Epidural Analgesia -A Self-Directed Learning Module 3rd

Epidural Analgesia

U N I V E R S I T Y O F W I S C O NU N I V E R S I T Y O F W I S C O NU N I V E R S I T Y O F W I S C O NU N I V E R S I T Y O F W I S C O N S I NS I NS I NS I N

H O S P I T A L A N D C L I N I C SH O S P I T A L A N D C L I N I C SH O S P I T A L A N D C L I N I C SH O S P I T A L A N D C L I N I C S

M A D I S O N , W IM A D I S O N , W IM A D I S O N , W IM A D I S O N , W I

Copyright , 2000, UW Hospital and Clinics Authority Board

A Self-Directed Learning Module Third Edition

Perission granted to modify or adopt provided written credit given to University of Wisconsin Hospital &

Clinics Copyright 2000 UWHC Authority Board

TABLE OF CONTENTS

I. Introduction 2 II. Content

Section 1 4 Benefits, Indications, and Contraindications Section 2 7 Pain Transmission / Modulation Section 3 9 The Epidural Space Section 4 11 Epidural Catheter Placement Section 5 13 Common Opioids and Local Anesthetics Section 6 17 Nursing Assessment, Documentation, and Management of Side Effects and Complications Section 7 22 Patient / Family Teaching Section 8 23 AP II Pump

III. Post-test 24 IV. References 28

First Authored 1997 by:

Susan L. Schroeder, RN, MS Clinical Nurse Specialist Department of Nursing

1 Permission granted to modify or adopt provided written credit given to University of Wisconsin

Hospital & Clinics Copyright 2000 UWHC Authority Board

UW Hospital and Clinics, Madison, WI

Revised 2000 by: Deb Gordon, RN, MS

Clinical Nurse Specialist Department of Nursing

UW Hospital and Clinics, Madison, WI

Sue Deeren RN, MS, NP Clinical Nurse Specialist

Department of Anesthesiology University of Wisconsin, Madison, WI

Michael Ford, MD

Assistant Professor Department of Anesthesiology

University of Wisconsin, Madison, WI

Mark Schroeder, MD Associate Professor

Department of Anesthesiology University of Wisconsin, Madison, WI

Produced by the Department of Nursing Resources and Development 3rd Ed, Copyright 2000 UW Board of Authority



INTRODUCTION Analgesia is now recognized as a significant contributor to clinical outcomes (1). The goal for pain management is to provide the best analgesia with the least amount of side effects. Epidural analgesia is a desirable method of pain relief because it provides true segmental analgesia with little or no contribution from systemic levels of opioids (2). All of which may lead to excellent analgesia with minimal side effects (2,3). Caring for patients who receive epidural analgesia requires specialized knowledge regarding the placement of the epidural catheter, management of the therapy, and monitoring for potential side effects/complications (1,3,4,5,6). This self-directed learning module is essential information for the nurse clinician who cares for patients receiving epidural analgesia.

After the completion of this self-directed learning module, nurse clinicians will be able to:

o Identify the benefits, indications and contraindications for

epidural analgesia. o Explain the transmission and modulation of pain stimuli as

related to epidural analgesia. o Identify the spinal cord anatomy as related to the placement of

the epidural catheter. o List the common medications used for epidural analgesia. o Identify potential complications from epidural analgesia, the

required monitoring of patients receiving epidural analgesia, and the specific actions to be taken if a complication occurs.

o Recognize common side effects from epidural analgesia, and list

appropriate actions to be taken in the management of these side effects.

o Describe required nursing assessment and documentation as related

to epidural analgesia. o Perform appropriate patient/family teaching for those patients

receiving epidural analgesia. o Demonstrate the programming and use of the Baxter AP II infusion

Pump.



Prior to completing the self-directed learning module:

o Review : 1. Nursing Policy & Procedure 6.13 Epidural and

Intrathecal Analgesia 2. AP II Programming Guide and/or Baxter AP II video o Attend AP II Pump Inservice Other recommended resources to review (available through Nursing Staff Development, 263-6490): de Leon-Casasola, O., Karabella, D., & Lema, M. (1996) Bowel function recovery after radical hysterectomies: Thoracic epidural bupivacaine-morphine versus intravenous patient-controlled analgesia with morphine: A pilot study. Journal of Clinical Anesthesia, 8, 87-92. Liu S, Carpenter RL, Neal JM. (1995). Epidural anesthesia and analgesia: their role in postoperative outcome. Anesthesiology 82(6) 1474-1506. Naber, L., Jones, G. & Halm, M. (1994). Epidural analgesia for effective pain control. Critical Care Nurse, October, 69-83. Pasero C. (1998). Epidural Analgesia For Acute Pain Management. American Society of Pain Management Nurses self directed learning program. ASPMN, Pensacola, FL. Pasero C, McCaffery M. (1999). Providing epidural analgesia: how to maintain a delicate balance. Nursing, August, 34-40.

Instructions for use of the self-directed learning module are:

1. Read the content material. 2. Complete the post-test. 3. Perform return demonstration on the use and programming of the AP

II pump to: Deb Gordon, RN, CNS, Nursing Staff Development Kathy Hansen, RN, CNS, Nursing Staff Development Sue Deeren, RN, NP, Anesthesiology Pain Resource Nurse on your Unit

o o • • • For clarification or questions regarding this self-directed learning module, please contact: Deb Gordon, RN, CNS, Nursing Staff Development 263-6488, or pager #7253



