- Email: [email protected]
PAIN MANAGEMENT IN TRAUMA
TRAUMA
0889-8537/99 $8.00
+ .OO
PAIN MANAGEMENT IN TRAUMA Nileshkumar Patel, MD, and Charles E. Smith, MD, FRCPC
Effective management of trauma victims necessitates a multidisciplinary approach that must include pain management specialists. This is because the effect of pain and the related stress response is almost always detrimental to patients. The immediate effects of pain, mediated by metabolic and neurohormonal mechanisms, lead to hyperglycemia, lipolysis, protein catabolism, increased antidiuretic and catecholamine levels, immunosuppression, and a hypercoagulable state (Table l ) . 1 8 Clinically, these manifest as hypertension, tachycardia, deep venous thrombosis, pulmonary embolism, immobility, splinting, ventilation perfusion mismatch, reduced gastrointestinal motility, water and salt retention, hypoxia, and infections. Collectively, these result in high morbidity, prolonged hospitalization, and higher costs. Adequate pain management in the acute setting also aids earlier rehabilitation and may reduce the incidence of long-term chronic pain syndromes. The purpose of this article is to familiarize readers with the factors that are important in the management of pain in the trauma setting, with emphasis on practicality. Although different regions of the body are considered separately, it is important to realize that trauma patients frequently present with injuries to multiple areas of the body, necessitating flexibility on the part of the pain management specialist. In the management of trauma patients, it is important to communicate with surgical colleagues. Issues such as monitoring of cerebral function need to be addressed in patients with head trauma. In patients with neurologic peripheral injuries, it is also often necessary to avoid the use of analgesic techniques that may reduce the surgeon’s ability to evaluate sensory and motor function.z8At all periods of intervention, the nature of current problems must be understood. This is best achieved by maintaining a current list of active problems because conditions are constantly changing in patients with
From the Pikeville College School of Osteopathic Medicine, Advanced Pain Management, Cudahy, Wisconsin (NP); and Department of Anesthesia, MetroHealth Medical Center, Case Western Reserve University, Cleveland, Ohio
ANESTHESIOLOGY CLINICS OF NORTH AMERICA
-
VOLUME 17 NUMBER 1 MARCH 1999
295
296
PATEL & SMITH
Table 1. CARDIOVASCULAR, METABOLIC, AND IMMUNE RESPONSE TO TRAUMA*
Sympathetic discharge and increased catecholamines Peripheral vasoconstriction Altered interstitial fluid matrix configuration Increased cardiac output Increased oxygen consumption Increased minute ventilation Increased lipolysis Increased muscle proteolysis Increased acute-phase proteins Increased gluconeogenesis and glycogenolysis Release of inflammatory mediators (e.g., tumor necrosis factor, leukotrienes) Activation of cytokine cascade and release of interleukins (IL1, IL2, IL6, IL8) Activation of complement cascade Activation of neutrophils Stimulation of lymphocytes Immunosuppression Hypercoagulable state 'Note that the magnitude and duration of change may vary considerably and are directly related to the phase and severity of injury. Adapted from Patel N, Smith CE: The effects of pain in the trauma patient. In Rosenberg AD, Bernstein R, Grande CM (eds):Perioperative Pain Management and Regional Anesthesia for the Trauma Patient. London, WB Saunders, 1998; with permission.
severe acute trauma, and this may influence the nature of the interventions that pain management specialists can offer. This article is divided into two sections. The first section deals with the management of acute trauma pain, and the second section highlights the commonly encountered chronic pain syndromes resulting from trauma. MANAGEMENT OF ACUTE PAIN Thoracic Trauma
In patients experiencing thoracic trauma, pain can arise from both penetrating (e.g., gunshot or stab wound) and blunt (eg., flail chest, multiple rib fractures, pulmonary contusion, pneumothorax, or disruption of the viscera and great vessels) injuries. The goal of adequate pain management is to improve ventilatory mechanics, allowing the patient to breathe deeply and to cough effectively to mobilize and clear secretions. Adequate pain control in the thoracic region not only prevents atelectasis and respiratory infections but more importantly can prevent episodes of hypoxia that may otherwise lead to the increased requirement for mechanical ~entilation.~, 'z 24, 33 In severely compromised patients with rib fractures, the use of aggressive techniques for controlling pain have reduced the need for mechanical ventilation.'",23 Interventional pain control techniques include intercostal nerve blocks and interpleural and epidural catheters to administer local anesthetic or opioid medications.'6,19, 27 Conventional Modes
Conventional modes of delivering analgesia, such as intramuscular (IM) administration of narcotics, provide inadequate analgesia because some periods
PAIN MANAGEMENT IN TRAUMA
297
of subtherapeutic narcotic blood levels depend on dosing intervals. Some issues also pertain to nursing delay leading to more frequent episodes of breakthrough pain. In addition, intramuscular administration of narcotics is time and resource intensive. The fact that larger doses of narcotics and narcotic-like agents are required means that patients suffer more side effects, including constipation, ileus, sedation, nausea, and vomiting. Intravenous Infusions
Intravenous infusions have certain advantages over IM, intermittent dosing regimens; however, even intravenous (IV) infusions do not provide optimal analgesia because inherent temporal variability exists in analgesic requirements in the trauma population. In addition, the initial dose titration is not only time intensive but also requires a long duration during which pain control is not adequate. Furthermore, episodes of hypoxia have been well documented in patients receiving IV infusions of narcotics. Intravenous Patient-ControlledAnalgesia
Intravenous patient-controlled analgesia (IVPCA) is a significant improvement over conventional modes of delivering narcotics to patients.' Because IVPCA allows patients to administer the medication to themselves during periods of alertness, this technique seems safe. Patients also have a sense of control when using IVPCA. The pain and oversedation cycles are reduced using this technique. The technique also is less demanding on nursing resources; however, its utility may be impaired by the significant costs involved in the acquisition and maintenance of computerized delivery pumps, pharmacy costs, and the need for personnel to monitor patients. Furthermore, neither IM nor IV analgesic routes seems to have any significant, positive influence on the stress response or morbidity (whereas the neuraxial route seems beneficial).*,13, 19, 34 The most frequently used opioid agonists in IVPCA are morphine and fentanyl (Table 2). Intercostal Nerve Blocks
Intercostal nerve blocks have been used for many years to treat rib-fracturerelated pain.7 The technique has repeatedly been shown to provide increased maximal inspiratory flow rates, superior analgesia, and better ability to cough and take deep breaths compared with other methods of pain contr01.~. *l The chief limitation of intercostal nerve blocks is that the relief of pain is temporary, lasting 6 to 12 hours or less. In addition, the risk for pneumothoraces limits its utility in the clinical setting. Although the technique is not complicated,
Table 2. GUIDELINES FOR INTRAVENOUS PATIENT-CONTROLLED ANALGESIA Opioid
Loading Dose
Morphine Hydromorphone Fentanyl Sufentanil Meperidine
0.054.1 mg/kg 0.014.02 mg/kg 0.5-1.0 pg/kg 0.074.1 pg/kg 0.5-1.0 mg/kg
Subsequent Dose
0.5-3.0 mg 0.14.5 mg 15-75 pg 2-10 pg 5-30 mg
Lockout (min)
Basal Ratelh
6-8 6-8 4 4 4-6 6-8
0.5-2.0 mg 0.14.3 mg 1 5 4 0 pg 2-8 Pg
5-20 mg
298
PATEL & SMITH
it may be difficult to perform if positioning poses a challenge in trauma patients?" Continuous intercostal nerve blockade has been shown to decrease pain scores and supplemental morphine use." lntrapleural Catheter
Interpleural catheter placed for thoracic pain has certain distinct advantages. Once the interpleural catheter is placed in an area close to the midpoint of the fractured ribs, one can use continuous infusions or intermittent injections to provide prolonged pain relief?] The major concerns with interpleural catheter placement are that the peak plasma levels of local anesthetics are relatively high. In addition, in patients with thoracostomy tubes, the risk of suctioning the injected local anesthetics must be guarded against. This is achieved by placing a catheter distant from the thoracostomy tube or delaying the suction of the thoracostomy tube for 15 to 30 minutes after injection of the local anesthetic through the interpleural catheter. Also, the use of interpleural catheters is patient-position-dependent.The tip of the catheter can migrate in certain patients, leading to inadequate analgesia. Epidural Analgesia Beneficial Effects
Epidural analgesia for thoracic pain has gained popularity since its first use in the late 1970s. This is because marked improvements in vital capacity and dynamic lung compliance have been shown with the use of local anesthetics and with narcotics administered through epidural catheters. An increase in functional residual capacity and a decrease in airway resistance have also been documented when analgesia is obtained through this route.'O, 34 The quality of analgesia is excellent such that deep respirations and coughing are possible, thereby preventing atelectasis.*O In addition, patients receiving continuous epidural analgesia (i.e., narcotics with or without local anesthetics) have been shown to have less ventilator-dependent time, decreased intensive care unit stays, shorter hospitalization, and decreased incidence of tracheostomies compared with control-matched groups with similar injury severity indices." In the trauma population, epidural analgesia leads to a lower incidence of respiratory depression, uses smaller doses of narcotics, and allows earlier ambulation and discharge compared with other modes of analgesia." The mortality rates, frequency of respiratory infections, and quality of pain relief reported by the patient are also superior in patients receiving epidural analgesia.I4 Limitations
