EMERGENCY SEDATION AND PAIN MANAGEMENT - PART 5 pps

17 Analgesia for the Emergency Back Pain Patient Donald Jeanmonod SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT NSAIDs Skeletal Muscle Relaxants Carisprodol Cyclobenzaprine Diazepam Metaxolone Orphenadrine Opiates Steroids Antidepressants Heat/Ice Physical therapy/Exercise therapy/Spinal Manipulation/Acupuncture Facet Injections/Epidural Injections FOLLOW-UP CONSIDERATIONS SUMMARY BIBLIOGRAPHY SCOPE OF THE PROBLEM Acute low back pain is a very common problem that affects 60–80% of adults during their lifetimes. Fifty percent of working-age adults will have at least one episode of low back pain during any given year. At any one point in time, 15–20% of the population will report having low back pain, 1% of the population will be temporarily disabled, and 1% of the U.S. population will be chronically disabled from back pain. This equates to 24.5 million adults in the United States reporting back pain during the year 2000. Low back pain usually starts between age 30 and 50, with the median age of onset a t 48 years. Men and women are equally affected by this problem and it crosses all social and racial boundaries. Epidemiologic studies have shown s imilar prevalence worldwide. Low back pain is second only to upper re- spiratory problems as the most common symptom-related reason for a physician visit. In 2000, 44 million pre- scriptions were written for low back pain, including prescriptions for nonsteroidal anti-inflammatory drugs (NSAIDs) (16.5%), COX-2 inhibitors (10%), and muscle relaxants (18.5%). Low back pain accounts for a huge financial expen- diture. Although patients who become disabled owing to low back pain represent less than 5% of those with low back pain problems, they account for up to 60% of the societal cos ts for this disorder. In 1990, the direct medical costs for treating low back pain exceeded $24 billion, and total expenditures of $35–56 billion have been estimated when disability costs are included. CLINICAL ASSESSMENT The majority of low back pain is due to mechanical musculo-ligamentous injury. Low back pain may arise 109 from spinal structures including ligaments, facet joints, vertebral body periosteum, perivertebral musculature and fascia, blood vessels, the annulus fibrosis, and nerve roots. However, up to 85% of patients with isolated low back pain cannot be given a precise neuroanatomical diagnosis. The remainder of the cases can be roughly divided between mechanical, nonmechanical, and vis- ceral causes (Table 17-1). The emergency provider’s approach to low back pain is not that different from the general practitioner’s. Because the majority of low back pai n is self-limiting and lacks a neuroanatomical diagnosis, imaging studies are usually of little utility. When assessing the patient, the emergency provider should be vigilant for the ‘‘Red Flags’’ that are indicators of a more serious cause of low back pain (Table 17-2). Although up to a third of patients may report a red flag symptom, only 1–10% of those will have potentially serious pathology (Table 17-3). The sensitivities and specificities of various historical and physical exam elements are included in Table 17-4. Neurologic involvement as a cause of pain is sug- gested by the presence of sciatica, neurogenic claudica- tion, or symptoms of cauda equina syndrome. Sciatica is a unilateral leg pain that usually extends past the knee and arises from a lumbar radiculopathy. The absence of sciatica makes the presence of a clinically important disc herniation unlikely. The presence of sciatica can be confirmed by the reproduction of pain on straight leg raise of less than 60  . Neurogenic claudication is the presence of leg pain on standing or after walking that mimics claudication, but unlike claudication, which improv es when a patient rests (even in an upright posture), neurogenic claudication often requires sitting with the back in flexion to relieve symptoms. Although the sensitivity of neurogenic claudication for the detection of spinal stenosis is only 60%, the specificity is thought to be quite high. Cauda equina syndrome is suggested by the presence of urinary retention (sensitivity 90%) with overflow incontinence, saddle anesthesia (sensitivity 75%), and bilateral lower Table 17-1. Differential diagnosis of low back pain Mechanical low back or leg pain Nonmechanical spinal conditions Visceral disease Lumbar strain or sprain Neoplasia Aortic aneurysm Degenerative disk disease Multiple myeloma Gastrointestinal disease Degenerative facet disease Metastatic carcinoma Pancreatitis Herniated disk Lymphoma Cholecystitis Spinal stenosis Leukemia Penetrating ulcer Osteoporetic compression Spinal cord tumors Renal disease fracture Retroperitoneal tumors Nephrolithiasis Spondylolisthesis Primary vertebral Pyelonephritis Traumatic fracture tumors Perinephric abscess Congenital disease Infection Genitourinary disease Kyphosis Osteomyelitis Prostatitis Scoliosis Septic diskitis Endometriosis Transitional vertebrae Paraspinous abscess Pelvic inflammatory Spondylolysis Epidural abscess disease Ligamentous instability Shingles Inflammatory arthritis Ankylosing spondylitis Psoriatic spondylitis Reiter’s syndrome Inflammatory bowel disease Osteochondrosis Paget’s disease Source: Adapted from Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992;268:760–765. 110 Analgesia for the Emergency Patient extremity weakness, pain, or sensory abnormalities (sensitivity 80%). Because 95% of disk herniations involve the L5 or S1 nerve roots, the physical exam should focus on the distal sensory and motor exam (Table 17-5). The most com- mon impairments are weakness of ankle and great toe dorisflexion (L5), loss of sensation on the foot (L5, S1), and loss of ankle reflex (S1). Although ankle plantar flexion is a function of the S1 nerve root, only severe impairments can be detected. Pin prick should be tested bilaterally for symmetry along the medial (L4), dorsal (L5), and lateral (S1) aspects of the feet, as this is more accurate than light touch or temperature. In the absence of findings suggestive of systemic disease or cauda equina syndrome, imaging is rarely needed unless patients have failed 6 weeks of conservative ther- apy. Plain radiographs can be used to identify fractures, but are not able to adequately date compression fractures. Table 17-2. Red flag indicators to prompt consideration of radiographic imaging for patients with acute back pain Indicators of cancer  History of cancer  Unexplained weight loss  Unrelenting night pain or pain at rest  Age > 70  Duration greater than 6 weeks Indicators of infection  Unexplained fever greater than 38  C (100.4  F) for greater than 48 hr  IV drug use  Immunosuppression Indicators of fracture  Recent significant trauma or milder trauma, age >50  Prolonged use of oral corticosteroids  Osteoporosis Indicators of cauda equina syndrome  Loss of bowel or bladder control  Saddle anesthesia  Symmetric distal numbness or leg weakness Other  Clinical suspicion of ankylosing spondylitis  Progressive neurological dysfunction Table 17-3. Prevalence of potentially severe causes of acute low back pain in primary care Etiology Prevalence (%) Compression fracture 4 Spondylolisthesis 3 Herniated disk 1–3 Neoplasia 0.7 Ankylosing spondylitis 0.3 Cauda equine syndrome 0.04 Infection 0.01 Spinal stenosis Unknown Source: Adapted from Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992;268:760–765. Analgesia for the Emergency Back Pain Patient 111 Patients with a high pretest probability for other serious diseases will require additional imaging, as plain radio- graphs are not sufficiently sensitive to detect other serious pathology. Computed tomography (CT) has the same sensitivity as magneti c resona nce imaging (MRI) i n detecting herniated disks and central stenosis. CT can detect pathology at the foraminal and extraforaminal nerve root, but is not effective f or evaluating the intrathecal Table 17-4. Sensitivity and specificity of history and physical exam for disease processes Disease to detect Historical or physical exam finding Sensitivity (%) Specificity (%) Cancer Age ! 50 years old 77 71 Previous history of cancer 31 98 Unexplained weight loss 15 94 Failure to improve after 1 month 31 90 No relief with bed rest 90 46 Duration of pain > 1 month 50 81 Age ! 