analgesia require an overall lower total dosage of narcotic than those who receive systemic narcotics via intramuscular (IM) injection, intravenous (IV) injection, or patient-controlled analgesia (PCA) [2,30]. In a study of epidural analgesia in lung transplant patients, patients who received medication via the epidural route had a duration of analgesia of 3.76 days versus 6.0 days in the IV PCA group before oral medications were started [18]. In cancer patients, longer-lasting analgesia without sedation means that patients are more alert, less depressed, more able to resume daily activities when possible, and more likely to be cared for at home [6].

In terms of patient response benefits, improved analgesia has been documented. Epidural narcotics provide more constant pain relief, without the peaks and valleys of serum drug levels associated with parenteral administration [29]. In one comparative analysis, three different epidural drug dosages or combinations were evaluated in patients undergoing thoracic, abdominal, orthopedic, or cardiac surgery for impact on pain intensity scores. Visual analog scale (VAS) pain scores were significantly lower in those receiving epidural fentanyl 5 mg/mL and bupivacaine 1 mg/mL, compared to ropivacaine 2 mg/mL or fentanyl 10 mg/mL and bupivacaine 1 mg/mL [31]. In another study, the probability of a VAS >40 mm was significantly lower in elective postoperative patients receiving epidural (20% probability) versus systemic narcotics (40% probability) [32]. The probability of having moderate-to-severe pain in the first 24-hour period was also significantly less in the epidural group.

The benefit of less sedation is directly related to the smaller narcotic dose required due to the longer duration associated with the epidural route. By remaining at the level of the spinal cord where they are injected, many epidural narcotics do not migrate to higher brain centers via the CSF or systemic circulation. This phenomenon, known as rostral spread, is responsible for the sedation and disorientation commonly associated with systemic narcotics [7]. Lipophilic drugs (e.g., fentanyl) are less likely to result in rostral spread than hydrophilic drugs (e.g., morphine).

Epidural analgesia leads to other clinical improvements and prevention of complications. Improvement in pulmonary function is yet another benefit of epidural analgesia. Patients receiving epidural narcotics experience an earlier improvement in pulmonary function tests (PFTs) when compared to those receiving systemic narcotics [7,33]. In one study of gastroplasty and thoracotomy patients, researchers identified that all patients had decreased PFTs [30]. However, the epidural patients had a less marked decrease in PFTs and returned to their preoperative values two days earlier than the systemic group.

In addition to an earlier restoration of pulmonary function, epidural patients experience fewer pulmonary complications. The incidence of atelectasis and pneumonia may be decreased because patients with more consistent pain control may have an increased ability to participate in pulmonary toilet activities, such as coughing and deep breathing [2,7,33,34]. Secondly, many patients receiving epidural narcotics spend less time on the ventilator and/or have less need for tracheostomy [35]. In one study, lung transplant patients who received epidural analgesia were extubated at an average of 1.46 days after surgery (range: 0.4 to 4.75 days) [23]. Reintubation rates have also been reported to be lower in lung transplant patients who received epidural analgesia (29%) versus IV PCA narcotics (55%) [18]. The reduction of these pulmonary comorbidities is especially significant for the critically ill patient in that gram-negative pneumonias may be associated with a mortality rate ranging from 33% to 70% [34,36].

Epidural narcotics may also decrease the metabolic-stress response associated with surgery and trauma. This response is characterized by an increased release of cortisol, catecholamines, and antidiuretic hormone causing hyperglycemia, sodium and water retention, potassium wasting, and muscle protein breakdown. Epidural narcotics reduce fluid mobilization and retention, the presence of which may further compromise the patient's pulmonary status and lead to respiratory distress and pulmonary edema. This clinical benefit is especially significant for congestive heart failure patients who have undergone upper abdominal surgery [7,34].

