Medical Management of the Orthopaedic Trauma Patient

Acute Pain Management, Regional Anesthesia Techniques, and Management of Complex Regional Pain Syndrome

Richard Gannon
Dean Mariano
Daniel J. Gianoli
Richard Sheppard

In 1995, the president of the American Pain Society, Dr. James Campbell, argued that pain was the “fifth vital sign” and suggested that to provide effective care, a patient’s pain should be quantified and treated. In 2001, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO; now The Joint Commission) recognized that “unrelieved pain has physical and psychological effects” and sought to provide care facilities with guidelines to improve access to pain assessment and management. The JCAHO guidelines sought (1) to promote respecting a patient’s right to be evaluated and treated for pain, and in particular for pain to be assessed at the initial evaluation and during all clinically relevant encounters, and (2) to educate patients and their families about available pain management strategies.

The continued evolution of health care from a paternalistic model to a more consumer-based model combined with the continued growth of the Internet and various social media platforms have placed a high value on care facility services and their image. Hospital surveys such as the ones provided by Hospital Consumer Assessment of Healthcare Provider and Systems (HCAHPS) seek to provide the public with data regarding patients’ perspectives on hospital care. These standardized surveys aim to obtain patients’ perspectives so that consumers may have an “apples to apples” comparison of their satisfaction with local facilities. In such surveys, pain management services are evaluated with the following questions: “During this hospital stay, how often was your pain well controlled?” and “During this hospital stay, how often did the hospital staff do everything they could to help you with your pain?”

Pain is a very personal experience, and despite the best efforts on the part of health care providers, it is common for there to be a disconnect between what healthcare providers view as adequate management and what patients experience. In a study of critically ill patients, 95% of surveyed house staff believed that they had achieved adequate pain control for their patients. However, 74% of patients rated their pain as being in the moderate to severe range. Recent studies have shown that pain scores do not necessarily correlate with global satisfaction ratings by patients. It has been suggested that although it is important to try to obtain adequate pain control, patient satisfaction scores correlate more strongly with the patient’s perception that caregivers were doing everything they could to provide pain control.

As clinicians, we tend to view pain as an invaluable part of the history and physical examination that can aid in determining a diagnosis. In truth, pain is an extremely complex and dynamic process that merits special attention. Over the past 2 decades, the way clinicians approach and treat acute pain processes has undergone a dramatic evolution. It has long been recognized that a patient’s exposure to noxious stimuli results in not only a stress response that can potentially increase morbidity and mortality but also a neuroendocrine response that may potentially lead to altered pain states and the development of chronic pain. Poorly controlled pain can lead to dysfunctions in a multitude of physiologic systems. Derangements in ventilation, hemodynamics, immune response, and coagulation complicate the care of patients, especially those who are acutely injured. Ultimately, this results in delayed mobilization, rehabilitation, and discharge. Given that today’s society expects sophisticated and effective treatments for their pain, coupled with the fact that reimbursement is becoming increasingly linked to patient satisfaction and participation in quality assurance programs, institutions and providers must be willing to take a more customized approach to pain management.

As our understanding of pain transmission and perception continues to deepen, it is evident that a multimodal, multidisciplinary approach is better suited to provide more tailored effective pain management.

Neurophysiology of Pain Processing

“Humans’” ability to successfully navigate and survive the environment is intimately tied to our ability to process both internal and external sensory information. At its core, the ability to transduce, transmit, and process sensory information is a protective mechanism. It is a highly evolved, complex, interconnected network of neurons that allow us to perceive and react to a variety of noxious and non-noxious stimuli. Processing of sensory information in higher brain centers results in the ability to learn from the experiences so that potentially harmful exposures can be minimized in the future. So important is our ability to sense noxious and potentially noxious stimuli that the system has extensive built-in redundancies as well as the ability to adapt. These features provide unique challenges to the clinicians who attempt to provide pain management. The redundancies and lack of a final common pathway for pain processing make it difficult to provide simple effective solutions for pain management. The plasticity of the system can reduce the effectiveness of what were once successful treatments for pain management and lead to chronic pain states. By providing a broad overview of this complex system, clinicians will be better equipped to provide effective treatment strategies.

Nociceptors and Primary Afferents

Sensory neurons are pseudounipolar and originate in the dorsal root ganglion. A single process projects from the soma and later splits. The peripheral limb goes to target structures to collect sensory information while a central process transmits sensory information to the spinal cord or brainstem. A variety of sensory neurons exist and can be classified by the diameter of their axon, the presence of myelination, and their transmission rate. As peripheral sensory axons approach their target structures, they branch to form a terminal arbor. Structures that have a high degree of spatial resolution for sensory discrimination have less branching or arborization. In the periphery, sensory neurons transduce chemical, mechanical, and thermal input into electrical signals that are carried to the central nervous system (CNS). Sensory axons that transduce non-noxious stimuli can possess specialized encapsulated nerve terminals that make them efficient at responding to specific stimuli such as mechanical distortion or vibration. Sensory nerves involved in nociception tend to be unencapsulated or have free endings and can respond to a variety of stimuli (thermal, mechanical, and chemical).