BENEFITS, INDICATIONS, AND CONTRAINDICATIONS

Section 1

1.1 BENEFITS Epidural analgesia provides very effective, prolonged segmental analgesia (3). Smaller doses of opioids can be used in the epidural route than systemic routes (parenteral or oral) since the opioid is administered more directly to the spinal opioid receptors. The smaller epidural dose of opioids decreases the potential for opioid-related side effects (3,6). In addition to opioids, local anesthetics can be administered epidurally in order to produce a neural blockade that provides analgesia. Local anesthetics and opioids can be used in combination, and are believed to act synergistically. This combination allows the concentration of local anesthetics and dose of opioids to be decreased. The following benefits have been found with epidural analgesia: o excellent analgesia(2,3,6,7) o less sedation (7) o earlier ambulation (8) o decreased incidence of pulmonary complications (7,8,9) o decreased incidence of venous thrombosis (9) o earlier return of bowel function (8,10) o decreased stress response (7) 1.2 INDICATIONS FOR EPIDURAL ANALGESIA o Post-operative pain management (3,4,5,6,11) Epidural analgesia appears to be most beneficial for the high-

risk surgical patient or for those recovering from extremely large or painful surgical procedures. Such procedures include thoracotomies, major upper abdominal, major abdominal vascular, and orthopedic surgeries. The epidural infusion provides a localized band of analgesia at the site of the incision.

o Multiple trauma (3,4,6) Epidural analgesia is especially beneficial for patients with

chest trauma, i.e.: rib fractures. The localized analgesia helps the patient overcome the pain induced splinting that contributes to the loss of pulmonary function which in turn may lead to atelectasis and pneumonia.

o Chronic pain (5,6,12) Epidural analgesia can be used in the treatment of patients

experiencing an acute exacerbation of Complex Regional Pain Syndrome (CRPS) by producing a sympathetic blockade using a local anesthetic. This provides improved analgesia, and allows the patient to participate in physical therapy which is vital in the control of their symptoms. Epidural analgesia may also be used for the treatment of other types of chronic pain such as cancer pain.



1.3 CONTRAINDICATIONS TO EPIDURAL ANALGESIA Epidural analgesia is contraindicated in the presence of: o Anticoagulation therapy (3,4,5,6,13,14)- *Note: see summary ASRA consensus

statement14 next page Anticoagulation therapy and neuraxial anesthesia used together

increase the risk of epidural hematoma which may lead to serious adverse effects such as permanent paralysis. Anticoagulation therapy should not be initiated or changed without first advising the Acute Pain Service.

o Coagulopathies (1,4,5,6,13,14) Patients experiencing coagulopathies are at an increased risk for

an epidural hematoma. o Decreased level of consciousness (13) Epidural analgesia may be implicated in any progression of

central nervous system dysfunction. Also pain management by epidural analgesia requires accurate reports of pain levels by patient.

o Systemic infection (4,5,6,13) Systemic infection or sepsis may lead to an infection in the

epidural space. o A localized infection at the insertion site of the epidural

catheter (4,5,6,13) A localized infection at the site of insertion may lead also to

an infection in the epidural space. o Increased intracranial pressure (6) An inadvertent dural puncture when trying to locate the epidural

space in a patient with increased intracranial pressure, increases the chance of cerebellar or tentorial herniation due to the loss of CSF.

o Lack of qualified nursing care to monitor patients for side

effects and complications (1,4,5,6,15) Epidural analgesia should only be used in hospital units where

the staff has received adequate training. Staff should be knowledgeable concerning epidural catheter placement, epidural medications, and the possible side effects and complications from epidural analgesia.



*SUMMARY OF THE AMERICAN SOCIETY OF REGIONAL ANESTHESIA'S CONSENSUS STATEMENTS ON NEUAXIAL ANESTHESIA AND ANTICOAGULATION14

ORAL ANTICOAGULANTS For patients on chronic oral anticoagulation, the anticoagulant therapy must be stopped and the prothrombin time (INR) measured prior to initiation of neuraxial block. The concurrent use of medications that affect other components of the clotting mechanisms may increase the risk of bleeding complications for patients receiving oral anticoagulants, and do so without influencing the prothrombin time and INR. These medications include aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), antiplatelet drugs, and heparin. Neurological testing of sensory and motor function should be performed routinely during epidural analgesia for patients on warfarin therapy. These checks should be continued after catheter removal for at least 24 hours, and longer if the INR was >1.5 at the time of catheter removal. ANTIPLATELET DRUGS Antiplatelet drugs, by themselves, appear to represent no added significant risk for the development of spinal hematoma in patients having epidural or spinal anesthesia. At this time, there do not seem to be specific concerns as to the timing of a single shot or catheter technique in relationship to the dosing of NSAIDs, postoperative monitoring, or timing of the neuraxial catheter removal. FIBRINOLYTIC AND THROMBOLYTIC DRUGS Patients receiving concurrent heparin with fibrinolytic and thrombolytic drugs are at high risk of adverse neuraxial bleeding during spinal or epidural anesthesia and should be cautioned against receiving spinal or epidural anesthetics except in highly unusual circumstances. If used, neurologic monitoring should be performed at least every 2 hours or more frequently, and the infusion should be limited to drugs minimizing sensory and motor blockade. STANDARD HEPARIN Subcutaneous (mini-dose) prophylaxis is not considered a contraindication to using neuraxial techniques. The risk of neuraxial bleeding may be reduced by delaying the heparin injection until at least one hour after the block or catheter placement. The catheter should be removed 1 hour before any subsequent heparin administration or 2-4 hours after the last heparin dose. Prolonged therapeutic anticoagulation appears to increase the risk of spinal hematoma formation, especially if combined with other anticoagulants or thrombolytics and neuraxial blocks should be avoided in this clinical setting. LOW MOLECULAR WEIGHT HEPARIN LMWH increases the risk of spinal hematoma. The decision to perform a neuraxial block must be made on an individual basis and if performed extreme vigilance of the patient's neurologic status is warranted. A single-dose spinal anesthetic may be the safest neuraxial technique and needle placement should occur at least 10-12 hours after a dose of LMWH. Patients receiving higher doses of LMWH (e.g. enoxaparin 1mg/kg twice daily) will require longer delays (24 hours). Neuraxial techniques should be avoided in patients administered a dose of LMWH two hours preoperatively (general surgery patients), since needle placement occurs during peak anticoagulant therapy. It is recommended that indwelling catheters be removed prior to initiation of LMWH. Timing of catheter removal is of paramount importance and should be delayed for at least 10-12 hours after a dose of LMWH. Subsequent doses of LMWH should be administered at least 2 hours or longer after catheter removal.