Certain factors that preclude the use of epidural analgesia techniques in the trauma population are important to recognize. For example, sufficient time may not be available for insertion of epidural catheters in patients with unstable or emergent presentation and who require surgical intervention. Also, the nature of injuries may not permit adequate positioning for catheter placement. Patients with spinal cord injuries or with coagulopathy are also poor candidates for epidural analgesia. The use of local anesthetics may be inappropriate in patients whose hemodynamic status would not tolerate a sympathectomy. Also, epidural
PAIN MANAGEMENT IN TRAUMA
299
Table 3. CLINICAL PROPERTIES, ADVANTAGES, AND DISADVANTAGES OF HYDROPHILIC EPIDURAL OPlOlDS (e.g., MORPHINE, HYDROMORPHONE) Properties
Slow onset Long duration High CSF solubility
Advantages
Prolonged single-dose analgesia Thoracic analgesia with lumbar administration Minimal doses compared with intravenous administration
Extensive CSF spread CSF
=
-
Disadvantages
Delayed onset of analgesia Unpredictable duration Higher incidence of side effects Delayed respiratory depression
cerebrospinal fluid
analgesia may be inappropriate if the use of local anesthetics hinders the evaluation of patients’ neurologic functioning. Other contraindications to the placement of epidural catheters include septicemia, untreated bacteremia, and alterations in mental status. Even with these limitations, many patients are candidates for postoperative epidural analgesia, particularly while in the surgical intensive care unit. Choice of Agent
The choice of opioids used for epidural anesthesia is determined by the lipid solubility of the agent, location of the catheter, and location of pain. Hydrophilic narcotics, such as hydromorphone or morphine, have delayed onset and prolonged duration, with increased incidence of respiratory depression (Table 3). On the other hand, lipid-soluble agents such as fentanyl and sufentanil, have faster onset of action, shorter duration of analgesia, and fewer respiratory side effects (Table 4). Larger doses of lipid-soluble agents are required, however, because the analgesic effects may not be locally mediated. Adverse effects of epidural narcotics include pruritus, sedation, nausea and vomiting, urinary retention, apnea, and seizures.32,35 A rare but worrisome complication is the compression of the spinal cord from epidural hematoma.15 This must be recognized and requires immediate surgical evacuation if paraplegia is to be prevented. The potential for epidural hematoma is increased if coagulation is impaired at the time of insertion or removal of the Factors associated with respiratory depression from neuraxial narcotics deserve particular attention. These include elderly age, poor general condition;
Table 4. CLINICAL PROPERTIES, ADVANTAGES, AND DISADVANTAGES OF LlPOPHlLlC EPIDURAL OPlOlDS (E.G., FENTANYL, SUFENTANIL) Properties
Rapid onset Short duration Low CSF solubility
Advantages
Disadvantages
Rapid analgesia Decreased side effects Ideal for continuous infusion or PCEA
Systemic absorption Brief single-dose analgesia Limited thoracic analgesia with lumbar administration
-
-
Minimal CSF spread CSF = cerebrospinal fluid; PCEA
=
patient-controlled epidural analgesia
300
PATEL & SMITH
concomitant use of CNS depressant drugs or systemic narcotics; and, as men35 tioned previously, the use of hydrophilic Epidural analgesia can be delivered in intermittent boluses as continuous infusion and as patient-controlled epidural analgesia. The site of catheter placement (lumbar or t h ~ r a c i c and ) ~ the dosing regimens appear in Tables 5 to 7. Nonthoracic Trauma
Benefits of Pain Management for Patients with Nonthoracic Trauma
Patients suffering from extremity injuries, especially those requiring vascular reanastomosis, can be helped significantly by pain management physicians. Sympathetic hyperactivity occurs reflexively in patients with vascular disruptions, amputations, and peripheral crush injuries. Techniques that diminish sympathetic activity, such as the use of regional anesthesia and sympathetic blocks, augment blood flow to the appropriate extremity and not only help with pain relief but also improve the surgical outcome. Brachial plexus blockade is commonly instituted for upper extremity injuries and revascularization procedures. The interscalene approach is used for the shoulder and upper arm, whereas the axillary route is preferred for hand and arm procedures. This permits long-term administration of local anesthetics either by intermittent injection or continuous infusion. Noninvasive Doppler flowmetry can be used to demonstrate improvement in blood flow in patients receiving brachial plexus blockade. Although brachial plexus blockade is easy to perform, its use may be limited if frequent neurologic evaluation is needed in the postsurgical period. In patients with femoral neck fractures (see also article by Rosenberg in this issue), the use of triple nerve blocks (i.e., femoral, obturator, and lateral femoral cutaneous nerves) provides analgesia for as many as 48 hours. Other advantages of peripheral nerve blocks include reduced narcotics use and facilitation of physical rehabilitation. For lower extremity surgery, IVPCA with morphine is instituted most often and provides adequate pain control because the stress response is less marked with extremity injury compared with thoracic and upper abdominal trauma. Blunt or penetrating injuries involving the abdominal cavity can lead to significant respiratory compromise and patient morbidity. The goal of treatment is to reduce splinting and guarding so as to prevent decreases in functional
Table 5. PHARMACOLOGY OF EPIDURAL OPlOlDS
Opioid
Relative Lipid Solubility
Morphine Hydromorphone Meperidine Methadone Fentanyl Sufentanil
1 1.4 28 82 580 1270
Dose
1-5 mgt 0.2-1.0 mg 30-100 mg 4-8 mg 50-200 pg 10-50 pg
Onset (min)
Duration (h)”
30-90 20-30 15-25 10-20 5-15 5-15
6-24 6-18
*Duration of analgesia varies widely; higher doses produce longer durations. tLower dose range recommended for elderly patients or thoracic site of injection.
6 8 6-8 2 4 2 4
PAIN MANAGEMENT IN TRAUMA
301
Table 6. SUGGESTED DOSING PROTOCOLS FOR THORACIC EPIDURAL
CATHETERS (T4-T8) Bupivacaine-Morphine (bupivacaine, 1 mg/rnL, and morphine, 0.05 mg/rnL infusion) Patient Age (Y)
Morphine Loading Dose (mg)
Bupivacaine Loading Dose 0.25-0.5% (mL)
Infusion Rate (mUh)
PCEA Dose (mL) 20-min Delay
1544 45-65 66-75 76 +
4 3 2 1
5-8 4-6 4-5 3 4
6 5 3 2
3 4 2.5-3.0 1.5-2.0 1-2
Bupivacaine-Fentanyl (bupivacaine, 1 .O rng/rnL, with or without fentanyl, 5 pg/rnL infusion) Patient Age (Y)
Fentanyl Loading Dose (mg)
Bupivacaine Loading Dose 0.25-0.5% (mL)
Infusion Rate (mUh)
PCEA Dose (mL) 10-min Delay
15-44 45-65 66-75 76 +
100 100 75 50
5-8 4-6 4-5 3 4
6 5 4 3
4 3 4 24 1.5-2.0
Hydromorphone-Bupivacaine(bupivacaine, 1.O rng/mL, with or without hydromorphone, 0.01 rng/rnL infusion) Patient Age (Y)
Hydromorphone Loading Dose (mg)
1544 45-65 66-75 76 +
0.8 0.6 0.4 0.2
PCEA
=
Bupivacaine Loading Dose 0.25-0.5% (mL)
5-8 p6
4-5 34
Infusion Rate (mW
PCEA Dose (mL) 15-min Delay
6 5 3 2
3 4 2.5-3.0 1.5-3.0 1-2
patient-controlled epidural analgesia
residual capacity, vital capacity, and maximum expiratory flow. The intermittent administration of IM narcotics is deemed to be inadequate in achieving these goals. Whenever permitted, aggressive techniques should be available for trauma patients just as they are available for patients undergoing elective upper abdominal surgery. Head-injured patients require continuous neurologic status monitoring. In the acute setting, it is difficult to achieve a balance between adequate pain control and sedative side effects that may hamper neurologic assessment. This is particularly an issue in multiply injured trauma patients, especially if mechanical ventilation is required?* In such cases, short-acting sedative agents ( e g , propofol) or nonsteroidal anti-inflammatory agents ( e g , ketorolac) administered parenterally often suffice. Regional Blockade Techniques
Awareness and appreciation of the anatomy, complications, and contraindications to regional anesthesia and analgesia techniques are necessary before
302
PATEL&SMITH
Table 7. SUGGESTED DOSING PROTOCOLS FOR LUMBAR EPIDURAL CATHETERS (L1 -L4) Bupivacaine-Fentanyl (bupivacaine,0.625-1 .O mg/mL and fentanyl, 5 pg/mL infusion) Patient Age (y)
Fentanyl Loading Dose (pg)
Bupivacaine Loading Dose 0.2545% (mL)
15-44 45-65 66-75 76
100-200 100-150 50-99 50
12-16 8-14 6-12
+
523
Infusion Rate (mm)
PCEA Dose (mL) 10-20-min Lockout
8-12 6-10 4-8 3-6
4-45
s 5 2 4 1.54.0
Morphine-Bupivacaine (morphine, 0.05 mg/mL infusion with or without bupivacaine,
0.625 ma/mL) Patient Age (y)
15-44 45-65 66-75 76 +
Morphine Loading Dose (mg)
Bupivacaine Loading Dose 0.2545% (mL)
4
10-14 6-12 5-8 4-6
3 2 1
Infusion Rate (mW
PCEA Dose (mL) 20-min Lockout
8 6
4
4
2-3 1-2
2
%4
~
Hydromorphone-Bupivacaine (hydromorphone,0.01 mg/mL infusion with or without
buDivacaine, 0.625 ma/mL1 Patient Age (y) 15-44 45-65 66-75 76 i-
Hydromorphone Loading Dose (mg)
Bupivacaine Loading Dose 0.2545% (mL)
0.8 0.6 0.4 0.2
10-14 6-12 5-8 4-6
Infusion Rate (mW 8 6
4 2
PCEA Dose (mL) 15-min Lockout 4
3-4 2-3 1-2
PCEA = patient-controlled epidural analgesia.
