Handbook of Clinical Anesthesia

Chapter 57

acute Pain Management

Appropriate management of patients with acute perioperative pain using multimodal or balanced analgesia is crucial (Macres SM, Moore PG, Fishman SM: Perioperative pain management. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1473–1504). Inadequate relief of postoperative pain has adverse physiologic effects that may contribute to significant morbidity and mortality, resulting in the delay of patient recovery and return to daily activities.

  1. Definition of Acute Pain

Acute pain has been defined as the normal, predicted, physiological response to an adverse chemical, thermal, or mechanical stimulus. Generally, acute pain resolves within 1 month. Acute pain-induced change in the central nervous system is known as neuronal plasticity. This can result in sensitization of the nervous system, resulting in allodynia and hyperalgesia.

  1. Anatomy of Acute Pain (Figs. 57-1 and 57-2 and Table 57-1)

α-δ Fibers transmit “first pain,” which is described as sharp or stinging in nature and is well localized. Polymodal C fibers transmit “second pain,” which is more diffuse in nature and is associated with the affective and motivational aspects of pain.

III. Pain Processing

Tissue injury tends to fuel neuroplastic changes within the nervous system, which results in both peripheral and central sensitization. Clinically, this can manifest as

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hyperalgesia (exaggerated pain response to a normally painful stimulus) or allodynia (painful response to a typically nonpainful stimulus) (Fig. 57-3).

 

Figure 57-1. Afferent pathways involved in nociceptive regulation.

  1. The four elements of pain processing are transduction, transmission, modulation, and perception (Fig. 57-4).

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Figure 57-2. Efferent pathways involved in nociceptive regulation.

  1. Modulationof pain transmission involves altering afferent neural transmission along the pain pathway. The dorsal horn of the spinal cord is the most common site for modulation of the pain pathway, and modulation can involve either inhibition

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or augmentation of the pain signals. Examples of inhibitory spinal modulation include release of inhibitory neurotransmitters (γ-aminobutyric acid, glycine) and activation of descending efferent neuronal pathways (release of norepinephrine, serotonin, and endorphins in the dorsal horn).

Table 57-1 Primary Afferent Nerves

Fiber Class

Diameter (µ)

Velocity

Effective Stimuli

Abeta (myelinated)

12–20

Group II (> 40–50 m/sec)

Low-threshold mechanoreceptors
Specialized nerve endings (pacinian corpuscles)

α-δ (myelinated)

1–4

Group III (<40 m/sec)

Low-threshold mechanical or thermal
High-threshold mechanical or thermal
Specialized nerve endings

C (unmyelinated)

0.5–1.5

Group IV (<2 msec)

High-threshold thermal, mechanical, and chemical
Free nerve endings

 

Figure 57-3. Pain sensitization. (Adapted with permission from Klemm D: Am Family Phys 63(10), 2001.)

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Figure 57-4. The four elements of pain processing are transduction, transmission, modulation and perception. 5HT = 5-hydroxytryptamine (serotonin); CCK = cholecystokinin; NE = norepinephrine; NMDA = N-methyl-D-aspartate; NO = nitric oxide; NSAID = nonsteroidal anti-inflammatory drug.

  1. Spinal modulation that results in augmentation of pain pathways is a consequence of neuronal plasticity. The phenomenon of “wind-up” is an example of central plasticity that results from repetitive C-fiber stimulation of wide-dynamic range (WDR) neurons in the dorsal horn.
  2. A multimodal approach to pain therapy should target all four elements of the pain processing pathway.
  3. Chemical Mediators of Transduction and Transmission (Table 57-2 and Fig. 57-5)
  4. Pain receptors include the NMDA (N-methyl-D-aspartate), AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid),

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kainite, and metabotropic receptors (Fig. 57-6).