PAIN TRANSMISSION MODULATION OF PAIN

Section 2

Definition of terms: Pain: An unpleasant sensory and emotional experience associated with the actual or potential tissue damage. Afferent Nerve: A nerve that transmits impulses from the periphery toward the central nervous system. Analgesia: Pain relief, the absence of pain in response to a stimulus that normally would be painful. Noxious stimulus: A stimulus that is damaging or potentially damaging to body tissue. Nociceptor: A nerve receptor that is preferentially sensitive to noxious or potentially noxious stimuli. Nociception: The process of encoding a painful sensation. Modulation: The process whereby nociceptive transmission is modified through a number of influences (16,17).

o o • • The body’s response to pain is protective in nature. Pain is a warning signal to which the body responds to prevent further injury. Noxious substances which are released in response to damaged tissue initiate the nociceptive transmission. Afferent nerve fibers respond to the nociceptive stimuli peripherally, and relay this information to the spinal cord. Most of the nociceptive input enters the spinal cord through the dorsal horn (16,17,18). In the dorsal horn, nociceptive neurotransmittors are released in response to the nociceptive input which activate the second-order dorsal horn neurons. The activation of the second order neurons results in: 1) spinal reflex responses such as acute vasoconstriction, muscle spasms, and increased sensitization of nociceptors; and 2) activation of the ascending tracts which transmits the nociceptive input to several regions within the brain (16,18). This is where several responses to pain occur including the perception of pain, and the emotional and behavioral responses.



The modulation of nociceptive input occurs at several sites including the opioid receptors located in the dorsal horn, and at opioid receptors located supraspinally in such areas as the cortex, hypothalamus and periaqueductal area. Neuropeptides such as enkephalin molecules (endogenous opioids) bind with the opioid receptors to modulate nociceptive input. Exogenous (administered) opioids work in a similar fashion. These opioid receptors provide the means by which spinal opioids are able to modulate pain transmission (18,19). (See diagram 1)



THE EPIDURAL SPACE

Section 3 The epidural space is a ‘potential space’ that contains fatty tissue and blood vessels; and is located between the bony vertebral canal and the outer surface of the dura mater. Moving towards the spinal cord from the epidural space are the membranes or meninges that cover the spinal cord. They are: 1) the dura mater; 2) the arachnoid mater; and 3) the pia mater which adheres tightly to the spinal cord and brain. The subarachnoid space is the area that lies between the arachnoid and pia mater, and contains the cerebral spinal fluid (CSF) (20,21). The vertebral column is stabilized by ligaments. The ligamentum flavum is the structure through which the epidural needle and catheter must pass when being inserted to reach the epidural space (2). (See Diagrams 2 & 3) The epidural space contains fat which surrounds and pads the spinal cord. This fat functions as a ‘depot’ for opioids and local anesthetics when these medications are administered for epidural analgesia (4,13). Opioids administered into the epidural space diffuse across the meninges and CSF to receptors in the dorsal horn of the spinal cord.





EPIDURAL CATHETER PLACEMENT

Section 4 A dermatome is the area of skin and soft tissue that is innervated by a single spinal nerve root. (See diagram 4) The epidural catheter is placed in a centrally located interspace so that all of the affected dermatomes would receive the benefits of the infusion (22,23). Under aseptic conditions, the epidural catheter is placed by a physician with the patient in the sitting or lateral fetal position. Proper placement of the catheter is verified by the physician through aspiration of the catheter and a small test dose of a local anesthetic. Once proper placement of the catheter is confirmed, the catheter is secured with tape and an occlusive, transparent dressing. The extra length of the catheter is then brought up over the shoulder, and secured with tape along its length. A .22 micron filter is attached between the catheter and the infusion tubing. The catheter and tubing should be clearly labeled as ‘EPIDURAL CATHETER’ (3,6,13).



Epidural catheters may be placed either in the thoracic, lumbar, or caudal spaces. Most often thoracic catheters are placed for the management of upper abdominal and thoracic sites of pain. However lumbar catheters may also be placed for these sites. Lumbar and caudal catheters are generally used for lower abdominal or lower extremity sites (22,23). If lumbar catheters are placed for upper abdominal or thoracic sites, a larger dose/volume of opioid may be needed. (See Diagram 5)



COMMON OPIOIDS AND LOCAL ANESTHETICS

Section 5

5.1 EPIDURAL OPIOIDS o Onset and duration of analgesia A spinal opioid’s ability to dissolve in fat (lipid solubility) influences its onset and duration of action. Lipophilic opioids such as fentanyl, easily penetrate the dura/arachnoid membranes and the spinal tissue, thus having a rapid onset of action. Unlike systemically administered opioids, drug metabolism does not influence the spinal opioids’ duration of action. The principle routes of clearance of epidurally administered opioids are through rapid vascular absorption or through slow rostral diffusion in the CSF with elimination at the arachnoid granulations. Thus, lipophilic opioids have a rapid onset of action but a limited duration (2,3,13,24). Meperidine, an intermediate lipophilic opioid, has a moderate onset of action and duration. Caution must be used with prolonged or high doses of meperidine, or with use in the elderly or patients with impaired renal or hepatic function. Meperidine is metabolized in the liver to normeperidine, a CNS neurotoxic metabolite which can produce irritability, tremors, agitation, myoclonus, and convulsions (25). Generally though, epidural meperidine infusions are at low doses and normeperidine toxicity is not a problem. Hydrophilic drugs (water soluble), such as morphine and hydromorphone, have difficulty penetrating the membranes, and diffuse more slowly. Therefore the onset of pain relief is slower. Hydrophilic opioids tend to accumulate in the CSF, and are transported rostrally to higher spinal levels eventually being eliminated at the arachnoid granulations. Since hydrophilic opioids have a greater ability for dermatomal spread than the lipophilic, this enables them to provide analgesia for larger areas. Conversely lipophilic opioids are limited in their ability to spread throughout several dermatomes due to their rapid penetration of spinal membranes and tissue. Additionally since hydrophilic opioids spread rostrally and linger longer in the CSF, their duration of action is longer. So hydrophilic opioids have a slower onset and a longer duration (2,13,24). (See Diagram 6 and refer to Table 1)