50 or hx of CA or unexplained Weight loss or failure to improve w/Rx 100 60 Osteomyelitis IVDA, UTI, or skin infection 40 – Spinal infection Fever 27–83 – Tenderness to percussion 86 60 Compression Fx Age ! 50 years old 84 61 Age ! 70 years old 22 96 Trauma 30 85 Corticosteroid use 6 99 Herniated disk Sciatica 95 88 Ipsilateral straight leg raise 80 40 Contralateral straight leg raise 25 90 Weakness on ankle dorsiflexion 35 70 Weakness on ankle plantar flexion 6 95 Weakness on great toe dorsiflexion 50 70 Impaired ankle reflex 50 60 Sensory loss 50 50 Spinal stenosis Neurogenic claudication 60 – Age ! 50 years old 90 70 Ankylosing spondylitis Age 40 years old 100 7 Pain not relieved supine 80 49 Morning back pain 64 59 Pain duration ! 3 months 71 54 Note: ca, cancer; IVDA, intravenous drug abuse; UTI, urinary tract infection. Source: Adapted from Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992;268:760–765. Table 17-5. Physical examination findings for specific nerve roots Nerve root Strength Sensory Reflex L2 Iliopsoas Anterior thigh, groin None L3 Quadriceps Anterior/lateral thigh Patella L4 Quadriceps and ankle dorsiflexion Medial ankle/foot Patella L5 Great toe dorsiflexion Dorsum of foot None S1 Ankle plantar flexion Lateral plantar foot Achilles 112 Analgesia for the Emergency Patient nerve root. MRI appears to be the superior modality for imaging the spine. PAIN CONSIDERATIONS The vast majority of patients will not have a readily identified neuroanatomical diagnosis for their low back pain. Expectations of an exact diagnosis, disease-specific treatment, and complete relief of pain lead patients to believe that their pathology has been missed or that their symptoms are doubted by the medical practitioner. Unsuccessful treatments reinforce a patient’s belief that the cause of their pain is not known, further adding to the psychological distress of chronic pain. Given that 90% of individuals will have resolution of pain by 6 weeks, initial therapy should be tailored to support patients through this initial period of pain. The patient should be encouraged to remain active during this period of time, being reassured that the pain asso- ciated with physical activity is not causing further damage to the spine. This avoids the imp airment that frequently accompanies chronic low back pain. Patients should be informed that up to 50% of those presenting with acute low back pain will have at least one recur- rence in the first 12 months. Further complicating the expression as well as the perception of pain are a number of psychosocial factors including depression, anxiety, job satisfaction, and the monetary reimbursement that may accompany disability from low back pain. Waddell has described a number of criteria on examination that might lead one to believe that a patient’s back pain is of nonorganic etiology (Table 17-6). Understanding the pain pathway helps one under- stand the treatment of low back pain. In the periphery, injury directly stimulates peripheral nerves or causes release of inflammatory mediators that stimulate noci- ceptors. The pain stimulus is transmitted to the spinal cord by fast-conducting, myelinated delta fibers and slow-conducting, unmyelinated C fibers. In the dorsal horn of the spinal cord, pain transmission is modulated by opioid receptors. Once a pain stimulus has become severe enough to result in central transmission, the signal is carried by the spinothalamic tracts to the medulla and thalamus and eventually to the cerebral cortex. The signal is once again modified by serotonin, norepinephrine, GABA, dopa- mine, and opioid receptors prior to effecting a response. NSAIDs and muscle relaxants, epidural and facet blocks, and exercise, physical therapy, and osteopathic manip- ulation modify the pain response at the level of the peripheral nerve. Opiates and transcutaneous electrical nerve stimulators have analgesic efficacy at the spinal level, and opiates, antidepressants, neuroleptics, and neurostimulants have efficacy at the cortical level. Pain should be initially managed with NSAIDs, muscle relaxants, and/or analgesics, with additional options considered if pain continues. PAIN MANAGEMENT NSAIDs U.S. guidelines on the