Additional studies have investigated the effects of epidural anesthesia on other patient outcomes. In one study on major vascular surgery, researchers found patients who had combined general and epidural anesthesia with postoperative epidural analgesia had significantly lower cardiac morbidity than those patients who only received general anesthesia with postoperative systemic opioid analgesia [37]. Epidural analgesia in high-risk cardiac surgical patients is associated with hemodynamic stability, decreased catecholamine response, good pulmonary function, and early extubation and discharge from intensive care [38]. Evidence of epidural anesthesia's impact on reducing thromboembolic, pulmonary, and gastrointestinal postoperative complications is also encouraging, and it is suggested that epidural anesthesia may be a significant factor in reducing gastrointestinal complications, such as postoperative ileus, in major abdominal surgery patients [39].

Earlier ambulation is the second patient response benefit of the epidural route. In one study of obese patients after upper abdominal surgery, epidural patients ambulated without assistance earlier than IM patients (23 hours versus 30 hours) [30]. Early mobilization may be a significant factor in reducing thromboembolic complications. In combination, improved pulmonary function and earlier mobilization are two of the most significant factors responsible for decreased morbidity and mortality and length of stay (LOS) in patients receiving epidural analgesia. While these findings are encouraging, more research is needed in various populations to compare the impact of epidural versus systemic narcotics on pulmonary complications and ambulation status, as well as on level of alertness and patients' ability to participate in their own care. For instance, in one study, more rapid rehabilitation was not found to be a benefit in elderly total knee replacement surgery patients who received epidural analgesia (compared to PCA) [40]. Additionally, epidural analgesia was not associated with better pain relief or higher patient satisfaction than PCA in this population.

Mixed findings have been reported in relation to LOS. In some studies, epidural analgesia has been associated with shorter hospital stays. In a study of rib fracture patients, those receiving epidural narcotics had a shorter intensive care unit (ICU) stay (6 days versus 18 days) and overall hospital stay (15 days versus 47 days) compared to patients receiving systemic narcotics [35]. In another study of patients undergoing spinal fusion with instrumentation, epidural analgesia with bupivacaine resulted in patients tolerating a full diet earlier and being discharged an average of 0.5 days sooner than the PCA group [41]. On the other hand, McBeath and colleagues found no difference in LOS in total knee or hip replacement patients receiving either continuous epidural morphine or bupivacaine or PCA opioids (morphine or meperidine) [42]. Additionally, a retrospective analysis of more than 1,500 thoracotomy patients showed no difference between LOS in patients receiving epidural analgesia versus systemic opioid-based therapy [43]. Other outcome benefits have been reported. A study of patients with multiple rib fractures found that epidural analgesia was associated with decreased rates of nosocomial pneumonia and shorter durations of mechanical ventilation [44,45]. More studies are warranted to address the impact that epidural analgesia has on the postoperative course, including the ICU and total hospital LOS [7].

Intermittent administration involves injecting a narcotic bolus at a timed interval and may be used with either acute or chronic pain conditions. The major advantage of intermittent injections is that dosing is based on each individual patient's need. Primary disadvantages include inconsistent analgesia and narcotic-related side effects due to redosing intervals and fluctuating narcotic blood levels; changes in respiratory rate and end-tidal carbon dioxide (CO₂) consistent with respiratory depression; and the need for a healthcare provider to administer the dose. The major nursing consideration associated with this route is that iodine-based topical antiseptic solutions should be used to prep the injection port prior to administration. The injection port should not be cleansed with alcohol or other antiseptics as these agents may cause neurotoxicity if they enter the epidural space [7,27].

Continuous infusions deliver epidural drugs at a constant rate by means of an infusion pump, avoiding the peaks and valleys associated with the intermittent technique. This method of administration provides more consistent analgesia due to a constant blood level of the prescribed opioid and also allows a lower total volume of drug to be infused at one time. As a result, fewer side effects, such as respiratory depression, occur with continuous infusions. In addition, the rate of the infusion may be titrated to the patient's response, providing the optimal level of analgesia. The major disadvantage of this route is reliance on an infusion pump and the potential for equipment malfunction [7].

PCA is another option for delivering a fixed rate of epidural narcotics. The major advantage of the PCA route is that the patient may administer additional bolus doses above and beyond the basal rate on an as needed basis. Therefore, this route gives the patient some control to alleviate their pain, especially when sudden increases in pain are experienced [6,7]. PCA has been shown to be both safe and efficacious in appropriately chosen adults, adolescents, and children, and many studies have shown that patients prefer this method of analgesia over intermittent injections [50,53,54].