Table 1 EPIDURAL OPIOIDS (25) DRUG LIPID SOLUBILITY ONSET DURATION Morphine 1 30 - 60 min. 6 - 24 hours Hydromorphone 10 15-30 6 - 18 hours Meperidine 30 5 - 10 min. 6 - 8 hours



Fentanyl 800 5 min. 4 - 6 hours

o Potency of epidural opioid analgesia The amount of opioid needed to provide a given level of analgesia is much smaller when administered per spinal route. This is due to the opioid being deposited in close proximity to the spinal cord opioid receptor sites. This reduces dose requirements, and improves the selectivity of spinal analgesia. Effective doses of opioids when administered intrathecally are even smaller due to the medication being deposited even closer to the receptor sites. When comparing 24 hour dose requirements of parenteral vs. epidural vs.



intrathecal morphine, it has been found to be a sequential 10 fold decrease i.e.: 50 - 70 mg of parenteral morphine = 5 mg of epidural morphine = 0.5 mg intrathecal morphine (26).



o Side effects of epidural opioid analgesia While the ability of hydrophilic opioids to remain in the CSF does provide some advantages such as prolonged duration, higher potency, and extended dermatomal spread, the progressive rostral spread may lead to potentially serious complications and/or mild side effects as discussed below. Respiratory depression with a hydrophilic opioid such as morphine may occur at two distinct times. ‘Early respiratory depression’, soon after administration, occurs mainly due to the vascular absorption and circulatory redistribution to the brain. This is similar to parenteral administration. ‘Delayed-onset respiratory depression’ occurs due to the rostral spread of the opioid via the CSF to the brainstem respiratory center. This may occur up to 24 hours later. With the use of lipophilic opioids, the ‘delayed-onset respiratory depression’ is less likely to occur due to the decreased tendency of lipophilic opioids to have a rostral spread. ‘Early-onset respiratory depression’ may occur though due to the rapid uptake and circulation to the brainstem respiratory center (2,3,4,5,6,13,24). The risk of respiratory depression is greatly increased if systemic opioids (IV, IM, or PO) are co-administered with epidural opioids. Nausea and vomiting are also related to rostral spread of the opioid in the CSF to the chemoreceptor trigger zone in the brainstem (2,4,5,6). This occurs in about 17% of post-operative patients, similar to patients receiving parenteral opioids (6,26). Fortunately, the incidence is reduced after repeated doses, and can often be managed with antiemetics Pruritus is frequently noted with epidural opioids, usually of the face and chest. A rash is not normally detected. The cause for pruritus is not clearly understood, but it may reflect alterations in spinal and trigeminal nerve processing (26,27,28). The modulation of nociceptive input is interpreted at a higher level as an itch. A recent study (29) indicates that there maybe changes in the spinal efferent outflow, causing histamine to be released at peripheral sites. Thus explaining why antihistamines may provide effective treatment (13,26). Another pruritus management option is to administer a mixed opioid agonist-antagonist such as nalpuphine (Nubain). Nalpuphine antagonizes mu opioid receptors which are thought to be associated with respiratory depression and pruritus and stimulates opioid kappa receptors, which produces analgesia. A typical dose of nalpuphine for pruritis is 2.5-5.0 mg IV q6 hours PRN. Urinary retention occurs most often but not exclusively in young males and is less likely with thoracic epidurals. It has been reported to occur due to the relaxation of the bladder detrusor muscle (13,26). 5.2 LOCAL ANESTHETICS



Dilute local anesthetics when injected on or near a nerve will result in the blockade of some nerve conduction. This may result in the absence of pain, while motor and other sensory functions may be unaffected. The term ‘differential block’ is used to describe this phenomenon. Some nerves are less readily blocked than others due to their size and extent of myelination. Local anesthetics administered epidurally interrupt the nociceptive input at the nerve roots as they return to the spinal column (28). Local anesthetics may differ according to: 1) potency; 2) speed of onset; 3) duration of activity; and 4) ability to cause a differential blockade of sensory and motor fibers (26). Bupivacaine, the most common local anesthetic used in continuous epidural infusions, has a high anesthetic potency, a prolonged duration of action, and will also provide adequate sensory analgesia with minimal blockade of motor function (28). Local anesthetics are relatively free of side effects. However, higher concentrations of local anesthetics will provide an increased motor block (possibly limiting ambulation) and/or a sympathetic blockade (resulting in resting or orthostatic hypotension). Patients receiving epidural local anesthetic should be kept well hydrated and monitored regularly for changes in lower extremity motor strength and orthostatic hypotension. A phenomenon called tachyphylaxis may also occur with the administration of local anesthetics. This is the development of an acute tolerance to the drug; the drug becomes less effective. The coadministration of epidural local anesthetics and opioids has been found to prevent the occurrence of tachyphylaxis. The exact mechanism for this is still unclear (28). Although rare, epidural administration of a local anesthetic can lead to high blood concentrations of local anesthetics causing symptoms of systemic local anesthetic toxicity. A number of factors influence the blood concentrations of local anesthetics such as the dose of the drug, site of injection, speed of the injection, or inadvertent injection directly into the blood vessels. Systemic side effects primarily involve the central nervous or cardiovascular systems (30,31). The initial symptoms of CNS toxicity are lightheadedness, dizziness, metallic taste, and ringing in the ears. This may progress to an excitatory phase with symptoms such as shivering, muscle twitching, tremors, and then generalized convulsions. CNS depression may follow resulting in a respiratory arrest. Cardiovascular systemic toxicity is initially noted by hypotension which may be transient but this may progress to profound hypotension, myocardial depression eventually resulting in cardiac arrest and death (32,33). 5.3 OPIOID AND LOCAL ANESTHETIC COMBINATIONS Opioids and local anesthetics are believed to act synergistically. By combining both in the epidural infusion, a decreased concentration of the local anesthetic and a lower dose of the opioid may be possible. This generally provides better analgesia with fewer side effects (2,13,34).