conducting these procedures. Because this is beyond the scope of this article, the reader is referred to standard textbooks of regional anesthesia.6, Thoracic Epidural Catheter Insertion
The paramedian approach is preferred to the midline approach because the steepness of the spine is avoided and identification of safe depth of the lamina and ligament is permitted. After sterile preparation and draping, superficial local infiltration is performed with a 25-gauge needle approximately 1 cm lateral to the spinous process. Deeper local infiltration is performed with a 4 cm 22gauge needle, which is then used to identify the vertebral lamina. The needle should be advanced until the lamina has been fully identified. Infiltration of the periosteum is performed, and the exploring needle is walked cranially to the upper border of the lamina, where the ligament flavum has its insertion. The 22-gauge needle is removed’and an 18-gauge Touhy needle is inserted in a similar fashion until the ligamentum flavum is encountered. The epidural space is then identified by the loss-of-resistance technique. Because the interspinous ligament is not encountered with the paramedian approach, true loss of
PAIN MANAGEMENT IN TRAUMA
303
resistance may not occur until the ligmentum flavum is engaged. Many physicians prefer to use continuous pressure on the plunger of a glass syringe with saline to optimize the sensitivity of bss of resistance. A key point is to avoid incorrect extreme lateral angulation of the needle. After the epidural space is identified, the epidural catheter is threaded and the Touhy needle withdrawn. A test dose of 3 to mL of 1.5% lidocaine with 15 pg of epinephrine is injected to identify potential spinal or intravascular catheter placement. The catheter is taped and secured. For patients with anticipated longer use of catheter, a microfilter is attached to the proximal end of the epidural catheter. Caution is taken to avoid contamination. Suggested dosing protocols are shown in Table 6. Lumbar Epidural Catheter Insertion
The bony landmarks are palpated and the L4 lumbar vertebra is identified at the level of the iliac crest. The L2-L3 and L3-L4 interspaces are most often used. An intradermal wheal is raised with the local anesthetic exactly over the chosen interspace, and deep infiltration of local anesthetic is made using a 25gauge, 4 cm needle. The Touhy needle is inserted into the middle of the interspace at right angles to the skin. The needle is then advanced until it is firmly engaged in the interspinous ligament and advanced to penetrate into the ligamentum flavum. A syringe containing air or saline is attached to the needle, and light, continuous pressure is maintained on the syringe plunger to identify the epidural space by loss of resistance. The most difficult part of the technique is to learn to control the advancing of the needle, which must not penetrate the epidural space beyond the needle bevel. The position of the hands and fingers on the needle and syringe is crucial. The index finger of the noninjecting hand may be held firmly against the patient‘s back to act as a resistance to sudden, forward movement. The epidural catheter is then inserted and the Touhy needle removed. Again, the intrathecal or intravascular placement of the catheter should be ruled out with 3 mL of 1.5% lidocaine and 15 pg of epinephrine. Brachial Plexus Blockade
Axillary Block. A 4-cm, 18- to 20-gauge short beveled needle attached to plastic extension tubing is used. The axillary artery is palpated continuously and the needle inserted just above the artery in the proximal portion of the axilla. It is directed toward the apex of the axilla. The needle is advanced slowly and kept close to the artery and in the same plane as the artery. Penetration of the neurovascular sheath is usually felt as a ”give” as the needle is advanced and paresthesias are elicited in the hand. If the needle is then left untouched, it is seen moving with arterial pulsation, confirming its close relationship to the artery. If the needle is advanced, it enters the artery, and it may be withdrawn and realigned. Alternatively, an insulated needle may be advanced within the neurovascular sheath with the aid of a nerve stimulator.” Insertion of a catheter over a needle and into the neurovascular sheath is possible. Them should be no obstruction to the forward movement of the catheter if the needle is corre~tlyplaced. The catheter can then be used for continuous, prolonged anesthesia. For the continuous infusion method, 0.25% bupivacaine is given at 10 mL/h. Alternatively, 0.5% bupivacaine with 1:200,000 epinephrine can be injected at intervals of 6 to 8 hours.
304
PATEL & SMITH
Interscalene Approach. The patient is supine with the head turned away from the side to be blocked. The interscalene groove is identified just lateral to the anterior scalene muscle at the level of the cricothyroid cartilage. A skin wheal is raised with local anesthetic, and a 20-gauge needle is inserted and directed caudally until paresthesias are identified below the shoulder. After ensuring the absence of aspiration of blood and cerebrospinal fluid, 20 to 40 mL of 1% lidocaine or 0.25% to 0.5% bupivacaine is injected. This provides analgesia for 3 to 10 hours depending on the agent. The incidence of ipsilateral phrenic nerve palsy is 100%; therefore, this approach should be used cautiously if pulmonary status is marginal. Three-in-OneBlock
The inguinal ligament and the femoral artery pulse are identified. The puncture site is below the inguinal ligament 1 to 2 cm lateral to the femoral artery. The insertion of the needle is in a slightly cranial direction until a paresthesia is elicited. The local anesthetic is injected at the site of the femoral nerve within the sheath. If an adequate volume is used, the local anesthetic diffuses proximally to block the femoral nerve, the lateral cutaneous nerve of the thigh, and the obturator nerve. A dose of 25 to 30 mL of 1% lidocaine or 0.5% bupivacaine is appropriate. This should provide analgesia for 4 to 12 hours for patients undergoing surgical correction of femoral nerve neck fractures. Interpleural Analgesia Technique
A Touhy needle is inserted into the pleural space approximately 8 to 10 cm from the spinous process at the eighth or ninth intercostal space. The loss-ofresistance technique is used and the movement of the syringe plunger observed with inspiration. An epidural catheter is inserted to a depth of 5 to 8 cm, and the needle is removed. The epidural catheter is placed as close to the site of injury as possible. The catheter is then aspirated for blood, fluid, or air. For post-thoracotomy pain, the catheter may be inserted by the surgeon under direct vision. The catheter is secured with a suture and a sterile dressing. Twenty milliliters of 0.5% bupivacaine are injected with 1:200,000 epinephrine. The chest tube (if present) is clamped for 15 to 30 minutes following the bolus dose injection to prevent the loss of the anesthetic agent. Repeat boluses are reinjected as needed on an average of 4 to 6 hours. For continuous infusion, the interpleural catheter is bolused with 0.4 mL/kg of 0.5% bupivacaine with epinephrine 1:200,000, followed by a continuous infusion of 0.25% bupivacaine at 0.1 to 0.2 mL/kg/h. CHRONIC PAIN SYNDROMES RESULTING FROM TRAUMA Delayed Pain in Trauma
Soft tissue injuries occur with all trauma. The degree of injury, treatment, and patient characteristics determine whether acutely injured trauma patients will develop chronic regional pain syndromes, myofascial pain syndromes, fibromylagia, chronic low back pain, phantom pain, or posttraumatic headaches. In patients sustaining thoracic trauma from rib fractures or thoracostomy tube placement and from surgical retractors a recognized long-term complication
PAIN MANAGEMENT IN TRAUMA
305
of neuropathic pain exists. This may result from neural entrapment or direct laceration of the nerve endings. The condition is very difficult to treat, and management often includes long-term use of narcotics to control pain. Fibromyalgia occurs in at least 10% of patients with a history of trauma. The syndrome does not always correlate with the severity of trauma, and even minor degrees of trauma can render patients disabled. The best outcomes in these patients are frequently the result of early recognition and aggressive therapy because treatment of established fibromyalgia is very challenging. Whiplash injuries and posttraumatic headaches cause another significant long-term problem in patients sustaining head and neck trauma. Posttraumatic headaches are ascribed to excessive muscle contraction, scarring, entrapment of sensory nerves at the site of injury, or vasodilation. Headaches can become chronic and are frequently difficult to treat. In the authors’ experience, posttraumatic headaches continue to improve over the initial 6 months after injury, following which is a significant plateau. Another sequela of head and neck trauma is disorders of the temporomandibular joint. Unless a Lefort fracture is also present, many temporomandibular disorders are not readily apparent after the initial injuries and must be sought and treated at the earliest possible interval to prevent any long-term consequences. Orthopedic injuries involving the lower extremities can lead to significant long-term morbidity because of alterations in posture and restriction of normal range of motion.8 Often, an ongoing limp and subsequent compensatory gait asymmetry are present. The goal of treatment of chronic posttraumatic pain is essentially to learn to recognize the symptoms and treat them early on to avoid any long-term sequelae. For patients, this includes pain, disability, and emotional and financial loss. For society, this involves increased resource utilization, including the use of medical and social services. Patients with trauma to the extremities may have sympathetic mediated pain, whereas amputees may experience postamputation, or phantom, limb pain (PLP). Postamputation (Phantom) Limb Pain
Chronic awareness of an amputated limb is a well-known phenomenon. PLP is characterized by sensory disturbances, including significant pain and aberrations in touch, temperature, and pressure sensations. The incidence of PLP decreases with time and may be as high as 100% in the immediate postamputation period, dropping to 5% to 10% after several years; however, the onset of pain may be weeks or months after the initial amputation. The characteristics of PLP are also time dependent. Initially, it is a shooting, sharp, localized pain that is later described as burning, cramping, and squeezing in nature. The pain is usually felt in the distal portion of the phantom limb, but with time, it can be felt more proximally. The pathophysiology of PLP is not established. Peripheral stimulation of injured nerve endings and trigger points cause severe, prolonged pain in PLP patients. Although stump revision and local anesthesia infiltrations reduce the pain, these modalities rarely provide complete or lasting relief. This suggests that the CNS may account for a significant portion of the pain. A component of PLP may be sympathetic mediated because burning dysesthesia, hypersensitivity to cold and light touch, local vasoconstriction, and excessive sweating are often described; however, sympathectomy has not been found to be highly successful in alleviating PLP symptoms. The spinal origin of PLP is suggested by efficacy
306
PATEL & SMITH
of intrathecal opiates in the treatment of patients with established PLP. Inhibitory influences from the midbrain are proposed to be sustained by afferent input from the normal limb, and cessation of the afferent sensory input on amputation is proposed to lead to reduction of inhibitory influences and uncontrolled pain. Although anxiety and depression may exacerbate PLP, they do not cause PLP. A lack of clear understanding of the pathophysiology of PLP means that no single therapeutic modality can be successful in the treatment of patients with PLP. Correctable contributing factors, such as stump pain, ill-fitting prostheses, lack of soft tissue padding, and localized ischemia and infections, should be addressed first. Physiotherapy and stress therapy are as important as pharmacokinetics and surgical interventions. Pharmacologic agents, including nonsteroidal anti-inflammatory drugs, antiepileptics, antidepressants, and narcotics, have all been tried and seem to have some temporary effect. In the short term, transcutaneous electrical stimulation has also been demonstrated to be effective. Patients with a history suggestive of sympathetic mediated pain benefit from a series of sympathetic blocks. Likewise, dorsal root rhizotomy and dorsal column stimulation may provide satisfactory analgesia for the short term. Multidisciplinary approaches seem to offer the greatest hope. Complex Regional Pain Syndromes
Complex regional pain syndromes (CRPS; formerly known as reflex sympathetic dystrophy or cuusulgiu) are a group of disorders characterized by pain and relief of pain following sympathetic blockade at some stage of the disease process. Reflex sympathetic dystrophy differs from causalgia by the absence of any major nerve damage. Any trauma (e.g., fractures, sprains, injections, minor injuries, or surgical incision) can lead to CRPS. Several hypotheses exist to explain the occurrence of CRPS, the most plausible being that the initial immediate response to trauma is the propagation of active potentials via c-nociceptor fibers through the dorsal root ganglion to the spinal cord, where wide-dynamic-range neurons are activated and sensitized. The wide-dynamic-range neurons remain sensitized and respond to activity in large-diameter A-mechanoceptors, which are activated by light touch. This state produces allodynia (i.e., pain arising from a stimulus that does not normally produce pain). The sympathetic nervous system has been shown to influence the function of the mechanoceptors. The same sensitized wide-dynamic-range neurons can respond to a mechanoceptor activity initiated by the sympathetic system in the sensory receptor. This state represents sympathetically mediated pain. Evidence shows that primary afferent nociceptor activity has heightened responsiveness to norepinephrine, so the actual pain may also be mediated by alpha-adrenergic receptors. Clinical hallmarks of CRPS are burning pain and hyperesthesia (i.e., exquisite sensitivity to stimulation). The onset of pain is usually days after trauma but may be weeks later. Pain is distal, around the site of trauma, diffuse in nature, and not conforming to any dermatomal or neural distribution. It is exacerbated by touch, air movement, cold, emotional stress, or dependent limb posture. Pain progresses proximally and may encompass the entire extremity with time. Associated changes include edema, followed by skin thinning and increased hair growth. Nails may become rigid and brittle. Muscle stiffness and soreness is seen early, with associated reduced strength, tremors, and dystonia. All movements are reduced, and bone demineralization ensues. CRPSs are staged as acute (I), dystrophic (11), and atrophic (111) (Table 8).