Implantable ports or infusion pumps are the last option for delivering epidural narcotics. Implantable devices are used for patients requiring long-term pain management, such as oncology populations. With implantable ports, the epidural catheter is surgically placed at the indicated interspace and then tunneled subcutaneously around the patient's trunk. The catheter exits on an accessible location of the abdomen so the injection port can be accessed for either intermittent or continuous infusions [6]. Nonprogrammable fixed-rate infusion pumps deliver a predetermined constant rate of infusion and allow for a change in the dose by changing the drug concentration in the reservoir. Programmable pumps (i.e., variable delivery rate pumps) allow for alterations to the dose, single doses, timed-specific doses, or changes in the continuous infusion rate [8].

Implantable ports consist of an implantable silicone catheter (sized from 4–12 F), and an implantable titanium or silicone port with a self-sealing rubber septum. This port contains an internal reservoir that can be repeatedly accessed by injection with a 90-degree non-coring needle. These needles vary from ½ to ¾ inches, and the appropriate needle length should be chosen based on the patient's size and the depth of the port. The needle should first be connected to extension tubing and flushed with 5 cc of normal saline. Using sterile technique, the site should be cleansed from the center of the port outward 2–3 inches in a circular motion first using alcohol, then followed with an iodine-based antiseptic. Accessing the port is done by stabilizing it between the thumb and index finger of the non-dominant hand. Using the other hand, the needle is inserted perpendicular to the center of the port. The needle should be pushed firmly through the patient's skin and portal septum until it hits the bottom of the platform. Once in the portal body, aspirate for blood; if positive, flush with 10 cc of normal saline. When ready for epidural analgesia, connect the infusion to the extension set and stabilize the needle in the port by covering with an occlusive dressing. To discontinue the infusion, keep the port stabilized between the thumb and index finger, hold needle firmly, and withdraw using even pressure [55,56,57].

It has been a customary nursing practice to cleanse the portal body with povidone-iodine-based solutions prior to accessing the port. This practice is done to disinfect the port and minimize the patient's risk of infection. One study investigated this practice and questioned whether or not a trace amount of povidone-iodine solution could pose some risk for toxicity, especially if the solution were systemically absorbed. In this study, three different techniques were compared: commercially available 10% povidone-iodine swabsticks, commercially available 10% povidone-iodine pledgets, and 4-inch square gauze pads saturated with 10% povidone-iodine solution. A significant difference was found with the three cleansing techniques, and the 10% povidone-iodine pledget introduced the least iodine contamination. The findings of this study are considered preliminary, and more research is needed before nurses routinely abandon the practice of using povidone-iodine for disinfection [19,58,59].

Infusion pumps may also be implanted into a subcutaneous pocket of the abdomen to administer continuous epidural infusions [7]. Both options require surgery and carry a potential for infection. Patients who are likely candidates for implantable ports or infusion pumps include those whose life expectancy is greater than a few months with pain below the mid-cervical dermatome that has been unsuccessfully treated with aggressive analgesics and is inappropriate for neurosurgical procedures [6]. Patient/family teaching for these patients should include an explanation of the procedure in terms the patient can understand, expectations for postoperative pain or discomfort and self-care responsibilities, medication preparation, the procedure for injection, assessing the exit site and tunnel area for signs and symptoms of infection, catheter care and dressing changes, refill schedules and procedures, obtaining supplies and narcotics, and follow-up care [9,27].

The most serious narcotic-related side effect associated with epidural analgesia is respiratory depression. It is manifested by a decrease in the depth of respirations or tidal volume, followed later by a decrease in respiratory rate. Initially, the patient may be able to maintain an adequate respiratory rate but the hyperventilation that occurs does not allow adequate oxygen CO₂ exchange. This impaired gas exchange leads to mental status changes indicative of increasing CO₂ levels. Therefore, a decrease in the patient's LOC or arousability is considered the first and the best indicator of respiratory depression [5]. Any changes in mentation, such as sedation or confusion, should be considered indicators of hypoxia and/or hypercarbia until ruled out by arterial blood gas levels. As discussed, frequent assessment of the patient's level of sedation is important for early detection and treatment [2]. Several factors place patients at greater risk for the development of respiratory depression (Table 4). Respiratory depression is rarely seen in chronic pain patients because many of these patients have developed a tolerance from previous narcotic administration [6].