5.4 COMMON EPIDURAL INFUSION Common Opioid Concentrations Common Local Anesthetics

Concentrations Morphine 50 mcg/ml Bupivacaine 0.1% (1mg/ml). Hydromorphone 10mcg/ml Bupivacaine 0.05% (0.5mg/ml) Fentanyl 2-5mcg/ml Ropivacaine 0.2% (2mg/ml) Meperidine 2mg/ml 5.5 COMMON INFUSION RATES 5-14 cc/hour



NURSING ASSESSMENT, DOCUMENTATION, AND MANAGEMENT

OF SIDE EFFECTS AND COMPLICATIONS

Section 6

6.1 GENERAL PATIENT MANAGEMENT o Maintain IV access while receiving epidural analgesia and for 8

hours following the last administration of medication. (3,13) o Epidural medications should be sterile, preservative-free (due to

the neurotoxicity of preservatives), and designated for intraspinal use. (6,26)

o Do not use alcohol on the epidural catheter or infusion tubing

due to the potential for neurotoxicity. (6,24) o No other opioid or CNS depressant should be administered to a

patient receiving epidural opioids due to the increased risk of respiratory depression. If the patient is anxious, agitated, and needs a sedative, notify the Acute Pain Service prior to starting the sedative. It may be prudent to stop the epidural infusion and provide analgesia through another route.

o No anticoagulation therapy should be initiated or changed before

notifying the Acute Pain Service. Anticoagulation therapy increases the risk of epidural hematoma. Timing of catheter placement and removal is of paramount importance in the presence of anticoagulation therapy.

o Review Epidural Physician Orders (13)

Noting: 1. The location of the epidural catheter 2. Initial preop opioid bolus dose, if given and when 3. Medication(s) ordered and the infusion rate 4. Specific recommendations for patient assessment 5. Orders to treat potential side effects/complications 6. When to notify the Anesthesiology Acute Pain Service Notify by using the P-A-I-N pager ( # 7 2 4 6 )

6.2 ASSESSMENT OF ANALGESIA LEVEL (3,5,13) Assessment: Assess the patient’s pain rating using patient-specific pain scale (e.g. 0-10) every 4 hours while awake, both at rest and with activity Documentation: Document patient’s pain ratings on Pain Management flow sheet (UWHC #48) Management: Notify the Acute Pain Service of inadequate analgesia



6.3 ASSESSMENT AND MANAGEMENT OF SIDE EFFECTS o Increased sedation / respiratory depression (2,3,4,5,6,13,22,31,35,36)

An increased sedation level will occur prior to respiratory

depression Assessment: Assess sedation level/respiratory rate every hour for the first 24 hours, then every 4 hours, preferably by the same nurse during each shift. Documentation: Document levels on the Pain Management flow sheet Warning: Do not administer systemic opioids or CNS

depressants without approval of the Acute Pain Service.

Management: Notify the Acute Pain Service of a sedation score of 4 and / or respiratory rate less than 10.

UWHC Sedation Scale: N = Normal sleep 1 = Anxious, agitated, or restless 2 = Calm, cooperative to tranquil (normal patient’s baseline without sedation) 3 = Quiet, drowsy, responds to verbal commands 4 = Asleep, brisk response to forehead tap or loud verbal stimuli 5 = Asleep, sluggish response to increasingly vigorous stimuli 6 = Unresponsive to painful stimuli

If the sedation score is 5 and the respiratory rate is less than 8

1. Stop the epidural infusion 2. Administer naloxone* as ordered on the Epidural Physician orders 3. Notify the Acute Pain Service

4. Administer oxygen, check the patient’s oxygen saturation

level • Naloxone is an opioid antagonist that reverses the effects of

opioids. Usual dose is 100mcg IV given over 1 minute. Caution must be taken to give it slowly because naloxone may cause cardiopulmonary symptoms such as ventricular tachycardia and pulmonary edema. The dose may need to be repeated every 3 - 5 minutes until the symptoms have been reversed.



• Patients should be monitored closely after naloxone administration because respiratory depression may recur due to the short half-life of naloxone (55 minutes). Repeat boluses or constant infusion may be necessary.



o Nausea / Vomiting (2,3,4,5,6,13,22,31)

Management: Administer anti-emetics as ordered, and notify the Acute Pain Service

if the nausea/vomiting persists. Assess for other possible causes and treat as appropriate.

o Pruritus (2,3,4,5,6,13,22,31)

Management: Administer diphenhydramine (antihistamine) or nalbuphine (opioid agonist-antagonist) as ordered prn, and notify the Acute Pain Service if the pruritus persists or becomes more severe. Assess for other possible causes and treat as appropriate.

o Urinary retention (2,3,4,5,6,13,22,31) Management: The patient may have a foley catheter placed, or be

straight catheterized prn. If the patient requies a second

straight catheterization consider placing a foley catheter. The Acute Pain Service recommends not to routinely discontinue the foley while the patient is still receiving a lumbar epidural infusion. The risk of urinary retention is greater in men and with lower (lumbar or caudal) catheter placement.

o Orthostatic hypotension (4,6,13,32,34)

Assessment: Assess BP and HR every 4 hours Assess for orthostatic changes prior to ambulating Management: Ensure adequate hydration and fluid replacement.

Notify the Acute Pain Service if changes are greater than 20% from baseline.

o Sensory / Motor function loss (3,4,5,13,30,31)

Assessment: Assess the patient for changes in sensory/motor function

at least every 4 hours and more frequently if there are changes. Ask the patient to point to numb and tingling skin areas, and to bend their knees and lift the buttocks off the mattress.

Management: Do not ambulate the patient if the patient complains of weakness, heaviness, or numbness/tingling in lower extremities

Notify the Acute Pain Service of changes noted in the patient’s sensory/motor function



6.4 ASSESS FOR POTENTIAL COMPLICATIONS OF EPIDURAL ANALGESIA o Epidural abscess (4,5,6,13,21,37)

Assessment: Assess the catheter insertion site every 8 hours for signs of infection i.e.: tenderness, erythema, swelling, drainage.