Table 57-2 Algogenic Substances

Substance

Source

Effect

Bradykinin

Macrophages
Plasma kininogen

Activates nociceptors

Serotonin

Platelets

Activates nociceptors

Histamine

Platelets
Mast cells

Produces vasodilation, edema, and pruritus
Potentiates the response of nociceptors to bradykinin

Prostaglandin

Tissue injury and cyclo-oxygenase pathway

Sensitizes nociceptors

Leukotriene

Tissue injury and lipo-oxygenase pathway

Sensitizes nociceptors

Excess hydrogen ions

Tissue injury and ischemia

Increases pain and hyperalgesia associated with inflammation

Cytokines (interleukins, TNF)

Macrophages

Excite and sensitize nociceptors

Adenosine

Tissue injury

Pain and hyperalgesia

Neurotransmit-ters (glutamate, substance P)

Antidromic release by peripheral nerve terminals after tissue injury

Substance P activates macrophages and mast cells
Glutamate activates nociceptors

Nerve growth factor

Macrophages

Stimulates mast cells to release histamine and serotonin
Induces heat hyperalgesia
Sensitizes nociceptors

TNF = tissue necrosis factor.

  1. Repetitive C-fiber stimulation of WDR neurons in the dorsal horn at intervals of 0.5 to 1.0 Hz may precipitate the occurrence of “wind-up” and central sensitization and secondary hyperalgesia (Fig. 57-7).

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Figure 57-5. Substances involved in nociception.

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Figure 57-6. Schematic representation of peripheral and spinal mechanism involved in neuroplasticity. AAMPA = α-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid; NK = neurokinin; NMDA = N-methyl-D-aspartate.

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Figure 57-7. Primary nociceptive transmission in the spinal cord. NMDA antagonists have an antihyperalgesic rather than an analgesic effect in the spinal cord. AMPA = α-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid; CGRP = calcitonin gene-related peptide; NK = neurokinin; NMDA = N-methyl-D-aspartate.

  1. The Surgical Stress Response

Although similar, postoperative pain and the surgical stress response are not the same. Surgical stress causes release of cytokines and precipitates adverse neuroendocrine and sympathoadrenal responses (increased secretion of the catabolic hormones [cortisol, glucagon, growth hormone, and catecholamines] and decreased secretion of the anabolic hormones [insulin and testosterone]) (Table 57-3).

  1. Preemptive Analgesia

The goal of preemptive analgesia is to prevent NMDA receptor activation in the dorsal horn which causes “wind-up,” facilitation, central sensitization expansion of receptive fields, and long-term potentiation, all of which may lead to a chronic pain state.

VII. Strategies for Acute Pain Management

The majority of postoperative pain is nociceptive in character. Evidence suggests that women experience more

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pain after surgery than men and therefore require more morphine to achieve a similar level of pain relief.

Table 57-3 Consequences of Poorly Managed Acute Pain

System

Consequences

Cardiovascular

Tachycardia
Hypertension
Increased cardiac workload

Pulmonary

Respiratory muscle spasm (splinting)
Decreased vital capacity
Atelectasis
Arterial hypoxemia
Increased risk of pulmonary infection

Gastrointestinal

Postoperative ileus

Renal

Increased risk of oliguria and urinary retention

Coagulation

Increased risk of thromboemboli

Immunologic

Impaired immune function

Muscular

Muscle weakness and fatigue

 

Limited mobility with increased risk of thromboembolism

Psychological

Anxiety

 

Fear and frustration, resulting in poor patient satisfaction

VIII. Assessment of Acute Pain (Fig. 57-8)

Common features of pain are usually reviewed during the assessment for acute pain (Table 57-4).

  1. Opioid Analgesics

Opioid Analgesics are the mainstay for the treatment of acute postoperative pain, and morphine is the “gold-standard” (Tables 57-5).

  1. Hydromorphoneis a semisynthetic opioid that has four to six times the potency of morphine, making it the ideal drug for long-term subcutaneous administration in opioid-tolerant patients.
  2. Fentanylis available for intravenous (IV), subcutaneous, transdermal, transmucosal, and neuraxial administration.

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Figure 57-8. Linear visual analogue scale and faces pain assessment tool.