Early-Onset Respiratory Depression

The incidence of early-onset respiratory depression is estimated to be less than 1%. It generally occurs within one to two hours of administration and is due to vascular uptake of the opioids from the epidural space. In other words, the narcotic is absorbed by the epidural veins into the systemic circulation. A second mechanism may be the rapid achievement of narcotic concentrations in the brain via the internal vertebral venous system [2,27,46,73].

Delayed-Onset Respiratory Depression

Delayed-onset respiratory depression is relatively uncommon, with an estimated incidence ranging from 0.3% to 5%. With an insidious onset, its peak incidence is 6 to 12 hours after the initial dose; however, it can occur up to 24 hours after administration of the last dose. Delayed-onset respiratory depression related to the lipid and water solubility of the opioids is caused by cephalad diffusion of the narcotic in the CSF to the fourth ventricle, where agonism with opioid receptors of central respiratory centers occurs. Peak CSF concentrations usually occur within five hours [2,27,46].

Because morphine is highly water soluble, it rapidly diffuses cephalad in the CSF via rostral spread. As a result, delayed-onset respiratory depression is more common with morphine. In contrast, fentanyl is highly lipid soluble with greater uptake by the spinal cord. Limited diffusion occurs into the CSF, and thus, respiratory depression in these patients is unlikely [2,5].

Treatment

The first step in managing patients with respiratory depression is withholding additional narcotic boluses or stopping the continuous epidural infusion. The patient should be placed on supplemental oxygen and arterial blood gases obtained. Naloxone, a narcotic antagonist, is also indicated to reverse the respiratory depressant effects, generally for respiratory rates less than eight breaths per minute. The goal of this treatment is to reverse the undesirable side effect while maintaining the beneficial analgesic effects. Naloxone is supplied in 0.4 mg/mL vials. The vial may be diluted with 9 mL of preservative-free normal saline to obtain a 0.04 mg/mL concentration. Small doses, ranging from 0.04–0.4 mg, are repeated (up to a maximum of 0.8 mg) until the desired effect is achieved [47].

After the initial dose, the patient should be continually assessed for the need for additional treatment. Because naloxone has a much shorter half-life (approximately 30 minutes) than narcotics (especially epidural narcotics), repeated administration by either bolus or an infusion may be needed to maintain sufficient plasma levels and reverse the respiratory depressant effects. Naloxone must be titrated slowly, as rapid narcotic reversal may result in hypertension, cardiac dysrhythmias, pulmonary edema, and cardiac arrest due to pain-induced activation of the sympathetic nervous system. Other causes of respiratory depression should be considered if improvement is not achieved with this treatment [47]. The return of pain is possible with naloxone administration, and it is important to review alternative pain management strategies with the patient because additional narcotic doses are not immediately advised [46].

Hypotension is a second potential narcotic-related side effect of epidural analgesia. However, as epidural narcotics have a localized action and do not produce sympathetic nervous system blockade, they generally have little effect on blood pressure. Therefore, if a patient who has received epidural narcotics becomes hypotensive, consider other more common etiologies. The hypotensive state may be a result of fluid volume changes or immobility postoperatively, in which case IV fluids are indicated [7,46]. More rarely, hypotension may be due to allergic reactions, ranging from mild urticaria to cardiovascular collapse. Treatment is determined by the severity of the reaction, from antihistamines to vasopressor support such as IV epinephrine. Other interventions to maintain airway, breathing, and circulation are indicated as needed [7].