PAIN MANAGEMENT IN TRAUMA
307
Table 8. STAGES OF COMPLEX REGIONAL PAIN SYNDROMES Characteristics
Symptoms and signs
Acute (1)
Dystrophic (2)
Atrophic (3)
Allodynia; warm, dry, swollen skin; soft edema; hair
Dysesthesia; cold, moist, cyanotic skin;
Coarse, thick, brittle hair; shriveled skin; disuse atrophy; contractures; severe osteoporosis; chronic persistent changes, unlikely to return to normal
excess;
hyperpathia; increased blood flow; increased temperature; patchy osteoporosis Onset of symptoms Clinical course
Within days of injury
Responds to
brawny edema;
coarse, decreased hair growth; thick, raised nails; decreased nail
growth; decreased temperature; decreased blood flow; diffuse osteoporosis Days or months from injury Responsive phase
treatment
Functional outcome
Impaired
6 1 2 mo after injury
Poor response to treatment
Restricted
Severely restricted
The diagnosis of CRPS is usually made clinically, but any test that shows alterations in blood flow, sweating, or temperatures may be of use in the diagnosis and follow-up of patients with CRPS. Most commonly, skin temperatures (measured with thermography, liquid crystal thermometry, or electronically with thermistors and thermocouples) are compared among extremities to evaluate the degree of asymmetry of sympathetic activity among affected and normal sides. A more definitive diagnosis is aided by the interruption of pathologic sympathetic activity by either pharmacologic means or by sympathetic blocks. Sympathetic blockade may be achieved at the ganglion level (cervicothoracic ganglion blockade for the upper extremity and lumbar sympathetic blockade for the lower extremity) or at the postganglion level (IV regional sympathetic blockade). Sympathetic blocks aid in diagnosis and therapy. Diagnostic blocks should be confirmed by the absence of provocation of pain by cold, stress, reversal of sympathetic effector responses, and return of normal sensation in the affected area. Thermography, sudomotor function evaluation, and plethysmography all provide objective measures of response to sympathetic block, but the most commonly used is a simple measure of distal temperatures before and after the block in the affected extremity because the loss of vasoconstriction results in an increase in the distal skin temperature. Effective physical therapy is the mainstay of treatment of patients with CRPS. The goal is to increase range of motion in the joint and muscle groups of the afflicted areas. Adequate analgesia must be provided with regional analgesia or sympathetic blockade to permit the necessary physical therapy. With sympathetic blocks, a "staircase" pattern is sought, with increasing pain relief for longer periods with each successive block. For more prolonged sympathectomy, chemical neurolysis (either 6% phenol or 50% alcohol) lasts weeks, but surgical sympathectomy may be an alternative if pain relief does not last.
ACKNOWLEDGMENT The authors thank Fran Hall for preparing the manuscript.
308
PATEL & SMITH
References 1. Ballantyne JL, Carr DB, Chalmers TC, et a1 Postoperative patient-controlled analgesia: Meta-analyses of initial randomized controlled trials. J Clin Anesth 5:182-193, 1993 2. Benzon HT, Wong HY, Belavic AM, et al: A randomized double-blind comparison of epidural fentanyl infusion versus patient-controlled analgesia with morphine for postthoracotomy pain. Anesth Analg 76316-322, 1993 3. Benzon HT: Post-thoracotomy epidural analgesia: Lumbar or thoracic placement? J Cardiothorac Vasc Anesth 7515-516, 1993 4. Bergh NP, Dottori 0, Lof BA, et al: Effect of intercostal nerve block on lung function after thoracotomy. Acta Anaesthiol Scand 18(Suppl 24):85-95, 1966 5. Bromage PR The control of post thoracotomy pain. Anaesthesia 44:445446, 1989 6. Brown DL: Atlas of Regional Anesthesia. Philadelphia, WB Saunders, 1992 7. Bryant LR, Trinkle JK, Wood RE: A technique for intercostal nerve block after thoracotomy. Ann Thorac Surg 11:388-391, 1971 8. Cohen S, Alagesan R, Alagesan R, et al: Acute and chronic posttraumatic pain. Problems in Anesthesia 8:487-517, 1994 9. Cousins MJ, Bridenbaugh PO (eds): Neural Blockade in Clinical Anesthesia and Management of Pain, ed 3, Philadelphia, Lippincott-Raven, 1998 10. Dittman M, Steenblock U, Kranzlin M, et al: Epidural analgesia or mechanical ventilation for multiple rib fractures. Intensive Care Med 8:89-92, 1982 11. Dryden CM, McMenermin I, Duthie DJR Efficacy of continuous intercostal bupivacaine for pain relief after thoracotomy. Br J Anaesth 70:508-510, 1993 12. Gibbons J, James 0, Quail A: Relief of pain in chest injury. Br J Anaesth 45:1136-1138, 1973 13. Glass PSA, Estok P, Ginsberg 8, et al: Use of patient controlled analgesia to compare the efficacy of epidural to intravenous fentanyl administration. Anesth Analg 74345351, 1992 14. Grass JA: Surgical outcome: Regional anesthesia and analgesia versus general anesthesia. Anesthesiol Rev 10117-125, 1993 15 Gustofsson H, Ruthberg H, Bengtsson M Spinal hematoma following epidural analgesia: Report of a patient with ankylosing spondylitis and a bleeding diathesis. Anaesthesia 43:220-222, 1988 16. Johnston JR, McCaughey W Epidural morphine: A method of management of multiple rib fractures. Anaesthesia 35:155-157, 1980 17. Kavanagh BE‘, Katz J, Sandler A N Pain control after thoracic surgery: A review of current techniques. Anesthesiology 81:737-759, 1994 18. Kehlet H: The-surgical stress response: Should it be prevented? Can J Surg 34:565567, 1991 19. Kehlet H, Dahl JB: The value of ”multimodal” or ”balanced analgesia” in postoperative pain treatment. Anesth Analg 771048-1056, 1993 Epidural anesthesia and analgesia: Their role in surgical 20. Liu S, Carpenter RL, Neal JM: outcome [review]. Anesthesiology 821474-1506, 1995 21. Liu M, Rock P, Grass JA, et al: Double-blind randomized evaluation of intercostal nerve blocks as an adjuvant to subarachnoid administered morphine for post-thoracotomy analgesia. Reg Anesth 20418-425, 1995 22. Mackersie RC, Karagianes TG: Pain management following trauma. Crit Care Clin 6:433-449, 1990 23. Mackersie RC, Shackford SR, Hoyt DB, et al: Continuous epidural fentanyl analgesia: Ventilatory function improvement with routine use in treatment of blunt chest trauma. J Trauma 271207-1212, 1987 24. O’Connor CJ: Thoracic epidural analgesia: physiologic effects and clinical applications. I Cardiothoracic Vasc Anesth 7595409. 1993 25. Owens EL, Kasten GW, Hessel EA: Spinal hematoma after lumbar puncture and heparinization. Anesth Analg 65:1201-1207, 1986 26. Pate1 N, Smith CE: The effects of pain in the trauma patient. In Rosenberg AD, Bemstein R, Grande CM (eds): Perioperative Pain Management and Regional Anesthesia for the Trauma Patient. London, WB Saunders, 1998
PAIN MANAGEMENT IN TRAUMA
309
27. Rankin AR, Comber RE: Management of fifty cases of chest injury with a regimen of epidural bupivacaine and morphine. Anaesth Intensive Care 12311-314,1984 28. Rauck RL: Trauma. In Raj PP (ed): Pain Medicine: A Comprehensive Review. St. Louis, Mosby-Year Book, 1996 29. Rosenberg A, Albert DB, Bemstein RL: Regional anesthesia for orthopaedic trauma. Problems in Anesthesia 842+$44,1994 30. Rawal N, Sjostrand U, Dahlstrom B, et al: Epidural morphine for post-operative pain relief A comparative study with intramuscular narcotic and intercostal nerve block. Anesth Analg 61:93-98, 1982 31. Safran D, Kuhlman G, Orhaut E, et al: Continuous intercostal blockade with lidocaine afler thoracic surgery. Anesth Analg 70345-349, 1990 32. Scherer R, Schmutzler M, Giebler R, et a1 Complications related to thoracic epidural analgesia: A prospective study in 1071 surgical patients. Acta Anaesthesiol Scand 3737&374,1993 33. Shulman M S Managing post thoracotomy pain. Problems in Anesthesia 4:37&392, 1990 34. Shulman M, Sandler AN, Bradley JW, et al: Post thoracotomy pain and pulmonary function following epidural and systemic morphine. Anesthesiology 61:569-575, 1984 35. Tanaka K, Watanabe R, Harada T, et a1 Extensive application of epidural anesthesia and analgesia in a university hospital: Incidence of complications related to technique. Reg Anesth 183438,1993
Address reprint requests to Charles E. Smith, MD Department of Anesthesiology MetroHealth Medical Center 2500 MetroHealth Drive Cleveland, OH 44109
0889-8537/99 $8.00
+ .OO
PAIN MANAGEMENT IN TRAUMA Nileshkumar Patel, MD, and Charles E. Smith, MD, FRCPC