treatment of low back pain state that there is good evidence for the use of NSAID med- ications for short-term symptom control (Figure 17-1, Table 17-7). The majority of randomized, controlled NSAID trials for acute low back pain have demonstrated the superior efficacy of NSAIDs over placebo, but none has demonstrated that one NSAID is superior to another. NSAIDs do not appear to be as effective in acute low back pain accompanied by the neurologic symptoms of sciatica or radiculopathy. There is conflicting evidence regarding the effectiveness of NSAIDs over acetaminophen, where neither has proven to be superior in the treatment of acute low back pain. Similarly, there is no evidence that NSAIDs are superior to muscle relaxants or opiates for the treatment of acute low back pain. NSAIDs tend to be well tolerated in the short-term treatment of back pain patients, with withdrawal rates of 2–13% secondary to side effects. Side effects are typically gastrointestinal, including abdominal pain and diarrhea, but can also include edema, dry mouth, rash, dizziness, headache, and fatigue. Adverse effects of NSAIDs include gastrointestinal bleeding, nephropathy, and worsening of heart failure and hypertension. There is no reported dif- ference in the number or severity of adverse events among trials of different NSAIDs. Skeletal Muscle Relaxants One comm only proposed mechanism of low back pain is the spasm-pain-spasm cycle. According to this theory, muscle spasm activates afferent pain fibers, which stimulate the anterior horn cells, causing increased Analgesia for the Emergency Back Pain Patient 113 Table 17-6. Waddell’s test Having three or more of the following five criteria is a strong indicator of a nonorganic cause of low back pain. Refer to the appropriate mental health individual if appropriate. 1. Superficial or nonanatomic tenderness a. Cutaneous hyperesthesia b. Pain on gently rolling the skin 2. Pain on simulated maneuvers a. Axial loading on the top of the head in upright individuals b. Pain on passive range of motion of the shoulder and hip in the same direction in the standing individual 3. Straight leg raising discrepancy a. Lying and sitting straight leg disparity b. Normal sitting straight leg raise with distraction 4. Nonphysiologic distal examination a. Stocking glove sensory distribution b. Pseudocogwheeling – voluntary muscle contraction with recurrent giving way 5. Overreaction Low back pain History and physical exam Uncomplicated low back pain Uncomplicated sciatica Suspect major mechanical injury Suspect infection Suspect major neurological injury NSAID ± muscle relaxant + early return to activity/work Immobilize Negative Labs and imaging Consult MRI Positive X-ray Consult Add opiate Consider antidepressant Consider physical modalities Negative Negative No improvement Positive Figure 17-1.Algorithm for evaluation of acute low back pain. 114 Analgesia for the Emergency Patient muscle contraction. For this reason, mu scle relaxants would be expected to have a significant affect, breaking the spasm-pain-spasm cycle. However, clinical and physiologic studies, including electromyogram (EMG) studies, have failed to support thi s hypothesis. The term ‘‘skeletal muscle relaxant’’ is a misnomer because at the usual prescribed doses, skeletal muscle relaxants do not depress neuronal conduction, neuromuscular transmis- sion, or muscle excitability and do not appear to relax skeletal muscle to a significant degree. Oral muscle relaxants have been shown to improve pain to a greater degree than placebo. A systematic re- view of the literature loo king at 40 trials demonstrated that skeletal muscle relaxants are as effective as NSAIDs for the treatment of acute low back pain, but found little benefit in the treatment of chronic low back pain. Comparisons of combination therapy of a NSAID plus a muscle relaxant compared to NSAID therapy alone have yielded conflicting results in comparative trials. The major side effects of skeletal muscle relaxants are similar for all the medications in this class, although there are some less common side effects that are unique to each agent. The primary side effects include central nervous system (CNS) effects, including headache, drowsiness, and dizziness, and GI effects, including nausea, vomiting, and anorexia. After prolonged administration of muscle relaxants, withdrawal symptoms may occur on abrupt cessation. Few studies have compared the various skeletal muscle relaxants for the management of acute back pain. Carisprodol Carisprodol is prescribed as 350 mg QID. Head-to-head studies of cyclobenzaprine and carisprodol demon- strated equal effectiveness and similar side-effect profiles except for autonomic side effects, which were more prevalent in cyclobenzeprine. Comparative studies of carisprodol to diazepam have demonstrated improved efficacy of carisprodol in relieving muscle stiffness, muscle tension, and activity impairment with less side effects than diazepam therapy. The major concern for carisprodol use is its potential for abuse. Meprobamate, a metabolite of carisprodol, is classified by the Food and Drug Administration (FDA) as a schedule IV controlled substance. Although carisprodol does not carry this classification by the FDA, many states have assigned it their own schedule IV classification Table 17-7. Medications for analgesia in acute back pain patients Generic name Brand name Dose Timing Metabolism Acetaminophen Tylenol 650–1,000 mg q4–6 hr Hepatic Ibuprofen Motrin, Advil 400–800 mg q6 hr Renal Ketorolac Toradol 30–60 mg IM, 30 mg IV q6 hr Renal Muscle relaxantss Baclofen Lioresal 5–20 mg q8 hr Renal Carisoprodol Soma 350 mg q6–8 hr Hepatic/renal Chlorzoxazone Parafon 500–750 mg q6–8 hr Hepatic Cyclobenzaprine Flexeril 5–20 mg q8 hr Renal Diazepam Valium 2–10 mg q6–8 hr Hepatic/renal Metaxalone Skelaxin 800 mg q6–8 hr Hepatic Methocarbamol Robaxin 1,500 mg, 1,000 mg IV/IM q6–8 hr Hepatic Orphenadrine Norflex 100 mg, 60 mg IV/IM q12 hr Hepatic Tizanidine Zanaflex 4–8 mg q6–8 hr Hepatic Opiates Codeine/APAP Tylenol #3, #4 30/300 mg, 60/300 mg q4–6 hr Hepatic/renal Hydrocodone/APAP Lortab, Vicodin 2.5–10/500 mg q4–6 hr Hepatic/renal Oxycodone/APAP Percocet, Roxicet, Tylox 2.5–10/325–650 mg Hepatic Propoxyphene/APAP Darvocet 100/650 mg q4 hr Hepatic Fentanyl Duragesic 1–2 mcg/kg Titrate Hepatic Hydromorphone Dilaudid 0.015 mg/kg Titrate Hepatic Morphine 0.1–0.2 mg/kg Titrate Hepatic/renal Analgesia for the Emergency Back Pain Patient 115 Cyclobenzaprine Cyclobenzaprine is prescribed in 5 or 10 mg tablets TID. A large, randomized controlled trial comparing cyclo- benzaprine at multiple doses to placebo demonstrated that cyclobenzaprine recipients had significant im- provement in all primary efficacy variables, including a 30% reduction in time to complete resolution of symptoms. A meta-analysis of 14 randomized controlled trials demonstrated that patients treated with cyclo- benzaprine were five times more likely to have symptom improvement at day 14. Adverse events in these trials were more common with the 10 mg dose than the 5 mg dose. Somnolence is reported in 18–38% of patients and dry mouth in 21–32%. Diazepam Diazepam in 5–10 mg doses is often prescribed as a muscle relaxant. A single study of 50 patients comparing diazepam to placebo failed to identify any benefit of diazepam for the treatment of acute low back pain, but demonstrated increased CNS side effects. Two studies of tetrazepam use in chronic low back pain have demonstrated superiority over placebo in treating chronic low back pain. Although there may be some benefit of benzodiazepines for the treatment of acute low back pain, appropriate evidence is currently lacking in the medical literature. Metaxolone The recommended dose of metaxolone is 800 mg TID. Although no quality trials of metaxolone have been published, the low incidence of sedation and short elimination half-life suggest that metaxolone may be a muscle relaxant with less likelihood of the typical side effects of this group of medications. The only random- ized controlled trials in the literature evaluating metaxolone include studies used for FDA approval from the 1960s and 1970s, where metaxolone demonstrated superiority to placebo in the treatment of acute low back pain or acute exacerbations of chronic low back pain. The majority of adverse events reported with its use