Local anesthetics are not specific to sensory afferent fibers, and they do block autonomic and motor efferent fibers. This sympathetic blockade can lead to hypotension and exacerbate or intensify postural hypotension due to hypovolemia. As a result, postural hypotension may restrict early ambulation and potentially increase morbidity. Therefore, assessment of the patient's motor strength prior to ambulation is critical [5,74]. Additionally, assistance with ambulation should be provided to ensure patient safety. Olson and colleagues identified several risk factors for postoperative hypotension in total knee arthroplasty patients who received epidural analgesics/anesthetics [75]. These risk factors included the use of preoperative diuretics, low diastolic blood pressure in the post-anesthesia unit, low postoperative systolic blood pressure on the day of surgery, total fluid intake first postoperative day, and low hemoglobin the third postoperative day. Assessment of these parameters in this population is important in the surveillance of postoperative epidural analgesia.

Pruritus is the most frequently reported narcotic-related side effect of epidural analgesia. The incidence ranges from 28% to 100%, occurring with both acute and chronic administration [2]. Pruritus tends to increase during pregnancy and with co-administration of steroids. The greater intensity of pruritus with epidural narcotics may occur from altered cutaneous sensation or from the effect of the narcotic on the central mechanism located in the medulla [46]. While pruritus is not dose-related, it may continue for the duration of the narcotics' effect. However, some reports identify that pruritus may abate in 48 to 72 hours in patients receiving continuous morphine administration [6,7].

Itching may be local or generalized on the face (especially the nose and palate), trunk, and legs. It may mimic an allergic reaction with a rash, wheals, or edema. An increase in body temperature may also be an exacerbating factor. Treatment is symptomatic, and patients may respond to antihistamines such as 25–50 mg diphenhydramine IM/IV every six to eight hours or 25 mg hydroxyzine IM. In some cases, pruritus may be severe enough to warrant the administration of naloxone titrated to relief. The standard dose of IV naloxone ranges from 0.04–0.4 mg for the treatment of narcotic-related side effects [47].

With an estimated incidence of 17% to 35%, nausea and vomiting may occur as the opioid diffuses from the site of the epidural injection to the chemoreceptor trigger zone for vomiting located in the 4th ventricle [2,46]. This side effect usually occurs four to six hours after administration and may be associated with activity, such as turning and coughing [7]. As with hypotension, searching for other causes of nausea and vomiting, such as abdominal distention or pain, should be attempted first.

Treatment is symptomatic with antiemetics such as prochlorperazine (2.5–10 mg every three to four hours IV, or 5–10 mg every three to four hours IM), metoclopramide (10–20 mg IV, IM), or droperidol (0.625–1.25 mg IV) [47]. However, use extreme caution with the concurrent administration of droperidol (maximum initial dose: 2.5 mg). Droperidol relieves nausea but may potentiate the respiratory depressant effects of epidural narcotics, as may other sedating medications, including midazolam, systemic narcotics, antihistamines, and psychotropics [47]. Small doses of naloxone may also be effective in reducing nausea and vomiting without interrupting analgesia [46].

Urinary retention is another frequently occurring narcotic-related side effect. With an incidence between 22% and 100%, it is the only narcotic-related side effect that does not appear to be dose-dependent [2,76]. It usually occurs in the first 24 to 48 hours and then resolves spontaneously. Signs and symptoms include a lack of urge to void and bladder distention. The underlying mechanism may be the action of the narcotic on the spinal nerves innervating the detrusor muscle, thereby altering bladder tone (atonia) and predisposing to bladder over distension and increased residual volumes [76]. For unknown reasons, urinary retention occurs more often in elderly men, patients with pre-existing bladder disorders, and during pregnancy and the postoperative period. A study of patients after total knee arthroplasty found that use of epidural analgesia was a significant predictor of urinary retention [77]. Urinary retention may lead to urinary tract infections, which in turn can cause hematogenous seeding and infection of the postoperative joint [6,46].

Nursing management involves monitoring intake and output and assessing for bladder distention. Many centers insert an indwelling Foley catheter for the duration that the epidural catheter remains in place. If a Foley catheter is not used, intermittent catheterization may be necessary. However, catheterization in some populations, like total knee arthroplasty, may in fact further increase the risk of infection [77]. The administration of bethanechol or 0.04–0.4 mg naloxone IV may also help reduce the occurrence of this side effect [46,47].

Although epidural catheters are small and the resistance to injection is high, patients may feel the expansion of the epidural space and/or the cooler temperature of the medication. Pain on injection is usually felt at the site where the catheter empties into the epidural space and is most often caused by injecting the medication too quickly. As it may also indicate infection or a misplaced catheter, full assessment of catheter placement by the physician is warranted when there is pain on injection [46].