Assess for changes in sensory/motor function every 4 hours including unexplained back pain, bowel or bladder dysfunction, fever, or neck stiffness.

Management: Notify the Acute Pain Service of any changes noted

o Epidural hematoma (6,13,21,35,38)

Assessment: Assess the catheter insertion site every 8 hours for pain and or swelling at the site.

Assess for changes in sensory/motor function every 4 hours,including progressive numbness, weakness, or bowel and bladder dysfunction

Warning: Do not administer Low Molecular Weight Heparin

without first advising the Acute Pain Service Management: Notify the Acute Pain Service of these symptoms

o Subdural puncture (6,13)

(The catheter may migrate into the subarachnoid space, causing an overdose of opioid and local anesthetic)

Assessment: Assess the patient for a sudden or progressive increase in side effects such as sedation, loss of sensory and motor function, hypotension Management: Notify the Acute Pain Service immediately

o Migration of catheter into epidural vessels (5,13)

(The catheter may migrate into the blood vessels of the epidural space, causing the medications to be delivered systemically)

Assessment: Assess the catheter for blood in the tubing Assess the patient’s pain level, inadequate analgesia may occur due to the small opioid dose being delivered systemically Assess the patient for symptoms of local anesthetic toxicity such as dizziness, lightheadedness, hypotension, agitation, seizures



Management: Notify the Acute Pain Service of any of these changes



6.5 CATHETER AND DRESSING CARE o Dressing care: Notify the Acute Pain Service to reinforce or change the dressing. The epidural catheter is secured with adhesive strips and covered with a clear adhesive dressing. Manipulation of the dressing may dislodge the epidural catheter from the epidural space. It is best if a member of the Acute Pain Service attends to the dressing so that assessment of the position of the catheter is noted. Do not change or reinforce the dressing (5,6). o Disconnection of the epidural catheter from the filter, or if the epidural catheter or filter is cracked: If disconnected, cover the ends with sterile gauze. Notify the Acute Pain Service immediately (13,22) If the catheter or filter is cracked (clear fluid may accumulate under dressing). Notify the acute pain service immediately (13,22,31). 6.6 DISCONTINUATION OF EPIDURAL CATHETER (31)

The Acute Pain Service will remove the epidural catheter. The decision to stop the epidural infusion and remove the epidural catheter is made by either the Acute Pain Service or the patient’s primary physicians. The Acute Pain Service will remove the epidural catheter. If an epidural catheter is removed accidentally, place the catheter and attached dressing into a plastic bag and label with the patient’s name. The APS will inspect the catheter to ensure it was removed without breakage.

6.7 TRANSITION TO ALTERNATIVE MODES OF ANALGESIA(30)

Studies are lacking and controversy exists over the correct ratios to use when switching opioid-naïve patients from various epidural opioids to parenteral or oral opioids. The nurse should discuss the plan and clarify responsibility for



pain management with the patient’s primary treatment team prior to epidural catheter removal.



PATIENT / FAMILY TEACHING

Section 7

The patient / family should be informed of the importance of pain management to their well-being, and that the staff is eager to provide adequate analgesia. The patient / family should be instructed on: 1. The use of pain rating scales 2. The different routes of analgesia administration

3. The possible side effects of the analgesic and the management of these side effects.

4. Activity levels expected of the patient while receiving epidural analgesia (1,13) The patient / family should also be given to read: Health Facts For You: • Pain Management ---- What Everyone Should Know (UWH #4299) • Epidural Analgesia (UWH #4322)



AP II PUMP

Section 8

1. Review the Acute Pain Service Guidelines for use of the pump and/or view the Baxter AP II video (available through the Nursing Staff Development office) 2. Attend inservice on use of AP II pump. 3. Return demonstration on use and programming of AP II pump to: Deb Gordon, RN Nursing Staff Development Kathy Hansen, RN Nursing Staff Development Sue Deeren, RN Anesthesiology Pain Resource Nurse on your unit

For more information, or for additional copies of this Self-Directed Learning Module, please call Nursing Staff Development at

263-6490.



III. POST-TEST

True or False (Please record your answers on the answer sheet provided)

_____ 1. Exogenous opioids bind with opioid receptors to modulate the nociceptive transmission. _____ 2. Fat in the epidural space functions as a ‘depot’ for the opioids and local anesthetics. _____ 3. Lipophilic opioids such as fentanyl, when

administered epidurally, have a rapid onset and a long duration of action.

_____ 4. Morphine, when administered epidurally, has a slower

onset but a longer duration of action when compared to fentanyl.

_____ 5. The dose of an opioid administered epidurally is

about the same as a parenteral dose. _____ 6. Common side effects of epidural opioids are nausea,

pruritus, and urinary retention. _____ 7. If the epidural catheter dressing is loose, the

nurse should reinforce the area with tape and a new occlusive dressing.

_____ 8. A sudden increase in a patient’s sedation level may

be due to the migration of the epidural catheter into the subarachnoid space.

_____ 9. All medications administered epidurally must be preservative-free. _____ 10. The epidural catheter insertion site should be

assessed every 8 hours for tenderness, swelling, erythema, or drainage.



o • • •



Case examples with multiple choice questions A 63 year old female was admitted to your unit at 1300 from the PACU following a (R) Thoracotomy for cancer. The patient had an epidural catheter inserted in the thoracic interspace 4 (T4) at 0700, and preservative-free Morphine 2.5mg at 0800. She received both a general anesthetic and an epidural infusion of bupivacaine during surgery. Surgery and her stay in the PACU were without complications. An epidural infusion of Morphine 50 mcg/ml and Bupivacaine 0.1% was started at 7cc/hr in the PACU. Your shift started at 2300, and received this report: Vital signs have been stable, currently BP 140/80 HR 88 RR 16 T 37.9 The patient is alert, and oriented x3 Epidural is infusing at 7 cc/hr The patient complained of incisional pain earlier, and received Morphine 2 mg IV at 1400 and 1600 Currently she denies pain 11. This patient should have her respiratory rate and level of sedation checked during your shift tonight: a. every 2 hours b. every 4 hours c. every hour d. one time this shift 12. At 0100 you note her respiratory rate is 6 / min. Prior to this you may have noticed: a. a fall in blood pressure b. an increased sedation level c. increased pain level d. none of the above 13. Upon discovering this patient with a respiratory rate of 6 / min., you assess the patient’s sedation level and rate it a 5. You should: a. call the Acute Pain Service b. stop the epidural infusion and monitor the patient c. stimulate the patient and call the Acute Pain Service d. stop the epidural infusion, administer Naloxone as ordered on the Physician Epidural Order sheet, and notify the Acute Pain Service 14. Earlier in the day, the patient had received IV Morphine for reports of increased pain. The patient: a. denied pain following the IV Morphine, this was appropriate b. should not have received IV Morphine along with the epidural infusion due to the increase risk of respiratory depression. The Acute Pain Service should be notified of inadequate analgesia c. should not have received IV Morphine with the epidural infusion, and the Surgery Service should be notified