Effective management of trauma victims necessitates a multidisciplinary approach that must include pain management specialists. This is because the effect of pain and the related stress response is almost always detrimental to patients. The immediate effects of pain, mediated by metabolic and neurohormonal mechanisms, lead to hyperglycemia, lipolysis, protein catabolism, increased antidiuretic and catecholamine levels, immunosuppression, and a hypercoagulable state (Table l ) . 1 8 Clinically, these manifest as hypertension, tachycardia, deep venous thrombosis, pulmonary embolism, immobility, splinting, ventilation perfusion mismatch, reduced gastrointestinal motility, water and salt retention, hypoxia, and infections. Collectively, these result in high morbidity, prolonged hospitalization, and higher costs. Adequate pain management in the acute setting also aids earlier rehabilitation and may reduce the incidence of long-term chronic pain syndromes. The purpose of this article is to familiarize readers with the factors that are important in the management of pain in the trauma setting, with emphasis on practicality. Although different regions of the body are considered separately, it is important to realize that trauma patients frequently present with injuries to multiple areas of the body, necessitating flexibility on the part of the pain management specialist. In the management of trauma patients, it is important to communicate with surgical colleagues. Issues such as monitoring of cerebral function need to be addressed in patients with head trauma. In patients with neurologic peripheral injuries, it is also often necessary to avoid the use of analgesic techniques that may reduce the surgeon’s ability to evaluate sensory and motor function.z8At all periods of intervention, the nature of current problems must be understood. This is best achieved by maintaining a current list of active problems because conditions are constantly changing in patients with
From the Pikeville College School of Osteopathic Medicine, Advanced Pain Management, Cudahy, Wisconsin (NP); and Department of Anesthesia, MetroHealth Medical Center, Case Western Reserve University, Cleveland, Ohio
ANESTHESIOLOGY CLINICS OF NORTH AMERICA
-
VOLUME 17 NUMBER 1 MARCH 1999
295
296
PATEL & SMITH
Table 1. CARDIOVASCULAR, METABOLIC, AND IMMUNE RESPONSE TO TRAUMA*
Sympathetic discharge and increased catecholamines Peripheral vasoconstriction Altered interstitial fluid matrix configuration Increased cardiac output Increased oxygen consumption Increased minute ventilation Increased lipolysis Increased muscle proteolysis Increased acute-phase proteins Increased gluconeogenesis and glycogenolysis Release of inflammatory mediators (e.g., tumor necrosis factor, leukotrienes) Activation of cytokine cascade and release of interleukins (IL1, IL2, IL6, IL8) Activation of complement cascade Activation of neutrophils Stimulation of lymphocytes Immunosuppression Hypercoagulable state 'Note that the magnitude and duration of change may vary considerably and are directly related to the phase and severity of injury. Adapted from Patel N, Smith CE: The effects of pain in the trauma patient. In Rosenberg AD, Bernstein R, Grande CM (eds):Perioperative Pain Management and Regional Anesthesia for the Trauma Patient. London, WB Saunders, 1998; with permission.
severe acute trauma, and this may influence the nature of the interventions that pain management specialists can offer. This article is divided into two sections. The first section deals with the management of acute trauma pain, and the second section highlights the commonly encountered chronic pain syndromes resulting from trauma. MANAGEMENT OF ACUTE PAIN Thoracic Trauma
In patients experiencing thoracic trauma, pain can arise from both penetrating (e.g., gunshot or stab wound) and blunt (eg., flail chest, multiple rib fractures, pulmonary contusion, pneumothorax, or disruption of the viscera and great vessels) injuries. The goal of adequate pain management is to improve ventilatory mechanics, allowing the patient to breathe deeply and to cough effectively to mobilize and clear secretions. Adequate pain control in the thoracic region not only prevents atelectasis and respiratory infections but more importantly can prevent episodes of hypoxia that may otherwise lead to the increased requirement for mechanical ~entilation.~, 'z 24, 33 In severely compromised patients with rib fractures, the use of aggressive techniques for controlling pain have reduced the need for mechanical ventilation.'",23 Interventional pain control techniques include intercostal nerve blocks and interpleural and epidural catheters to administer local anesthetic or opioid medications.'6,19, 27 Conventional Modes
Conventional modes of delivering analgesia, such as intramuscular (IM) administration of narcotics, provide inadequate analgesia because some periods
PAIN MANAGEMENT IN TRAUMA
297
of subtherapeutic narcotic blood levels depend on dosing intervals. Some issues also pertain to nursing delay leading to more frequent episodes of breakthrough pain. In addition, intramuscular administration of narcotics is time and resource intensive. The fact that larger doses of narcotics and narcotic-like agents are required means that patients suffer more side effects, including constipation, ileus, sedation, nausea, and vomiting. Intravenous Infusions
Intravenous infusions have certain advantages over IM, intermittent dosing regimens; however, even intravenous (IV) infusions do not provide optimal analgesia because inherent temporal variability exists in analgesic requirements in the trauma population. In addition, the initial dose titration is not only time intensive but also requires a long duration during which pain control is not adequate. Furthermore, episodes of hypoxia have been well documented in patients receiving IV infusions of narcotics. Intravenous Patient-ControlledAnalgesia
Intravenous patient-controlled analgesia (IVPCA) is a significant improvement over conventional modes of delivering narcotics to patients.' Because IVPCA allows patients to administer the medication to themselves during periods of alertness, this technique seems safe. Patients also have a sense of control when using IVPCA. The pain and oversedation cycles are reduced using this technique. The technique also is less demanding on nursing resources; however, its utility may be impaired by the significant costs involved in the acquisition and maintenance of computerized delivery pumps, pharmacy costs, and the need for personnel to monitor patients. Furthermore, neither IM nor IV analgesic routes seems to have any significant, positive influence on the stress response or morbidity (whereas the neuraxial route seems beneficial).*,13, 19, 34 The most frequently used opioid agonists in IVPCA are morphine and fentanyl (Table 2). Intercostal Nerve Blocks
Intercostal nerve blocks have been used for many years to treat rib-fracturerelated pain.7 The technique has repeatedly been shown to provide increased maximal inspiratory flow rates, superior analgesia, and better ability to cough and take deep breaths compared with other methods of pain contr01.~. *l The chief limitation of intercostal nerve blocks is that the relief of pain is temporary, lasting 6 to 12 hours or less. In addition, the risk for pneumothoraces limits its utility in the clinical setting. Although the technique is not complicated,
Table 2. GUIDELINES FOR INTRAVENOUS PATIENT-CONTROLLED ANALGESIA Opioid
Loading Dose
Morphine Hydromorphone Fentanyl Sufentanil Meperidine
0.054.1 mg/kg 0.014.02 mg/kg 0.5-1.0 pg/kg 0.074.1 pg/kg 0.5-1.0 mg/kg
Subsequent Dose
0.5-3.0 mg 0.14.5 mg 15-75 pg 2-10 pg 5-30 mg
Lockout (min)
Basal Ratelh
6-8 6-8 4 4 4-6 6-8
0.5-2.0 mg 0.14.3 mg 1 5 4 0 pg 2-8 Pg
5-20 mg
298
PATEL & SMITH
it may be difficult to perform if positioning poses a challenge in trauma patients?" Continuous intercostal nerve blockade has been shown to decrease pain scores and supplemental morphine use." lntrapleural Catheter
Interpleural catheter placed for thoracic pain has certain distinct advantages. Once the interpleural catheter is placed in an area close to the midpoint of the fractured ribs, one can use continuous infusions or intermittent injections to provide prolonged pain relief?] The major concerns with interpleural catheter placement are that the peak plasma levels of local anesthetics are relatively high. In addition, in patients with thoracostomy tubes, the risk of suctioning the injected local anesthetics must be guarded against. This is achieved by placing a catheter distant from the thoracostomy tube or delaying the suction of the thoracostomy tube for 15 to 30 minutes after injection of the local anesthetic through the interpleural catheter. Also, the use of interpleural catheters is patient-position-dependent.The tip of the catheter can migrate in certain patients, leading to inadequate analgesia. Epidural Analgesia Beneficial Effects
Epidural analgesia for thoracic pain has gained popularity since its first use in the late 1970s. This is because marked improvements in vital capacity and dynamic lung compliance have been shown with the use of local anesthetics and with narcotics administered through epidural catheters. An increase in functional residual capacity and a decrease in airway resistance have also been documented when analgesia is obtained through this route.'O, 34 The quality of analgesia is excellent such that deep respirations and coughing are possible, thereby preventing atelectasis.*O In addition, patients receiving continuous epidural analgesia (i.e., narcotics with or without local anesthetics) have been shown to have less ventilator-dependent time, decreased intensive care unit stays, shorter hospitalization, and decreased incidence of tracheostomies compared with control-matched groups with similar injury severity indices." In the trauma population, epidural analgesia leads to a lower incidence of respiratory depression, uses smaller doses of narcotics, and allows earlier ambulation and discharge compared with other modes of analgesia." The mortality rates, frequency of respiratory infections, and quality of pain relief reported by the patient are also superior in patients receiving epidural analgesia.I4 Limitations