Table 57-4 Features of Pain Commonly Addressed During Assessment

Onset of pain
Temporal pattern of pain
Site of pain

Radiation of pain
Intensity (severity) of pain
Exacerbating features (what makes the pain start or get worse?)
Relieving factors (what prevents the pain or makes it better?)
Response to analgesics (including attitudes and concerns about opioids)
Response to other interventions
Associated physical symptoms
Associated psychological symptoms
Interference with activities of daily living

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Table 57-5 Opioid Equianalgesic Dosing

Drug

Intravenous, Intramuscular, or Subcutaneous Dose

Oral Dose

Morphine

10 mg

30 mg

Hydromorphone (Dilaudid)

1.5–2.0 mg

6–8 mg

Hydrocodone (Vicodin)

 

30–45 mg

Oxymorphone (Opana IR and ER)

1 mg

10 mg

Oxycodone (Percocet, OxyContin)

10–15 mg

20 mg

Levorphanol (Levo-Dromoran)

2 mg

4 mg

Fentanyl

100 µg

 

Meperidine (Demerol)

100 mg

300 mg

Codeine

100 mg

200 mg

Methadone

Conversion ratio is variable

 

  1. Sufentanil.The high intrinsic potency of sufentanil makes it an excellent choice for epidural analgesia in opioid-dependent patients.
  2. Methadoneis well absorbed from the gastrointestinal (GI) tract. With repetitive dosing, methadone can accumulate. Opioid rotation is a useful technique to restore analgesic sensitivity in highly tolerant patients, and methadone is a common choice for opioid rotation.
  3. Non-Opioid Analgesic Adjuncts (Table 57-6)

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been proven effective in the treatment of postoperative pain. In addition, they are opioid sparing and can significantly decrease the incidence of opioid-related side effects such as postoperative nausea and vomiting and sedation. Platelet dysfunction, GI ulceration, and an increased risk of nephrotoxicity are several reasons why the nonselective NSAIDs may be avoided in the perioperative period.

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Table 57-6 Adult Dosing Guidelines for Non-opioid Analgesics

Drug

Route

Half-Life (hr)

Dose (mg)

Para-aminophenols

     

Acetaminophen

Oral

0.25

500–1000 mg every 4–6 hr Maximum daily dose in healthy adults: 4000 mg

Salicylates

Acetylsalicylic acid

Oral

0.25

500–1000 mg every 4–6 hr
Maximum daily dose in healthy adults: 4000 mg

Diflunisal

Oral

8–12

500 mg every 8–12 hr
Loading dose: 1000 mg

Choline magnesium
Trisalicylate

Oral

9–17

1000–1500 mg every 12 hr

NSAID's
Propionic Acids

Ibuprofen

Oral

2

400 mg every 4–6 hr

Naproxen

Oral

12–15

250 mg every 6–8 hr

Ketoprofen

Oral

2.1

25–50 mg every 6–8 hr

Oxaprozin

Oral

42–50

600 mg every 12–24 hr

Indoleacetic Acids

Indomethacin

Oral

2

25 mg every 8–12 hr

Sulindac

Oral

7.8

150 mg every 12 h

Etodolac

Oral

7.3

300–400 mg every 12 hr

Pyrrolacetic Acids

Ketorolac

IV

6

30 mg initially followed by 15–30 mg every 6–8 hr, not to exceed 5 days

Phenylacetic Acids

Diclofenac potassium

Oral

2

50 mg every 8 hr

Enolic Acids (Oxicams)

Meloxicam

Oral

15–20

7.5–15.0 mg every 24 hr

Piroxicam

Oral

50

20–40 mg every 24 hr

Naphthyalkalone

Nabumetone

Oral

22.5

500–750 mg every 8–12 hr

COX-2 Inhibitor

Celecoxib

Oral

11

100–200 mg every 12 hr

COX = cyclo-oxygenase; IV = intravenous.

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  1. NMDA receptor antagonists(ketamine, dextromethorphan) may be analgesic adjuncts.
  2. α2-Adrenergic agonists(clonidine, dexmedetomidine) may be administered perioperatively to provide analgesia, sedation, and anxiolysis.
  3. Gabapentinand pregabalin are effective analgesics not only for the treatment of neuropathic pain syndromes but also for the treatment of postoperative pain. When these drugs are combined with an NSAID, the combination has been shown to be synergistic in attenuating the hyperalgesia associated with peripheral inflammation.
  4. Lidocainehas been shown to be analgesic, antihyperalgesic, and anti-inflammatory after IV administration.
  5. Glucocorticoidspossess analgesic, anti-inflammatory, and antiemetic effects.
  6. Methods of Analgesia
  7. Patient-Controlled Analgesia (PCA)is any technique of pain management that allows patients to administer their own analgesia on demand.
  8. The five variables associated with all modes of PCA include bolus dose, incremental (demand) dose, lockout interval, background infusion rate, and 1-hour and 4-hour limits (Table 57-7).
  9. Risk Factors for Use of Opioid Patient-Controlled Analgesia(Table 57-8)
  10. Neuraxial Analgesia.Since the discovery of the opioid receptor, the intrathecal administration of opioids and the epidural administration of opioids plus a local anesthetic have produced significant pain control.