include gastrointestinal effects. Orphenadrine Few studies have addressed the use of orphenadrine. The benefit of this medication includes its ability to be used as an intravenous or intramuscular injection. A high quality study demonstrated that a single intravenous dose produced significant relief in 45 min when com- pared to placebo. Opiates Narcotic analgesics are commonly prescribed for back pain. There are few studies in the literature evaluating the effectiveness of opiates in the treatment of acute back pain, but a wealth of clinical experience suggests that they are efficacious for pain syndromes. A few principles should be considered in prescribing narcotics. In treating an acute episode in the emergency department, opiate options include oral therapy or in- travenous therapy. Intramuscular (IM) and subcutane- ous (SC) injections have unreliable and erratic drug absorption, and it is difficult to give repeated doses secondary to patient discomfort. Because IM and SC delivery routes have an onset of action that approx- imates that of oral agents, there is no benefit to these methods. The maximum dose of oral analgesics com- bined with acetaminophen or ibuprofen is limited by the presence of the nonnarcotic portion of the medication. Codeine, propoxyphene, hydrocodone, and oxycodone are common narcotic preparations in this class. Studies have demonstrated that physicians routinely ineffectively treat pain with intravenous opiates. The typical dose of morphine is 0.1–0.15 mg/kg, with similar equipotent dosing of hydromorphone as 0.015 mg/kg, and fentanyl as 1–2 mcg/kg. Side effects of narcotics include CNS depression, nausea mediated by histamine release, gastroparesis, constipation, and hypotension. Steroids Steroids are occ asionally used by practitioners for the treatment of acute low back pain, particularly in those patients with a radicular component. Data regarding the utility of treating acute low back pain with steroids are lacking. A single study comp aring systemic steroids to placebo for the treatment of acute low back pain did not dem- onstrate any benefit of a dexamethasone taper when compared to placebo with pain assessments at 7 days, less than 1 year, and greater than 1 year. A more recent article evaluating large dose IV corticosteroids for sciatica demonstrated a statistically significant, but 116 Analgesia for the Emergency Patient clinically irrelevant decrease in pain at 3 days, but no lasting effect (see reference 10). Antidepressants There is no available evidence to sup port the use of antidepressants for acute low back pain management. However, there is evidence that antidepressants effective in blocking norepinephrine reuptake (tricyclics and tetracyclics) are mildly to moderately effective in de- creasing chronic low back pain. Heat/Ice A Cochrane review evaluating data through 2005 found that heated wraps applied to the low back provided short- term pain relief and improvement in disability when compared to placebo tablets or nonheated wraps. One study comparing heat to ibuprofen or acetaminophen found that a heated back wrap provided significantly better relief than ibuprofen or acetaminophen at 1 and 4 days of therapy. Likewise, heat has compared favorably to both exercise and educational booklets. Studies of heat vs cold, cold vs placebo, or cold vs other interventions have been few and of poor methodological quality. Physical therapy/Exercise therapy/Spinal Manipulation/Acupuncture A recent meta-analysis reviewed 11 of the highest quality studies of the MacKenzie technique of physical therapy for low back pain. Although there was a statistical benefit to physical therapy for low back pain, the dif- ference between physical therapy and other techniques is probably not clinically meaningful. A meta-an alysis identifying 11 trials of exercise ther- apy for acute low back pain found no benefit over no treatment or other conservative therapies. There was moderate evidence to suggest that exercise is effective in the care of subacute and chronic low back pain. For years, bed rest had been advocated based on the obser- vation that certain types of back pain get better with rest. Studies have