Certain factors that preclude the use of epidural analgesia techniques in the trauma population are important to recognize. For example, sufficient time may not be available for insertion of epidural catheters in patients with unstable or emergent presentation and who require surgical intervention. Also, the nature of injuries may not permit adequate positioning for catheter placement. Patients with spinal cord injuries or with coagulopathy are also poor candidates for epidural analgesia. The use of local anesthetics may be inappropriate in patients whose hemodynamic status would not tolerate a sympathectomy. Also, epidural
PAIN MANAGEMENT IN TRAUMA
299
Table 3. CLINICAL PROPERTIES, ADVANTAGES, AND DISADVANTAGES OF HYDROPHILIC EPIDURAL OPlOlDS (e.g., MORPHINE, HYDROMORPHONE) Properties
Slow onset Long duration High CSF solubility
Advantages
Prolonged single-dose analgesia Thoracic analgesia with lumbar administration Minimal doses compared with intravenous administration
Extensive CSF spread CSF
=
-
Disadvantages
Delayed onset of analgesia Unpredictable duration Higher incidence of side effects Delayed respiratory depression
cerebrospinal fluid
analgesia may be inappropriate if the use of local anesthetics hinders the evaluation of patients’ neurologic functioning. Other contraindications to the placement of epidural catheters include septicemia, untreated bacteremia, and alterations in mental status. Even with these limitations, many patients are candidates for postoperative epidural analgesia, particularly while in the surgical intensive care unit. Choice of Agent
The choice of opioids used for epidural anesthesia is determined by the lipid solubility of the agent, location of the catheter, and location of pain. Hydrophilic narcotics, such as hydromorphone or morphine, have delayed onset and prolonged duration, with increased incidence of respiratory depression (Table 3). On the other hand, lipid-soluble agents such as fentanyl and sufentanil, have faster onset of action, shorter duration of analgesia, and fewer respiratory side effects (Table 4). Larger doses of lipid-soluble agents are required, however, because the analgesic effects may not be locally mediated. Adverse effects of epidural narcotics include pruritus, sedation, nausea and vomiting, urinary retention, apnea, and seizures.32,35 A rare but worrisome complication is the compression of the spinal cord from epidural hematoma.15 This must be recognized and requires immediate surgical evacuation if paraplegia is to be prevented. The potential for epidural hematoma is increased if coagulation is impaired at the time of insertion or removal of the Factors associated with respiratory depression from neuraxial narcotics deserve particular attention. These include elderly age, poor general condition;
Table 4. CLINICAL PROPERTIES, ADVANTAGES, AND DISADVANTAGES OF LlPOPHlLlC EPIDURAL OPlOlDS (E.G., FENTANYL, SUFENTANIL) Properties
Rapid onset Short duration Low CSF solubility
Advantages
Disadvantages
Rapid analgesia Decreased side effects Ideal for continuous infusion or PCEA
Systemic absorption Brief single-dose analgesia Limited thoracic analgesia with lumbar administration
-
-
Minimal CSF spread CSF = cerebrospinal fluid; PCEA
=
patient-controlled epidural analgesia
300
PATEL & SMITH
concomitant use of CNS depressant drugs or systemic narcotics; and, as men35 tioned previously, the use of hydrophilic Epidural analgesia can be delivered in intermittent boluses as continuous infusion and as patient-controlled epidural analgesia. The site of catheter placement (lumbar or t h ~ r a c i c and ) ~ the dosing regimens appear in Tables 5 to 7. Nonthoracic Trauma
Benefits of Pain Management for Patients with Nonthoracic Trauma
Patients suffering from extremity injuries, especially those requiring vascular reanastomosis, can be helped significantly by pain management physicians. Sympathetic hyperactivity occurs reflexively in patients with vascular disruptions, amputations, and peripheral crush injuries. Techniques that diminish sympathetic activity, such as the use of regional anesthesia and sympathetic blocks, augment blood flow to the appropriate extremity and not only help with pain relief but also improve the surgical outcome. Brachial plexus blockade is commonly instituted for upper extremity injuries and revascularization procedures. The interscalene approach is used for the shoulder and upper arm, whereas the axillary route is preferred for hand and arm procedures. This permits long-term administration of local anesthetics either by intermittent injection or continuous infusion. Noninvasive Doppler flowmetry can be used to demonstrate improvement in blood flow in patients receiving brachial plexus blockade. Although brachial plexus blockade is easy to perform, its use may be limited if frequent neurologic evaluation is needed in the postsurgical period. In patients with femoral neck fractures (see also article by Rosenberg in this issue), the use of triple nerve blocks (i.e., femoral, obturator, and lateral femoral cutaneous nerves) provides analgesia for as many as 48 hours. Other advantages of peripheral nerve blocks include reduced narcotics use and facilitation of physical rehabilitation. For lower extremity surgery, IVPCA with morphine is instituted most often and provides adequate pain control because the stress response is less marked with extremity injury compared with thoracic and upper abdominal trauma. Blunt or penetrating injuries involving the abdominal cavity can lead to significant respiratory compromise and patient morbidity. The goal of treatment is to reduce splinting and guarding so as to prevent decreases in functional
Table 5. PHARMACOLOGY OF EPIDURAL OPlOlDS
Opioid
Relative Lipid Solubility
Morphine Hydromorphone Meperidine Methadone Fentanyl Sufentanil
1 1.4 28 82 580 1270
Dose
1-5 mgt 0.2-1.0 mg 30-100 mg 4-8 mg 50-200 pg 10-50 pg
Onset (min)
Duration (h)”
30-90 20-30 15-25 10-20 5-15 5-15
6-24 6-18
*Duration of analgesia varies widely; higher doses produce longer durations. tLower dose range recommended for elderly patients or thoracic site of injection.
6 8 6-8 2 4 2 4
PAIN MANAGEMENT IN TRAUMA
301
Table 6. SUGGESTED DOSING PROTOCOLS FOR THORACIC EPIDURAL
CATHETERS (T4-T8) Bupivacaine-Morphine (bupivacaine, 1 mg/rnL, and morphine, 0.05 mg/rnL infusion) Patient Age (Y)
Morphine Loading Dose (mg)
Bupivacaine Loading Dose 0.25-0.5% (mL)
Infusion Rate (mUh)
PCEA Dose (mL) 20-min Delay
1544 45-65 66-75 76 +
4 3 2 1
5-8 4-6 4-5 3 4
6 5 3 2
3 4 2.5-3.0 1.5-2.0 1-2
Bupivacaine-Fentanyl (bupivacaine, 1 .O rng/rnL, with or without fentanyl, 5 pg/rnL infusion) Patient Age (Y)
Fentanyl Loading Dose (mg)
Bupivacaine Loading Dose 0.25-0.5% (mL)
Infusion Rate (mUh)
PCEA Dose (mL) 10-min Delay
15-44 45-65 66-75 76 +
100 100 75 50
5-8 4-6 4-5 3 4
6 5 4 3
4 3 4 24 1.5-2.0
Hydromorphone-Bupivacaine(bupivacaine, 1.O rng/mL, with or without hydromorphone, 0.01 rng/rnL infusion) Patient Age (Y)
Hydromorphone Loading Dose (mg)
1544 45-65 66-75 76 +
0.8 0.6 0.4 0.2
PCEA
=
Bupivacaine Loading Dose 0.25-0.5% (mL)
5-8 p6
4-5 34
Infusion Rate (mW
PCEA Dose (mL) 15-min Delay
6 5 3 2
3 4 2.5-3.0 1.5-3.0 1-2
patient-controlled epidural analgesia
residual capacity, vital capacity, and maximum expiratory flow. The intermittent administration of IM narcotics is deemed to be inadequate in achieving these goals. Whenever permitted, aggressive techniques should be available for trauma patients just as they are available for patients undergoing elective upper abdominal surgery. Head-injured patients require continuous neurologic status monitoring. In the acute setting, it is difficult to achieve a balance between adequate pain control and sedative side effects that may hamper neurologic assessment. This is particularly an issue in multiply injured trauma patients, especially if mechanical ventilation is required?* In such cases, short-acting sedative agents ( e g , propofol) or nonsteroidal anti-inflammatory agents ( e g , ketorolac) administered parenterally often suffice. Regional Blockade Techniques
Awareness and appreciation of the anatomy, complications, and contraindications to regional anesthesia and analgesia techniques are necessary before
302
PATEL&SMITH
Table 7. SUGGESTED DOSING PROTOCOLS FOR LUMBAR EPIDURAL CATHETERS (L1 -L4) Bupivacaine-Fentanyl (bupivacaine,0.625-1 .O mg/mL and fentanyl, 5 pg/mL infusion) Patient Age (y)
Fentanyl Loading Dose (pg)
Bupivacaine Loading Dose 0.2545% (mL)
15-44 45-65 66-75 76
100-200 100-150 50-99 50
12-16 8-14 6-12
+
523
Infusion Rate (mm)
PCEA Dose (mL) 10-20-min Lockout
8-12 6-10 4-8 3-6
4-45
s 5 2 4 1.54.0
Morphine-Bupivacaine (morphine, 0.05 mg/mL infusion with or without bupivacaine,
0.625 ma/mL) Patient Age (y)
15-44 45-65 66-75 76 +
Morphine Loading Dose (mg)
Bupivacaine Loading Dose 0.2545% (mL)
4
10-14 6-12 5-8 4-6
3 2 1
Infusion Rate (mW
PCEA Dose (mL) 20-min Lockout
8 6
4
4
2-3 1-2
2
%4
~
Hydromorphone-Bupivacaine (hydromorphone,0.01 mg/mL infusion with or without
buDivacaine, 0.625 ma/mL1 Patient Age (y) 15-44 45-65 66-75 76 i-
Hydromorphone Loading Dose (mg)
Bupivacaine Loading Dose 0.2545% (mL)
0.8 0.6 0.4 0.2
10-14 6-12 5-8 4-6
Infusion Rate (mW 8 6
4 2
PCEA Dose (mL) 15-min Lockout 4
3-4 2-3 1-2
PCEA = patient-controlled epidural analgesia.