Table 57-7 Universal Intravenous Opioid Patient-Controlled Analgesia Regimens for Opioid-Naïve Adult Patient

Opioid

Demand Dose

Lockout (min)

Basal Infusion

Morphine

1–2 mg

6–10

0–2 mg/hr

Hydromorphone

0.2–0.4 mg

6–10

0.4 mg/hr

Fentanyl

20–50 µg

5–10

0–60 µg/hr

Sufentanil

4–6 µg

5–10

0–8 µg/hr

Tramadol

10–20 mg

6–10

0–20 mg/hr

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Table 57-8 Relative Risk Factors Associated with Patient-Controlled Analgesia

Pulmonary disease
Obstructive sleep apnea
Renal or hepatic dysfunction
Congestive heart failure
Closed head injury
Altered mental status
Lactating mothers

  1. Epidural analgesiais a critical component of multimodal perioperative pain management and improved patient outcome.
  2. The efficacy of an epidural technique is determined by numerous factors, including catheter incision site congruency, choice of analgesic drugs, rates of infusion, duration of epidural analgesia, and type of pain assessment (rest vs dynamic).
  3. Ideally, the epidural catheter is positioned congruent with the surgical incision (Table 57-9).
  4. A local anesthetic plus an opioid in the epidural space is the most common drug combination and is believed to have a synergistic effect.
  5. Epidurally administered opioids have the distinct advantage of producing analgesia without causing significant sympatholytic effect or motor blockade.
  6. Analgesia occurs by way of a spinal mechanism (diffusion of drug into the spinal fluid) and

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through a supraspinal mechanism after systemic adsorption. Opioids with intermediate lipophilicity (hydromorphone, alfentanil, meperidine) have the ability to easily move between the aqueous and lipid regions of the arachnoid membrane and therefore have high meningeal permeability, which potentially confers higher bioavailability in the spinal cord. Nevertheless, morphine has greater bioavailability in the spinal cord than alfentanil, fentanyl, and sufentanil.

Table 57-9 Guidelines for Adult Epidural Catheter Dosing Regimen*

Recommended adult dose for epidural bupivacaine (should not exceed 400 mg in 24 hours)
Surgical dermatome: Catheter placement
   Lumbar (total knee, arthroplasty, or lower extremity bypass surgery)
   Low thoracic (exploratory laparotomy, or xiphopubic incision)
   Mid to high thoracic (thoracotomy or sternotomy)

*Rate of infusion, 2–10 mL/hr.

  1. In general, epidural administration of hydrophilic opioids tends to have a slow onset, a long duration, and a mechanism of action that is primarily spinal in nature. Epidural administration of lipophilic opioids, on the other hand, has a quick onset, a short duration, and a mechanism of action that is primarily supraspinal and secondary to rapid systemic uptake.
  2. Adjuvant medications that may enhance analgesia include clonidine and ketamine.
  3. Extended-release epidural morphine (DepoDur) consists of morphine encapsulated within a liposome delivery system, which provides controlled release of morphine for up to 48 hours. DepoDur is only approved for lumbar epidural administration.
  4. Intrathecal analgesiais provided with a variety of opioid analgesics (morphine, hydromorphone, meperidine, methadone, fentanyl, sufentanil) (Table 57-10).
  5. Hydrophilic opioids (morphine) traverse the dura slowly, bind to epidural fat poorly, and slowly enter the plasma. They tend to have a slow onset of action and a long duration and provide a broad band of analgesia. Delayed respiratory depression is more common with hydrophilic opioids secondary to rostral spread.
  6. Lipophilic opioids (fentanyl) rapidly cross the dura, are quickly sequestered into epidural fat, and promptly enter the systemic circulation. Lipophilic opioids tend to have a rapid onset of action, a short duration, and a narrow band of analgesia. Delayed respiratory depression is less of a problem with the lipophilic opioids.