demonstrated that prolonged immobiliza- tion with back rest can actually be harmful in the treatment of acute low back pain. A Cochrane review of studies comparing spinal ma- nipulation versus sham treatments for acute low back pain demonstrated that although patients receiving spinal manipulation had a clinically significant response compared to sham treatment, the analgesic difference between groups did not reach statistical significance. There is no evidence in the medical literature to support the use of spinal manipulation for chronic low back pain. When compared to other accepted therapies for low back pain, of both acute and chronic duration, spinal manipulation does not appear to provide signif- icant pain relief or functional improvement. A Cochrane review of 35 randomized controlled trials of acupuncture vs placebo or sham treatment for low back pain was only able to identify three relevant trials. These studies were of small sample size and poor methodological quality, preventing decisive conclusions. Facet Injections/Epidural Injections A Cochrane review to determine the effectiveness of in- jection therapy in the treatment of acute and chronic low back pain found, on pooled analysis of the four ran- domized, placebo-controlled trials, no significant benefit to epidural corticosteroid injections. It is difficult to draw conclusions from these trials secondary to the degree of heterogeneity in patients, medications, injection techni- ques, small sample sizes, and the significant effects of placebo (20–30% recovery in the placebo group). FOLLOW-UP CONSIDERATIONS Patients evaluated for acute low back pain should be treated with NSAIDs with or without a muscle relaxant and referred to a primary care physician for continued treatment. Although 79% of back pain patients see only the initial physician who began their care for low back pain, a substantial minority (21%) will see multiple providers. The suggestion of disc herniation (symptoms of sciatica) should not rule out a course of conservative therapy. Ultimately, the decision to pursue a more aggressive surgical approach is based on clinical factors, not radio- graphic studies. This decision is also typically based on the presence of severe, uncontrolled pain, profound or progressive neurologic symptoms, or failure to respond to conservative therapy (Table 17-8). SUMMARY Most acute low back pain is self-limited, does not require radiographic evaluation, and will resolve in 6 weeks. After the initial health-care provider has ruled Analgesia for the Emergency Back Pain Patient 117 out potentially serious causes of low back pain, treat- ment should emphasize NSAID therapy. Opiates and skeletal muscle relaxants can be added to the pain medication regimen for more severe pain at the cost of added CNS side effects. Patients should be encouraged not to use bed rest for prolonged periods of time and should be referred to a primary care physician for reevaluation and further treatment if the back pain persists. BIBLIOGRAPHY 1. Bigos S, Bowyer O, Braen G, et al. Acute low back problems in adults. Clinical practice guideline no. 14. AHCPR Publ no. 95-0642. 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Indications for surgical referral of the back pain patient  Symptoms of cauda equina syndrome (loss of bowel/bladder function, saddle anesthesia, bilateral lower extremity weakness, pain, and numbness)  Progressive or severe neurologic deficit  Persistent neuromotor deficit after 6 weeks of conservative therapy  Persistent sciatica after 6 weeks of conservative therapy  Persistent and disabling low back and leg pain from spinal stenosis 118 Analgesia for the Emergency Patient [...]