Postdural puncture headache, caused by epidural catheter placement, has an incidence ranging from less than 1% to 70%, depending on the needle used (size and type), procedure, and age and sex of the patient. Incidence has been found to be inversely related to the experience of the anesthetist [78]. Postdural puncture headache occurs more often in adults younger than 40 years of age, and men are affected twice as often as women [2,79]. Commonly, the headache occurs within 48 hours of the puncture and lasts from days to weeks [78]. Dural puncture may be intentional, as with intrathecal catheter placement, or accidental during epidural insertion, causing CSF to leak from the intrathecal space through the puncture hole and resulting in a decrease in CSF volume and intracranial pressure.

The use of smaller, blunt-ended needles has been shown to minimize the size of the dural opening and speed closure of the puncture [2]. One study found that use of the smallest gauge needles (of all styles) drops incidence rates of postdural puncture headache consistently below 4% in procedures not intended to pierce the dura [78]. Another study compared the force required for puncture associated with various needle designs and gauges in samples of bovine dura and found that, among needles of the same gauge, there was a significant variation in the amount of required force and CSF leakage based on design [80]. For example, pencil-point style needles required greater penetrating force and caused significantly less leakage than same gauge Quincke needles; however, for all styles, the smaller gauges resulted in less CSF loss upon puncture. More recent studies report that pencil-point needles are superior to cutting needles at reducing the occurrence of postdural headache, headache severity, and the need for epidural blood patches to seal the puncture [81,82].

The resultant headache is postural in nature, exacerbated by an upright position (such as standing), coughing, or shaking the head and is relieved by lying flat. It is the result of stretch and tension on pain-sensitive intracranial vessels, nerves, and tentorium when the upright position is assumed. The headache is described as dull or throbbing, occurring in the frontal or occipital regions. Other signs and symptoms that are often associated include nausea and vomiting, diplopia, photophobia, tinnitus, and diminished hearing. Conservative management includes bedrest, hydration (which helps the production of CSF), analgesics and antiemetics, and use of an abdominal binder. An autologous epidural blood patch may also be utilized to seal the dural puncture and prevent further leakage of CSF. With this technique, 10 cc of the patient's blood is removed from a peripheral vein and injected through an epidural needle at the location of the dural puncture. The patient's blood migrates and forms a venous clot to seal the dural puncture and stop the CSF leak. The blood patch has a success rate of 89% to 95% and is associated with few complications in low-risk (i.e., not immunocompromised) patients [7,79].

As with any indwelling percutaneous and tunneled catheter, there is the risk of superficial or deep skin and soft tissue infection with epidural analgesia, a risk that varies directly with the length of time the catheter is left in place. Careful aseptic insertion technique with a minimum of trauma, good skin surface and dressing management, and regular inspection of the catheter site for signs of inflammation are each important in minimizing the risk of infection.

Bacterial colonization of the subcutaneous catheter tract and tip is thought to be a major precursor to clinical infection. The rate of epidural catheter colonization has been assessed prospectively in 205 patients receiving short-term postoperative analgesia [83]. In one study of cultures obtained at the time of catheter removal, the rate of colonization of the subcutaneous and tip segments of the catheter was 10.5% and 12.2%, respectively. Skin flora, such as coagulase-negative staphylococci (CoNS), accounted for the majority of isolates. Eleven patients had positive catheter tip cultures: seven CoNS, one Staphylococcus aureus, one Enterococcus, and one Acinetobacter; all had the same organism isolated in large numbers from the adjacent skin and catheter segment sites. Identified risk factors for bacterial colonization of the catheter were adverse catheter site events (e.g., accidental hub disconnection, damage to dressing), adjacent skin colonization, and blood transfusion. The authors concluded that strict aseptic technique at catheter placement and careful attention to maintenance of skin sterility adjacent to the site should reduce rates of catheter tip colonization and decrease the incidence of catheter-related infection [83].