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Table 57-10 Intrathecal Analgesia

Surgical Procedure

Intrathecal Drug Dose*

Labor analgesia

Sufentanil 2.5–5.0 µg

Cesarean section

Morphine 100 µg
Addition of clonidine (60 µg) is synergistic and can increase the duration of spinal analgesia after cesarean section but also increases intraoperative sedation

Outpatient knee arthroplasty

Fentanyl (25–50 µg) improves intraoperative analgesia without prolonging postoperative motor blockade

Total knee arthroplasty

Morphine (200–300 µg)

Total hip arthroplasty

Morphine (100–200 µg)

Thoracotomy and major abdominal surgery

Morphine (500 µg)
Incidence of side effects (nausea and vomiting, urinary retention, pruritus) increases with doses >300 µg

*Intrathecal hydromorphone, 50–100 µg, approximates intrathecal morphine, 100–200 µg.

  1. Other useful analgesic additives include the α2-agonists, NSAIDs, NMDA receptor antagonists, acetylcholinesterase inhibitors, adenosine, epinephrine, and benzodiazepines (Table 57-11).
  2. Peripheral Nerve Blockade.Single injection of peripheral nerve blockade may provide pain control that is superior to opioids with fewer side effects. Single injection techniques are limited in duration, but continuous peripheral nerve block techniques may extend the benefits of peripheral nerve blockade well into the postoperative period (Table 57-12).
  3. The Brachial Plexus
  4. The interscalene blockis the ideal peripheral nerve block for painful orthopaedic and vascular procedures performed on the shoulder and upper arm but is a poor choice for forearm and hand surgery because the ulnar nerve is commonly spared.
  5. The supraclavicular approachto the brachial plexus provides anesthesia to the entire upper

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extremity with a single injection of local anesthetic. The safety of this approach has improved dramatically with the use of ultrasonography.

Table 57-11 Intrathecal Analgesia

Intrathecal Drug

Dosing

Comments

Clonidine

15–45 µg improves the quality of spinal blockade in outpatient surgery

Side effects increase significantly at intrathecal doses >150 µg

Epinephrine

0.1–0.6 mg
Produces dose-related increase in the return of motor function and micturition

Not recommended for outpatient surgery

Neostigmine

6.25–50 µg Produces dose-related increase in motor blockade, time for resolution of the block, and nausea and vomiting

Further studies of the appropriate intrathecal dose that optimizes analgesia while minimizing side effects are needed

  1. The infraclavicular blockis ideally suited for surgical procedures below the mid-humerus such as the hand, wrist, forearm, or elbow. The block targets the brachial plexus at the level of the cords, where it is in close proximity to the axillary artery. Ultrasound guidance has dramatically improved the safety and success of the infraclavicular approach.
  2. The Lumbar Plexus
  3. Psoas compartment blockis indicated for major surgeries of the hip and knee. When combined with sciatic nerve blockade, virtually any surgical procedure can be performed on the lower extremity. The incidence of sciatic nerve injury after total knee arthroplasty, unrelated to regional anesthesia technique, is reported to be in the range of 0.2% to 2.4%. Sciatic nerve blockade can mask these complications.

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Table 57-12 Recommended Dosing Regimen of Local Anesthetics for Continuous Peripheral Nerve Blockade

Catheter

Drug

Rate of nfusion

Patient Controlled Analgesia Bolus (mL)

Lockout (min)

Interscalene

Ropivacaine 0.2%
Bupivacaine 0.15%–0.2%

5–8 mL/hr

2–4

15–20

Infraclavicular

Ropivacaine 0.2%
Bupivacaine 0.15%–0.2%

5–8 mL/hr

2–4

15–20

Femoral

Ropivacaine 0.2%
Bupivacaine 0.15%–0.2%

5–10 mL/hr

5–10

30–60

Popliteal

Ropivacaine 0.2%
Bupivacaine 0.15%–0.2%

5–8 mL/hr

2

15–20

Paravertebral

Ropivacaine 0.2%
Bupivacaine 0.25% with
1:400,000
epinephrine

0.1–0.2 mL/kg/hr
0.1 mL/kg/hr

 

 

  1. Femoral Nerve Block.Although the nerve can be visualized with ultrasonography both above and below the inguinal ligament, it is ideally visualized at the level of the inguinal crease; at this level, the nerve is positioned approximately 0.5 cm lateral to the femoral artery. The nerve provides motor innervation to the quadriceps femoris, sartorius, and pectineus muscles as well as sensory innervation to the anterior thigh and knee and the medial aspect of the lower extremity terminating as the saphenous nerve. Femoral nerve blockade is tremendously effective for postoperative pain control after arthroscopic reconstruction of the anterior cruciate ligament with patellar tendon autograft.