conducting these procedures. Because this is beyond the scope of this article, the reader is referred to standard textbooks of regional anesthesia.6, Thoracic Epidural Catheter Insertion
The paramedian approach is preferred to the midline approach because the steepness of the spine is avoided and identification of safe depth of the lamina and ligament is permitted. After sterile preparation and draping, superficial local infiltration is performed with a 25-gauge needle approximately 1 cm lateral to the spinous process. Deeper local infiltration is performed with a 4 cm 22gauge needle, which is then used to identify the vertebral lamina. The needle should be advanced until the lamina has been fully identified. Infiltration of the periosteum is performed, and the exploring needle is walked cranially to the upper border of the lamina, where the ligament flavum has its insertion. The 22-gauge needle is removed’and an 18-gauge Touhy needle is inserted in a similar fashion until the ligamentum flavum is encountered. The epidural space is then identified by the loss-of-resistance technique. Because the interspinous ligament is not encountered with the paramedian approach, true loss of
PAIN MANAGEMENT IN TRAUMA
303
resistance may not occur until the ligmentum flavum is engaged. Many physicians prefer to use continuous pressure on the plunger of a glass syringe with saline to optimize the sensitivity of bss of resistance. A key point is to avoid incorrect extreme lateral angulation of the needle. After the epidural space is identified, the epidural catheter is threaded and the Touhy needle withdrawn. A test dose of 3 to mL of 1.5% lidocaine with 15 pg of epinephrine is injected to identify potential spinal or intravascular catheter placement. The catheter is taped and secured. For patients with anticipated longer use of catheter, a microfilter is attached to the proximal end of the epidural catheter. Caution is taken to avoid contamination. Suggested dosing protocols are shown in Table 6. Lumbar Epidural Catheter Insertion
The bony landmarks are palpated and the L4 lumbar vertebra is identified at the level of the iliac crest. The L2-L3 and L3-L4 interspaces are most often used. An intradermal wheal is raised with the local anesthetic exactly over the chosen interspace, and deep infiltration of local anesthetic is made using a 25gauge, 4 cm needle. The Touhy needle is inserted into the middle of the interspace at right angles to the skin. The needle is then advanced until it is firmly engaged in the interspinous ligament and advanced to penetrate into the ligamentum flavum. A syringe containing air or saline is attached to the needle, and light, continuous pressure is maintained on the syringe plunger to identify the epidural space by loss of resistance. The most difficult part of the technique is to learn to control the advancing of the needle, which must not penetrate the epidural space beyond the needle bevel. The position of the hands and fingers on the needle and syringe is crucial. The index finger of the noninjecting hand may be held firmly against the patient‘s back to act as a resistance to sudden, forward movement. The epidural catheter is then inserted and the Touhy needle removed. Again, the intrathecal or intravascular placement of the catheter should be ruled out with 3 mL of 1.5% lidocaine and 15 pg of epinephrine. Brachial Plexus Blockade
Axillary Block. A 4-cm, 18- to 20-gauge short beveled needle attached to plastic extension tubing is used. The axillary artery is palpated continuously and the needle inserted just above the artery in the proximal portion of the axilla. It is directed toward the apex of the axilla. The needle is advanced slowly and kept close to the artery and in the same plane as the artery. Penetration of the neurovascular sheath is usually felt as a ”give” as the needle is advanced and paresthesias are elicited in the hand. If the needle is then left untouched, it is seen moving with arterial pulsation, confirming its close relationship to the artery. If the needle is advanced, it enters the artery, and it may be withdrawn and realigned. Alternatively, an insulated needle may be advanced within the neurovascular sheath with the aid of a nerve stimulator.” Insertion of a catheter over a needle and into the neurovascular sheath is possible. Them should be no obstruction to the forward movement of the catheter if the needle is corre~tlyplaced. The catheter can then be used for continuous, prolonged anesthesia. For the continuous infusion method, 0.25% bupivacaine is given at 10 mL/h. Alternatively, 0.5% bupivacaine with 1:200,000 epinephrine can be injected at intervals of 6 to 8 hours.
304
PATEL & SMITH
Interscalene Approach. The patient is supine with the head turned away from the side to be blocked. The interscalene groove is identified just lateral to the anterior scalene muscle at the level of the cricothyroid cartilage. A skin wheal is raised with local anesthetic, and a 20-gauge needle is inserted and directed caudally until paresthesias are identified below the shoulder. After ensuring the absence of aspiration of blood and cerebrospinal fluid, 20 to 40 mL of 1% lidocaine or 0.25% to 0.5% bupivacaine is injected. This provides analgesia for 3 to 10 hours depending on the agent. The incidence of ipsilateral phrenic nerve palsy is 100%; therefore, this approach should be used cautiously if pulmonary status is marginal. Three-in-OneBlock
The inguinal ligament and the femoral artery pulse are identified. The puncture site is below the inguinal ligament 1 to 2 cm lateral to the femoral artery. The insertion of the needle is in a slightly cranial direction until a paresthesia is elicited. The local anesthetic is injected at the site of the femoral nerve within the sheath. If an adequate volume is used, the local anesthetic diffuses proximally to block the femoral nerve, the lateral cutaneous nerve of the thigh, and the obturator nerve. A dose of 25 to 30 mL of 1% lidocaine or 0.5% bupivacaine is appropriate. This should provide analgesia for 4 to 12 hours for patients undergoing surgical correction of femoral nerve neck fractures. Interpleural Analgesia Technique
A Touhy needle is inserted into the pleural space approximately 8 to 10 cm from the spinous process at the eighth or ninth intercostal space. The loss-ofresistance technique is used and the movement of the syringe plunger observed with inspiration. An epidural catheter is inserted to a depth of 5 to 8 cm, and the needle is removed. The epidural catheter is placed as close to the site of injury as possible. The catheter is then aspirated for blood, fluid, or air. For post-thoracotomy pain, the catheter may be inserted by the surgeon under direct vision. The catheter is secured with a suture and a sterile dressing. Twenty milliliters of 0.5% bupivacaine are injected with 1:200,000 epinephrine. The chest tube (if present) is clamped for 15 to 30 minutes following the bolus dose injection to prevent the loss of the anesthetic agent. Repeat boluses are reinjected as needed on an average of 4 to 6 hours. For continuous infusion, the interpleural catheter is bolused with 0.4 mL/kg of 0.5% bupivacaine with epinephrine 1:200,000, followed by a continuous infusion of 0.25% bupivacaine at 0.1 to 0.2 mL/kg/h. CHRONIC PAIN SYNDROMES RESULTING FROM TRAUMA Delayed Pain in Trauma
Soft tissue injuries occur with all trauma. The degree of injury, treatment, and patient characteristics determine whether acutely injured trauma patients will develop chronic regional pain syndromes, myofascial pain syndromes, fibromylagia, chronic low back pain, phantom pain, or posttraumatic headaches. In patients sustaining thoracic trauma from rib fractures or thoracostomy tube placement and from surgical retractors a recognized long-term complication
PAIN MANAGEMENT IN TRAUMA
305
of neuropathic pain exists. This may result from neural entrapment or direct laceration of the nerve endings. The condition is very difficult to treat, and management often includes long-term use of narcotics to control pain. Fibromyalgia occurs in at least 10% of patients with a history of trauma. The syndrome does not always correlate with the severity of trauma, and even minor degrees of trauma can render patients disabled. The best outcomes in these patients are frequently the result of early recognition and aggressive therapy because treatment of established fibromyalgia is very challenging. Whiplash injuries and posttraumatic headaches cause another significant long-term problem in patients sustaining head and neck trauma. Posttraumatic headaches are ascribed to excessive muscle contraction, scarring, entrapment of sensory nerves at the site of injury, or vasodilation. Headaches can become chronic and are frequently difficult to treat. In the authors’ experience, posttraumatic headaches continue to improve over the initial 6 months after injury, following which is a significant plateau. Another sequela of head and neck trauma is disorders of the temporomandibular joint. Unless a Lefort fracture is also present, many temporomandibular disorders are not readily apparent after the initial injuries and must be sought and treated at the earliest possible interval to prevent any long-term consequences. Orthopedic injuries involving the lower extremities can lead to significant long-term morbidity because of alterations in posture and restriction of normal range of motion.8 Often, an ongoing limp and subsequent compensatory gait asymmetry are present. The goal of treatment of chronic posttraumatic pain is essentially to learn to recognize the symptoms and treat them early on to avoid any long-term sequelae. For patients, this includes pain, disability, and emotional and financial loss. For society, this involves increased resource utilization, including the use of medical and social services. Patients with trauma to the extremities may have sympathetic mediated pain, whereas amputees may experience postamputation, or phantom, limb pain (PLP). Postamputation (Phantom) Limb Pain
Chronic awareness of an amputated limb is a well-known phenomenon. PLP is characterized by sensory disturbances, including significant pain and aberrations in touch, temperature, and pressure sensations. The incidence of PLP decreases with time and may be as high as 100% in the immediate postamputation period, dropping to 5% to 10% after several years; however, the onset of pain may be weeks or months after the initial amputation. The characteristics of PLP are also time dependent. Initially, it is a shooting, sharp, localized pain that is later described as burning, cramping, and squeezing in nature. The pain is usually felt in the distal portion of the phantom limb, but with time, it can be felt more proximally. The pathophysiology of PLP is not established. Peripheral stimulation of injured nerve endings and trigger points cause severe, prolonged pain in PLP patients. Although stump revision and local anesthesia infiltrations reduce the pain, these modalities rarely provide complete or lasting relief. This suggests that the CNS may account for a significant portion of the pain. A component of PLP may be sympathetic mediated because burning dysesthesia, hypersensitivity to cold and light touch, local vasoconstriction, and excessive sweating are often described; however, sympathectomy has not been found to be highly successful in alleviating PLP symptoms. The spinal origin of PLP is suggested by efficacy
306
PATEL & SMITH
of intrathecal opiates in the treatment of patients with established PLP. Inhibitory influences from the midbrain are proposed to be sustained by afferent input from the normal limb, and cessation of the afferent sensory input on amputation is proposed to lead to reduction of inhibitory influences and uncontrolled pain. Although anxiety and depression may exacerbate PLP, they do not cause PLP. A lack of clear understanding of the pathophysiology of PLP means that no single therapeutic modality can be successful in the treatment of patients with PLP. Correctable contributing factors, such as stump pain, ill-fitting prostheses, lack of soft tissue padding, and localized ischemia and infections, should be addressed first. Physiotherapy and stress therapy are as important as pharmacokinetics and surgical interventions. Pharmacologic agents, including nonsteroidal anti-inflammatory drugs, antiepileptics, antidepressants, and narcotics, have all been tried and seem to have some temporary effect. In the short term, transcutaneous electrical stimulation has also been demonstrated to be effective. Patients with a history suggestive of sympathetic mediated pain benefit from a series of sympathetic blocks. Likewise, dorsal root rhizotomy and dorsal column stimulation may provide satisfactory analgesia for the short term. Multidisciplinary approaches seem to offer the greatest hope. Complex Regional Pain Syndromes
Complex regional pain syndromes (CRPS; formerly known as reflex sympathetic dystrophy or cuusulgiu) are a group of disorders characterized by pain and relief of pain following sympathetic blockade at some stage of the disease process. Reflex sympathetic dystrophy differs from causalgia by the absence of any major nerve damage. Any trauma (e.g., fractures, sprains, injections, minor injuries, or surgical incision) can lead to CRPS. Several hypotheses exist to explain the occurrence of CRPS, the most plausible being that the initial immediate response to trauma is the propagation of active potentials via c-nociceptor fibers through the dorsal root ganglion to the spinal cord, where wide-dynamic-range neurons are activated and sensitized. The wide-dynamic-range neurons remain sensitized and respond to activity in large-diameter A-mechanoceptors, which are activated by light touch. This state produces allodynia (i.e., pain arising from a stimulus that does not normally produce pain). The sympathetic nervous system has been shown to influence the function of the mechanoceptors. The same sensitized wide-dynamic-range neurons can respond to a mechanoceptor activity initiated by the sympathetic system in the sensory receptor. This state represents sympathetically mediated pain. Evidence shows that primary afferent nociceptor activity has heightened responsiveness to norepinephrine, so the actual pain may also be mediated by alpha-adrenergic receptors. Clinical hallmarks of CRPS are burning pain and hyperesthesia (i.e., exquisite sensitivity to stimulation). The onset of pain is usually days after trauma but may be weeks later. Pain is distal, around the site of trauma, diffuse in nature, and not conforming to any dermatomal or neural distribution. It is exacerbated by touch, air movement, cold, emotional stress, or dependent limb posture. Pain progresses proximally and may encompass the entire extremity with time. Associated changes include edema, followed by skin thinning and increased hair growth. Nails may become rigid and brittle. Muscle stiffness and soreness is seen early, with associated reduced strength, tremors, and dystonia. All movements are reduced, and bone demineralization ensues. CRPSs are staged as acute (I), dystrophic (11), and atrophic (111) (Table 8).