Epidural catheter-associated infections are of two types: superficial (skin and soft tissue) and deep (meninges, epidural space). In one review, the incidence of superficial infection was 4.3%, while reported deep infection rates were much less frequent, ranging from 0% to 0.7% [23]. Common mechanisms of infection include contamination of the exit site and spread along the catheter tract, contamination during needle or catheter insertion, hematogenous seeding from a distant focus of infection, and intraluminal spread via contaminated epidural infusion solutions. Difficult catheter insertions that result in undue trauma at the level of the dura may play a role in the development of epidural space infection. The incidence of infection appears to vary with the site of catheter placement, as one report found that the risk of infection was highest with thoracic epidural catheter usage [23]. One retrospective analysis found that tunneling of thoracic epidural catheters is associated with a lower risk of catheter-related infections [84]. Early local signs of catheter-site infection are erythema, warmth, tenderness, subcutaneous induration, and drainage from the catheter tract [7].

Epidural Abscess or Hematoma

The development of an epidural abscess or hematoma deep to the catheter site is a rare yet potentially serious complication. Bleeding into the epidermal space, from catheter placement trauma or erosion of an epidural venule or arteriole, tends to occur early after catheter insertion and is extremely rare unless the patient has a coagulopathy (e.g., thrombocytopenia, clotting factor deficiency, anticoagulant therapy). As indicated, the incidence of epidural abscess is less than 1% [23].

While rare, epidural hematoma and abscess are potentially life-threatening complications. Clinically, both present as a mass effect: localized pain, swelling or tenderness at the catheter site, radiculopathy, and other spinal cord compression signs [7]. Compression of sensory and motor neural elements in and about the spinal cord results in a variety of neurologic deficits. These include heaviness, numbness and tingling, lancinating pain, and loss of motor function below the affected level (e.g., lower extremities with lumbar catheters). Therefore, the patient's neurologic status should be assessed at least every four hours, including degree of back discomfort, motor strength, and sensory level. The physician should be notified if the patient reports new or unexpected degree of back pain, experiences a change in sensation, or is found to have loss of sensation or diminished motor strength in the extremities. Careful neurologic examination and consideration of magnetic resonance imaging should follow [7,23].

Occlusion of the epidural catheter may be due to various causes. The most common causes include the development of a blood or fatty clot within the catheter, contact of the tip of the catheter against an epidural vein, or kinking of the catheter [7]. Some epidural catheters are virtually kink-resistant due to the coil housed within the lumen of the catheter. If the epidural catheter does become occluded, the patient will not receive analgesia and will complain of returning pain [7]. In this situation, reassessment of catheter patency and placement is warranted.

After the epidural catheter is placed and the needle is removed, it is unlikely that the catheter will migrate and penetrate the dura. While dural puncture most often occurs during placement, the catheter must always be aspirated to verify correct placement prior to administering an epidural narcotic. The catheter dressing should also be assessed routinely to confirm that it is dry and intact. If the dressing is wet and catheter migration is suspected, notify the physician [7].

If the epidural catheter does migrate, a larger amount of narcotic may enter the CSF. With increased analgesia, the patient has a greater risk of respiratory depression, cardiovascular collapse, and neurologic changes, such as altered LOC, seizures, and paresthesias [7]. In these situations, the narcotic should be withheld until catheter placement can be reassessed and alternative routes for the administration of analgesics should be selected.

If the patient is receiving local anesthetics and the epidural catheter migrates into the subarachnoid space, these agents can infuse directly into the CSF and cause the level of blockade to rise. This blockade may affect the respiratory muscles. In addition, local anesthetic toxicity may occur when serum concentrations of the drug elevate. Signs of symptoms of toxicity include tinnitus, visual disturbances, and seizures [5].

Another rare catheter-related complication is shearing or breakage of the epidural catheter. This complication most often occurs during insertion or removal of the catheter. Shearing can be avoided by taping and stabilizing the catheter securely after insertion. Avoid bending the catheter. Again, if the dressing is wet or the catheter is leaking fluid, notify the physician [7]. If the catheter breaks off, the tip is generally not removed as these catheters are nontoxic and non-allergenic. If neurologic sequelae or infection develops, the catheter tip is retrieved surgically [4].