... abdominal pain BMJ 1992;3 05: 55 4 55 6 126 3 Pace S, Burke TF Intravenous morphine for early pain relief in patients with acute abdominal pain Acad Emerg Med 1996;3:1086–1092 4 LoVecchio F, Oster N, Sturmann K, Nelson LS, Flasher S The use of analgesics in patients with acute abdominal pain J Emerg Med 1997; 15: 7 75 779 5 Jones P Early analgesia for acute abdominal pain (letter) BMJ 1992;3 05: 1020–1021... the prevention and treatment of these conditions (Table 2 1-4 ) PAIN MANAGEMENT The management of chronic pain requires a consistent, multimodal pain management strategy (Table 2 1 -5 ) Patients with chronic pain often present urgently in two distinct situations: an exacerbation from their baseline of their chronic pain despite their ongoing therapy or an untreated state of their baseline pain owing to a...Analgesia for the Emergency Back Pain Patient 22 Hayden JA van Tulder MW, Malmivaara AV, Koes BW Meta-analysis: Exercise therapy for nonspecific low back pain Ann Intern Med 20 05; 142:7 65 7 75 23 Hagen KB, Jamtvedt G, Hilde G, Winnem MF The updated Cochrane review of bed rest for low back pain and sciatica Spine 20 05; 30 :54 2 54 6 119 24 Assendelft, WJJ, Morton, SC, Yu Emily,... Spinal manipulative therapy for low-back pain A Cochrane review Cochrane Libr 2006;447:3 25 Nelemans PJ, diBie RA, deVet HC, Sturmans F Injection therapy for subacute and chronic benign low back pain Spine 2001;26 :50 1 51 5 18 Analgesia for the Acute Abdomen Patient Martha L Neighbor SCOPE OF PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT DYSPEPSIA FOLLOW-UP CONSIDERATIONS SUMMARY BIBLIOGRAPHY... Skiendzielewski JJ Relief of myocardial ischemia pain with a gastrointestinal cocktail Am J Emerg Med 19 85; 3(3):208–209 21 Dickinson MW The ‘‘GI Cocktail’’ in the evaluation of chest pain in the emergency department J Emerg Med 1996;14(2):2 45 246 22 Welling LR, Watson WA The emergency department treatment of dyspepsia with antacids and oral lidocaine Ann Emerg Med 1990;19(7):7 85 788 23 Berman DA, Porter RS, Graber... 2004;27(3):2 25 231 4 Hoppe H, Studer R, Kessler TM, et al Alternate or additional findings to stone disease on unenhanced computerized tomography for acute flank pain can impact management J Urol 2006;1 75: 17 25 1730 5 Nishikawa K, Morrison A, Needleman P Exaggerated prostaglandin biosynthesis and its influence on renal resistance in the isolated hydronephrotic rabbit kidney J Clin Invest 1977 ;59 :1143–1 150 Analgesia... impacted stones and, therefore, preventing progression to inflammation and cholecystitis PAIN MANAGEMENT The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) for the treatment of the biliary colic patient has been documented in multiple small- to medium-sized randomized controlled studies of varying quality (Table 2 0-1 ) These trials have shown benefit not only in terms of pain control, but... or in their own adaptive mechanisms to try and tolerate pain, rather than to a decrease in their perception Recurrent pain syndromes can include back pain, myofascial pain syndrome, migraine syndrome, sickle cell disease, and inflammatory bowel disease CLINICAL ASSESSMENT Chronic pain may be associated with different painrelated signs and symptoms than acute pain It is typically not associated with sympathetic... system activation or specific findings of tissue injury Many 1 35 136 Analgesia for the Emergency Patient Table 2 1-1 Acute, chronic, and chronic malignant pain Acute pain Chronic pain (nonmalignant) Chronic pain (malignant) Associated pathology Present Variably present Present Prognosis Predictable recovery Unpredictable recovery Increasing pain and possibility of death Fear of loss of control, variable... develop a common goal and further facilitate communication Analgesia for Chronic Pain Patient PAIN CONSIDERATIONS Pain can generally be described as nociceptive or neuropathic Nociceptive pain results from the activation of primary peripheral nociceptors in response to noxious stimuli Somatic pain is sharp and well localized; visceral pain tends to be diffuse and radiating Nociceptive pain also results . low back pain. Ann Intern Med 20 05; 142:7 65 7 75. 23. Hagen KB, Jamtvedt G, Hilde G, Winnem MF. The updated Cochrane review of bed rest for low back pain and sciatica. Spine 20 05; 30 :54 2 54 6. 24 for the management of acute back pain. Carisprodol Carisprodol is prescribed as 350 mg QID. Head-to-head studies of cyclobenzaprine and carisprodol demon- strated equal effectiveness and similar. pain: A review of carisoprodol, cyclobenzoprine hydrochloride, and metaxalone. Clin Ther 2004;26:1 355 –1367. 15. Browning R, Jackson JL, O’Malley PG. Cyclobenzoprine and low back pain. A meta-analysis.