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  1. Saphenous nerve blockadeis frequently combined with a lateral popliteal block or sciatic block for procedures involving the lower leg. The saphenous nerve is the only branch of the lumbar plexus below the knee and is the largest sensory terminal branch of the femoral nerve.
  2. Sacral Plexus
  3. After foot and ankle surgery, sciatic nerve blockade provides safe, effective, and long-lasting postoperative analgesia. Ultrasound guidance provides real-time visualization and high-quality images of the sciatic nerve.
  4. Paravertebral blockademay provide segmental analgesia for numerous surgical procedures (thoracotomy, mastectomy, nephrectomy, cholecystectomy, rib fractures, video-assisted thorascopic surgery, inguinal and abdominal procedures).

XII. Continuous Peripheral Nerve Blockade Caveats

Hemorrhagic complications, rather than neurologic deficits, appear to be the predominant risk associated with the performance of peripheral nerve blockade in anticoagulated patients.

XIII. Complications from Regional Anesthesia

The comparative safety of regional anesthesia compared with general anesthesia cannot be accurately determined. Serious complications associated with the performance of regional anesthesia include cardiac arrest, radiculopathy, cauda equina syndrome, and paraplegia (Table 57-13). The incidences of cardiac arrest and neurologic complications are higher after spinal anesthesia than after all other types of regional procedures.

XIV. Perioperative Pain Management of Opioid-Dependent Patients

The onus for the identification of opioid-dependent patients rests with the surgical team, preoperative evaluation staff, and anesthesia team (Table 57-14).

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Table 57-13 Risk Factors for Nerve Injury During the Performance of Regional Anesthesia

Variable

Risk Factors

Patient

Body habitus
Pre-existing neurologic disorder (diabetes mellitus, past chemotherapy)
Male gender
Advanced age

surgical

Direct surgical trauma or stretch
Prolonged tourniquet time
Hematoma
Infection
Tightly applied casts or surgical dressings
Patient positioning

Regional anesthesia

Mechanical injury from the needle or catheter
Chemical neurotoxicity from the local anesthetic
Ischemic injury to the nerve

  1. Preoperative managementinvolves determining the patient's “baseline” opioid requirement and instruction to the patient to take his or her normal opioid dose on the day of surgery.
  2. Patients maintained on methadone should continue their “baseline” dose throughout the perioperative period. Patients receiving greater than 200 mg/day of methadone may develop a prolonged QT interval, which places them at risk for torsades de pointes (a baseline electrocardiogram should be obtained).
  3. Full antagonists (naloxone, naltrexone) and the partial agonists–antagonists (nalbuphine, pentazocine, butorphanol) should be avoided because they precipitate withdrawal symptoms in opioid-dependent patients.
  4. Intraoperative managementof opioid-dependent patients requires the prudent use of fentanyl, morphine, or hydromorphone to provide effective intraoperative anesthesia and postoperative analgesia and to prevent opioid withdrawal. This requires the administration of the patient's “baseline” opioid requirement plus his or her intraoperative requirements secondary to surgical stimulation.

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Table 57-14 Surgical Guidelines for Perioperative Pain Management of Opioid-Tolerant Patients

Preoperative
Evaluation: Early recognition and high index of suspicion.
Identification: Identify factors such as total opioid dose requirement and previous surgery or trauma.
Consultation: Meet with addiction specialists and pain specialists for perioperative planning.
Reassurance: Discuss patient concerns related to pain control, anxiety, and risk of relapse.
Medication: Calculate the opioid dose requirement and modes of administration; provide anxiolytics as needed.
Intraoperative
Maintain baseline opioids (oral, transdermal, intravenous).
Increase the intraoperative and postoperative opioid dose to compensate for tolerance. Provide peripheral neural or plexus blockade (consider neuraxial techniques).
Use non-opioids as analgesic adjuncts.
Postoperative
Plan preoperatively for postoperative analgesia (include an alternative).
Maintain baseline opioids.
Use multimodal analgesic techniques.
Use patient-controlled analgesia (use as primary therapy or as supplementation for neuraxial techniques).
Continue neuraxial opioids.
Continue continuous neural blockade.
After Discharge
If surgery provides complete pain relief, opioids should be tapered rather than abruptly discontinued.
Develop a pain management plan before hospital discharge (provide adequate doses of opioid and non-opioid analgesics).