PAIN MANAGEMENT IN TRAUMA
307
Table 8. STAGES OF COMPLEX REGIONAL PAIN SYNDROMES Characteristics
Symptoms and signs
Acute (1)
Dystrophic (2)
Atrophic (3)
Allodynia; warm, dry, swollen skin; soft edema; hair
Dysesthesia; cold, moist, cyanotic skin;
Coarse, thick, brittle hair; shriveled skin; disuse atrophy; contractures; severe osteoporosis; chronic persistent changes, unlikely to return to normal
excess;
hyperpathia; increased blood flow; increased temperature; patchy osteoporosis Onset of symptoms Clinical course
Within days of injury
Responds to
brawny edema;
coarse, decreased hair growth; thick, raised nails; decreased nail
growth; decreased temperature; decreased blood flow; diffuse osteoporosis Days or months from injury Responsive phase
treatment
Functional outcome
Impaired
6 1 2 mo after injury
Poor response to treatment
Restricted
Severely restricted
The diagnosis of CRPS is usually made clinically, but any test that shows alterations in blood flow, sweating, or temperatures may be of use in the diagnosis and follow-up of patients with CRPS. Most commonly, skin temperatures (measured with thermography, liquid crystal thermometry, or electronically with thermistors and thermocouples) are compared among extremities to evaluate the degree of asymmetry of sympathetic activity among affected and normal sides. A more definitive diagnosis is aided by the interruption of pathologic sympathetic activity by either pharmacologic means or by sympathetic blocks. Sympathetic blockade may be achieved at the ganglion level (cervicothoracic ganglion blockade for the upper extremity and lumbar sympathetic blockade for the lower extremity) or at the postganglion level (IV regional sympathetic blockade). Sympathetic blocks aid in diagnosis and therapy. Diagnostic blocks should be confirmed by the absence of provocation of pain by cold, stress, reversal of sympathetic effector responses, and return of normal sensation in the affected area. Thermography, sudomotor function evaluation, and plethysmography all provide objective measures of response to sympathetic block, but the most commonly used is a simple measure of distal temperatures before and after the block in the affected extremity because the loss of vasoconstriction results in an increase in the distal skin temperature. Effective physical therapy is the mainstay of treatment of patients with CRPS. The goal is to increase range of motion in the joint and muscle groups of the afflicted areas. Adequate analgesia must be provided with regional analgesia or sympathetic blockade to permit the necessary physical therapy. With sympathetic blocks, a "staircase" pattern is sought, with increasing pain relief for longer periods with each successive block. For more prolonged sympathectomy, chemical neurolysis (either 6% phenol or 50% alcohol) lasts weeks, but surgical sympathectomy may be an alternative if pain relief does not last.
ACKNOWLEDGMENT The authors thank Fran Hall for preparing the manuscript.
308
PATEL & SMITH
References 1. Ballantyne JL, Carr DB, Chalmers TC, et a1 Postoperative patient-controlled analgesia: Meta-analyses of initial randomized controlled trials. J Clin Anesth 5:182-193, 1993 2. Benzon HT, Wong HY, Belavic AM, et al: A randomized double-blind comparison of epidural fentanyl infusion versus patient-controlled analgesia with morphine for postthoracotomy pain. Anesth Analg 76316-322, 1993 3. Benzon HT: Post-thoracotomy epidural analgesia: Lumbar or thoracic placement? J Cardiothorac Vasc Anesth 7515-516, 1993 4. Bergh NP, Dottori 0, Lof BA, et al: Effect of intercostal nerve block on lung function after thoracotomy. Acta Anaesthiol Scand 18(Suppl 24):85-95, 1966 5. Bromage PR The control of post thoracotomy pain. Anaesthesia 44:445446, 1989 6. Brown DL: Atlas of Regional Anesthesia. Philadelphia, WB Saunders, 1992 7. Bryant LR, Trinkle JK, Wood RE: A technique for intercostal nerve block after thoracotomy. Ann Thorac Surg 11:388-391, 1971 8. Cohen S, Alagesan R, Alagesan R, et al: Acute and chronic posttraumatic pain. Problems in Anesthesia 8:487-517, 1994 9. Cousins MJ, Bridenbaugh PO (eds): Neural Blockade in Clinical Anesthesia and Management of Pain, ed 3, Philadelphia, Lippincott-Raven, 1998 10. Dittman M, Steenblock U, Kranzlin M, et al: Epidural analgesia or mechanical ventilation for multiple rib fractures. Intensive Care Med 8:89-92, 1982 11. Dryden CM, McMenermin I, Duthie DJR Efficacy of continuous intercostal bupivacaine for pain relief after thoracotomy. Br J Anaesth 70:508-510, 1993 12. Gibbons J, James 0, Quail A: Relief of pain in chest injury. Br J Anaesth 45:1136-1138, 1973 13. Glass PSA, Estok P, Ginsberg 8, et al: Use of patient controlled analgesia to compare the efficacy of epidural to intravenous fentanyl administration. Anesth Analg 74345351, 1992 14. Grass JA: Surgical outcome: Regional anesthesia and analgesia versus general anesthesia. Anesthesiol Rev 10117-125, 1993 15 Gustofsson H, Ruthberg H, Bengtsson M Spinal hematoma following epidural analgesia: Report of a patient with ankylosing spondylitis and a bleeding diathesis. Anaesthesia 43:220-222, 1988 16. Johnston JR, McCaughey W Epidural morphine: A method of management of multiple rib fractures. Anaesthesia 35:155-157, 1980 17. Kavanagh BE‘, Katz J, Sandler A N Pain control after thoracic surgery: A review of current techniques. Anesthesiology 81:737-759, 1994 18. Kehlet H: The-surgical stress response: Should it be prevented? Can J Surg 34:565567, 1991 19. Kehlet H, Dahl JB: The value of ”multimodal” or ”balanced analgesia” in postoperative pain treatment. Anesth Analg 771048-1056, 1993 Epidural anesthesia and analgesia: Their role in surgical 20. Liu S, Carpenter RL, Neal JM: outcome [review]. Anesthesiology 821474-1506, 1995 21. Liu M, Rock P, Grass JA, et al: Double-blind randomized evaluation of intercostal nerve blocks as an adjuvant to subarachnoid administered morphine for post-thoracotomy analgesia. Reg Anesth 20418-425, 1995 22. Mackersie RC, Karagianes TG: Pain management following trauma. Crit Care Clin 6:433-449, 1990 23. Mackersie RC, Shackford SR, Hoyt DB, et al: Continuous epidural fentanyl analgesia: Ventilatory function improvement with routine use in treatment of blunt chest trauma. J Trauma 271207-1212, 1987 24. O’Connor CJ: Thoracic epidural analgesia: physiologic effects and clinical applications. I Cardiothoracic Vasc Anesth 7595409. 1993 25. Owens EL, Kasten GW, Hessel EA: Spinal hematoma after lumbar puncture and heparinization. Anesth Analg 65:1201-1207, 1986 26. Pate1 N, Smith CE: The effects of pain in the trauma patient. In Rosenberg AD, Bemstein R, Grande CM (eds): Perioperative Pain Management and Regional Anesthesia for the Trauma Patient. London, WB Saunders, 1998
PAIN MANAGEMENT IN TRAUMA
309
27. Rankin AR, Comber RE: Management of fifty cases of chest injury with a regimen of epidural bupivacaine and morphine. Anaesth Intensive Care 12311-314,1984 28. Rauck RL: Trauma. In Raj PP (ed): Pain Medicine: A Comprehensive Review. St. Louis, Mosby-Year Book, 1996 29. Rosenberg A, Albert DB, Bemstein RL: Regional anesthesia for orthopaedic trauma. Problems in Anesthesia 842+$44,1994 30. Rawal N, Sjostrand U, Dahlstrom B, et al: Epidural morphine for post-operative pain relief A comparative study with intramuscular narcotic and intercostal nerve block. Anesth Analg 61:93-98, 1982 31. Safran D, Kuhlman G, Orhaut E, et al: Continuous intercostal blockade with lidocaine afler thoracic surgery. Anesth Analg 70345-349, 1990 32. Scherer R, Schmutzler M, Giebler R, et a1 Complications related to thoracic epidural analgesia: A prospective study in 1071 surgical patients. Acta Anaesthesiol Scand 3737&374,1993 33. Shulman M S Managing post thoracotomy pain. Problems in Anesthesia 4:37&392, 1990 34. Shulman M, Sandler AN, Bradley JW, et al: Post thoracotomy pain and pulmonary function following epidural and systemic morphine. Anesthesiology 61:569-575, 1984 35. Tanaka K, Watanabe R, Harada T, et a1 Extensive application of epidural anesthesia and analgesia in a university hospital: Incidence of complications related to technique. Reg Anesth 183438,1993
Address reprint requests to Charles E. Smith, MD Department of Anesthesiology MetroHealth Medical Center 2500 MetroHealth Drive Cleveland, OH 44109