d. none of the above o o • •



A healthy 61 year old male is S/P Colon Resection had an epidural catheter inserted in the T 12 interspace prior to surgery, and has Morphine 50 mcg/ml and Bupivacaine 0.1% infusing currently at 10 cc/hr. On Post-op Day (POD)#1, he had increased pain so the infusion was increased from 8cc/hr to 10cc/hr. On POD#2, you are to ambulate the patient. Currently he is denying pain. 15. As you prepare to ambulate the patient, he reports that his legs feel heavy and areas on his thighs feel numb. This is most likely due to: a. the local anesthetic in the epidural infusion b. generalized post-op weakness c. lying in one position too long during the night d. development of an epidural abcess 16. Prior to ambulating the patient, you should: a. assess his lower extremities for any further changes in

sensory / motor function, and notify the Acute Pain Service of his symptoms i.e.: heaviness, numbness, or other changes

b. stop the epidural infusion prior to ambulating the patient c. not worry about these symptoms d. notify the Surgical Service

o • • •

A 29 year old male, S/P a Total Colectomy-Pouch, had an epidural catheter placed at T 9 prior to surgery and is receiving Morphine 50 mcg/ml and Bupivacaine 0.1% at 8 cc/hr for pain management. The patient has been progressing very well. He has denied pain at rest, and reports a ‘2-3’ pain level with ambulation which he has been satisfied with for the last two days. In the early hours of POD#3, the patient reports that over the last 2 hours his pain at rest has increased from ‘0’ to ‘5-6’. The nurse assesses the patient for any other physical changes and finds none. 17. The nurse should: a. also assess the epidural infusion pump and tubing for problems such as kinked tubing, and assess the catheter site for catheter displacement or leakage b. just notify the Acute Pain Service c. wait another hour and reassess patient d. just notify the Surgical Service 18. When patients have inadequate analgesia, the nurse should notify: a. the Surgical Service b. the anesthesiologist who inserted the epidural catheter c. the Acute Pain Service in the morning d. the Acute Pain Service

o • • •



On your unit is a 42 year old female who is S/P (R) Thoracotomy, and had an epidural catheter inserted at the interspace T 6 preoperatively. She is receiving an infusion of Meperidine 2mg/ml and Bupivacaine 0.1% at 6cc/hr. Today (POD#1), you are to start to ambulate the patient. She denies incisional pain, numbness or heaviness in her legs. She does tell you that when she sat up in bed this am she felt very dizzy. 19. Prior to ambulating her, the nurse should: a. make sure there is adequate help prior to getting her out of bed b. check for orthostatic changes in the patient’s heart rate and blood pressure c. just notify the Surgical Service d. none of the above 20. On POD#3, the surgeons request that the epidural catheter be discontinued. The nurse should: a. discontinue the catheter b. remind the Surgical Service to discontinue the catheter c. should notify the Acute Pain Service, who will discontinue the catheter d. none of the above

o • • •



IV. REFERENCES 1. Macintrye, P.E. & Ready,L.B. (1996). Acute pain: significance

and assessment. In P.E. Macintrye & L.B. Ready, Acute Pain Management A Practical Guide (pp.1-12). London: W.B. Saunders.

2. VadeBoncouer, T.R. & Ferrante, F.M. (1993). Epidural and

subarachnoid opioids. In F.M. Ferrante & T.R. VadeBoncouer (Eds.), Post-operative Pain Management (pp.279-303). New York: Churchill Livingstone.

3. Grichnik, K. & Ginsberg, B. (1992). Epidural analgesic for

patients recovering from surgery. In R. Sinatra, A. Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp.243-252). St. Louis: Mosby-Year Book.

4. Pasero C. (1998). Epidural Analgesia For Acute Pain Management.

American Society of Pain Management Nurses self directed learning program. ASPMN, Pensacola, FL.

5. Pasero C., & McCaffery M. (1999). Providing epidural analgesia:

how to maintain a delicate balance. Nursing, August, 34-40. 6. Naber, L., Jones, G., & Halm, M. (1994). Epidural analgesia for

effective pain control. Critical Care Nurse, October, 69-83. 7. Liu S., Carpenter R.L., & Neal J.M. (1995). Epidural anesthesia

and analgesia: their role in postoperative outcome. Anesthesiology, 82(6) 1474-1506.

8. Anderson G., Rasmussen H., Rosenstock C., Bleemer T., Engb/ek J.,

Christensen M., & Ording H. (2000). Postoperative pain control by epidural analgesia after transabdominal surgery: efficacy and problems encountered in daily routine. Acta Anaesthesiol Scand,44, 296-301.

9. Mann C., Pouzeratte Y., Boccara G., Peccoux C., Vergne C., et

al., (2000). Comparison of intravenous or epidural patient controlled analgesia in the elderly after major abdominal surgery. Anesthesiology 92(2), 433-441.

10. Horlocker T.T., Wedel D.J., (1998). Neuraxial block and low

molecular weight heparin: balancing perioperative analgesia and thromboprophylaxis. Regional Anesthesia Pain Medicine 23 Supp.