  1. Because of chronic opioid administration, opioid doses may need to be increased 30% to 100% vis-à-vis the opioid-naïve patient.
  2. The optimal intraoperative dose of opioid varies considerably from patient to patient; therefore, monitoring intraoperative vital signs such as heart rate, pupil size, and respiratory rate can be useful and allows the clinician to avoid the negative consequences of overdosing or underdosing the patient with opioid.
  3. Titrating fentanyl, morphine, or hydromorphone to a respiratory rate of 12 to 14 breaths/min and a moderately miotic pupil is recommended.

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  1. It is also recommend that patients who are receiving chronic methadone therapy may receive an additional intraoperative dose of 0.1 mg/kg IV, which can be titrated to hemodynamic effect and pupillary response.
  2. Postoperative Management
  3. Upon arrival to the recovery room, IV opioids may be administered on an “as needed” basis; however, initiation of an IV PCA opioid with both a basal and incremental (bolus) dose minimizes the risk of breakthrough pain.
  4. Non-opioid co-analgesics (low-dose ketamine) are opioid sparing and should be part of any multimodal perioperative pain management regimen in opioid-dependent patients.
  5. Regional anesthesia (peripheral nerve blockade, epidural analgesia) is highly recommended in this patient population.
  6. Careful monitoring of the patient for excessive sedation and respiratory depression is mandatory, and caregivers in the recovery room and on the postsurgical units should be alerted to the potential risk for respiratory depression when parenteral and neuraxial opioids are combined.
  7. Organization of Perioperative Pain Management Services

The effective management of pain is a crucial component of good perioperative care and recovery from surgery. Unrelieved pain and inadequate pain relief have detrimental physiologic and psychological effects on patients by slowing their recovery. The key components to establishing a successful perioperative pain management service begins with an institutional commitment to support the service. The team must be built around a physician leader with training and experience in pain medicine, and other anesthesiologists must be available to support the service.

XVI. Special Considerations in the Perioperative Pain Management of Children

Acute pain management in children undergoing surgery and invasive procedures offers several specific and unique challenges for anesthesiologists (Table 57-15).

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Table 57-15 Challenges for Acute Pain Management in Children

Importance of the child's parents and siblings
Unavoidable preoperative fear and anxiety (adversely impact postoperative pain and recovery from surgery)
Developmental and communications issues
Difficulty in evaluating the effectiveness of treatment

  1. Nonparenteral Analgesics
  2. Non-opioid analgesics(oral or suppository acetaminophen, ibuprofen, ketorolac) are important adjuvant analgesic therapies, often with oral midazolam.
  3. Opioid Analgesics.Codeine in combination with acetaminophen is commonly used with good effect for the management of moderate postoperative pain in ambulatory patients. Intranasal sufentanil can also be used to manage preoperative anxiety and postoperative analgesia in children.
  4. Patient-Controlled Analgesia.There are safety concerns with use of PCA in children that mandate a high level of surveillance with respect to the functioning of the equipment and careful patient monitoring that may be a limitation to its use in infants. PCA by proxy is a safety risk because there is no complete assurance that parents will be competent in assessing the intensity of their child's pain or be able to regulate bolus doses to avoid opioid overdosage.
  5. Epidural neuraxial analgesia(single-shot technique or continuous catheter technique) has become a key component of the perioperative pain management plan for infants and young children undergoing abdominal, urologic, and orthopaedic procedures.
  6. Nerve Blocks in Children.The introduction of small stimulating needles and ultrasound imaging along with long-acting local anesthetics and continuous catheter techniques in selected patients has resulted in an increase in the use of peripheral nerve blocks in children undergoing orthopaedic extremity procedures. Combined ilioinguinal and iliohypogastric nerve blocks performed under ultrasound guidance to reduce the volume of the injection have gained increasing interest for effective pain management in children undergoing inguinal herniorrhaphy.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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