11. Liu S.S., Mulroy M.F. (1998). Neuraxial anesthesia and

analgesia in the presence of standard heparin. Regional Anesthesia Pain Medicine. 23 Supp.

12. de Leon-Casasola, O.A., Karabella, D. & Lema, M.J. (1996).

Bowel function recovery after radical hysterectomies: Thoracic epidural bupivacaine-morphine versus intravenous patient-



controlled analgesia with morphine: A pilot study. Journal of Clinical Anesthesia, 8, 87-92.

13. Agency for Health Care Policy and Research (1992). Clinical

Practice Guidelines: Acute Pain Management: Operative or Medical Procedures and Trauma, Pub. No. 92-0032, Rockville, MD.

14. American Society of Regional Anesthesia. Neuraxial Anesthesia

and Anticoagulation Consensus Statements. American Society of Regional Anesthesia Consensus Conference, Chicago, Il, May 2-3, 1998.

15. Byas-Smith, M. (1992). Management of acute exacerbations of

chronic pain syndromes. In R. Sinatra, A. Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp.432-444). St. Louis: Mosby-Year Book.

16. Macintrye, P.E. & Ready, L. B. (1996). Epidural and

intrathecal analgesia. In P.E. Macintrye & L.B. Ready, Acute Pain Management A Practical Guide (pp. 114-151). London: W.B. Saunders.

17. Ready, L. B. (1990). Spinal opioids in the management of

acute and post-operative pain. Journal of Pain and Symptom Management, 5 (3), 138-145.

18. Jones, S.J. (1992). Anatomy of pain. In R. Sinatra, A.

Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp.8-28). St. Louis: Mosby-Year Book.

19. Katz, N. & Ferrante, F.M. (1993). Nociception. In F.M.

Ferrante & T.R. VadeBoncouer (Eds.), Post-operative Pain Management (pp.17-67). New York: Churchill Livingstone.

20. Willens, J.S. (1996). Introduction to pain management. In

E. Salerno & J. Willens (Eds.), Pain Management Handbook An Interdisciplinary Approach (pp.3-38). St. Louis: Mosby-Year Book.

21. Aimone, L.D. (1992). Neurochemistry and modulation of pain.

In R. Sinatra, A. Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp.29-43). St. Louis: Mosby-Year Book.

22. Jasinski, D.M. & Snyder, C. J. (1996). Invasive

interventions. In E. Salerno & J.S. Willens (Eds.), Pain Management Handbook An Interdisciplinary Approach (pp.429-464). St. Louis: Mosby-Year Book.

23. Paice, J.A. & Buck, M.M. (1993). Intraspinal devices for

pain management. Nursing Clinics of North America, 28 (4), 921-935.

24. Lubenow, T. R. (1992). Epidural analgesia: Considerations

and delivery methods. In R. Sinatra, A. Hord, B. Ginsberg & L.



Preble (Eds.), Acute Pain Mechanism and Management (pp.233-242). St. Louis: Mosby-Year Book.

25. Mather, L.E. (1986). Pharmacokinetic studies of meperidine. In

K.M., Foley, C.E., Inturrisi (Eds.), Advance in Pain Research and Therapy, Vol 8, (pp.155-165). Raven Press, New York, pp 155-165.

26. Sinatra, R. (1992). Spinal opioids analgesia: an overview.

In R. Sinatra, A. Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp.225-232). St. Louis: Mosby-Year Book.

27. Macintrye, P.E. & Ready, L.B. (1996). Pharmacology of

opioids. In P.E. Macintrye & L.B. Ready, Acute Pain Management A Practical Guide (pp.13-40). London: W.B. Saunders.

28. Sinatra, R. (1992). Pharmacokinetics and pharmacodynamics of

spinal opioids. In R. Sinatra, A. Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp. 102-111). St. Louis: Mosby Year Book.

29. Zakowski, M., Ramanathan, S., Khoo, P., et al. (1990).

Plasma histamine with intraspinal morphine in cesarean section. Anesth Analg, 70, S448.

30. Pasero, C., Portenoy, R.K., McCaffery, M. (1999). In

McCaffery, M., Pasero, C. Eds., Pain: Clinical Manual (pp. 214-258). St.Louis: Mosby.

31. Mulroy M.F., Norris M.C., Kiu S.S. (1997). Safety steps for

epidural injection of local anesthetics: review of the literature and recommendations. Anesth Analg, 85, 1346-1356.

32. Macintrye, P.E. & Ready, L.B. (1996). Pharmacology of local

anesthetics. In P.E. Macintrye & L.B. Ready, Acute Pain Management A Practical Guide (pp. 41-52). London: W.B. Saunders.

33. Denson, D.D. & Mazoit, J.X. (1992). Physiology and

pharmacology of local anesthetics. In R. Sinatra, A. Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp.124-139). St. Louis: Mosby-Year Book.

34. Ferrante, F.M. & VadeBoncouer, T.R. (1993). Epidural

analgesia with combinations of local anesthetics and opioids. In F.M. Ferrante & T.R. VadeBoncouer (Eds.), Post-operative Pain Management (pp.305-333). New York: Churchill Livingstone.

35. Olsson, G.L., Reed, B.A., & Vanderveer, B.L. (1992). Nursing

education regarding epidural and intrathecal opioids. In R. Sinatra, A. Hord, B. Ginsberg, & L. Preble (Eds.), Acute Pain Mechanism and Management (pp. 570-584). St. Louis: Mosby-Year Book.



36. Ready, L.B., Loper, K.A., Nessly, M., & Wild, L. (1991). Post-operative epidural morphine is safe on surgical wards. Anesthesiology, 75 (3), 452-456.

37. Ngan Kee, W.D., Jones, M.R., Thomas, P. & Worth, R.J. (1992).

Extradural abscess complicating extradural analgesia for caesarean section. British Journal of Anaesthesia, 69, 647-652.

38. Metzger, G. & Singbartl, G. (1991). Spinal epidural hematoma

following anesthesia versus spinal subdural hematoma. Two case reports. Acta Anaesthesiol Scan, 35, 105-107



Notes:

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Epidural Analgesia -A Self-Directed Learning Module 3rd