When a stimulus is sufficient to evoke a response, an electrical impulse is generated. Discharge of the axon is directly related to the intensity of the stimulus. As stimulus intensity increases, the frequency of discharge increases proportionately. Low-threshold sensory neurons, such as Aβ fibers, are triggered by non-noxious stimuli. An increase in terminal discharge frequency of these fibers gives us the ability to perceive the change in stimulus. For example, non-nociceptive neurons that transduce temperature information at 30° C will increase their firing frequency as the temperature increases over a non-noxious range, resulting in the sensation of warmth. Aδ fibers are small (in diameter), myelinated neurons containing both low- and high-threshold terminals. Activation of these terminals can be initiated by non-noxious stimuli. As the stimulus intensifies, firing frequency continues to increase even when the stimulus enters an aversive range. Small unmyelinated C fibers are slow conducting and possess high-threshold terminals. Because these fibers transduce a variety of noxious stimuli such as chemical, mechanical, and thermal, they are often referred to as polymodal. When a noxious stimulus is present, high-threshold terminals from both the Aδ and C polymodal fibers are activated. Because Aδ fibers have higher conduction velocity, their activation produces sharp and focal first pain. Information carried by slowly conducting C polymodal fibers is perceived as dull, achy second pain.

In general, nociceptive neurons fall within the classification system presented. However, this is an oversimplification, and it should be noted that sensory neurons with the ability for nociception range in cell size, axon diameter, and degree of myelination. More recent efforts to find nociceptive-specific attributes have led researchers to investigate cellular markers such as protein and ion channels. To date, no particular cellular markers are exclusive to nociceptive neurons.

From a functional standpoint, nociceptors have two unique qualities. First, they have the ability to transduce and transmit noxious stimuli. Second, they have the ability to sensitize. After the application of noxious stimuli, nociceptors adapt in such a way that they become more excitable. A rise in the resting membrane potential produces a state by which less stimulation is required to produce activation. This phenomenon is referred to as primary hyperalgesia . Sensitization is an important process; if left unchecked, it can lead to the sensitization of higher order neurons within the CNS. Studies have shown that the alteration of ion channels that lead to sensitization are a result of the chemical milieu that develops after tissue damage. Although researchers have identified numerous chemical mediators that contribute to sensitization, it is apparent that products from the cyclooxygenase (COX) pathway play important roles. Nonsteroidal antiinflammatory drugs (NSAIDs) have been shown to be effective agents in combating primary hyperalgesia.

Central Nervous System Relay and Processing

A transverse section of the spinal cord reveals areas of white and gray matter. The white matter is an arrangement of myelinated tracts of ascending and descending axons, and the gray matter is composed of cell bodies. Cell bodies within the gray matter vary by location. The Rexed classification system divides these locations into 10 distinct laminae ( Fig. 14A-1 ).

Figure 14A-1

Rexed lamina classification system.

The central processes of the sensory neurons enter the spinal cord through the dorsal roots. These processes synapse on cell bodies located throughout the dorsal horn (laminae I–VI) as well as around the central canal (laminae X). Nociceptive neurons primarily synapse in laminae I, II, V, VI, and X. In addition to making synaptic contact at the neurons’ level of entry, they may travel rostrally or caudally along Lissauer tract, reaching areas up to six spinal segments away. Generally speaking, nociceptive afferents responsible for encoding information from cutaneous structures tend to localize their input in a single spinal level. Afferents originating in visceral or deep structures demonstrate collateralized branching, which enter Lissauer tract accessing distant spinal segments and a variety of laminae.

As stated previously, second-order neurons located within the grey matter can vary by location. Lamina I, or the marginal zone, contains a heterogeneous group of cell bodies that form the outermost portion of the dorsal horn. This portion of the dorsal horn is highly innervated with afferent inputs that are primarily from C polymodal and Aδ fibers. Afferents from these fibers release excitatory amino acids (glutamate) and neuropeptides (substance P, calcitonin gene-related peptide) that activate cell bodies within the lamina to continue signal transduction. Projections from these second-order neurons continue to supraspinal structures such as the medulla, midbrain, and thalamus. Alternatively, they can act intrasegmentally or intersegmentally as interneurons form synapses with cell bodies in other laminae.

Lamina II, or the substantia gelatinosa, also contains a heterogeneous group of cell bodies. These cells receive direct nociceptive input from C fibers as well as indirect input from the Aδ fibers of lamina I. In addition to primary nociceptive inputs, the cell bodies of this lamina receive serotonergic and noradrenergic connections from descending axonal projections. Although these cells have some projections to supraspinal structures, the vast majority are involved in interneuron connections with a dense network of axonal and dendritic arborizations forming axodendritic, dendrodenritic, and axoaxonic synapses. These interneurons can release inhibitory neurotransmitters, such as γ-aminobutyric acid (GABA), and their cell bodies exhibit complex responses with the ability to undergo prolonged periods of excitation or inhibition. The structure and function of these interneurons suggest that they play a significant role in the regulation of afferent signal transmission.

Laminae III, IV, and V are known collectively as the nucleus proprius. Afferent information to this area is primarily from large, highly myelinated, low-threshold Aβ fibers. Cell bodies in this lamina send their projections to overlying lamina as well as into the dorsal columns. In addition to input from low-threshold fibers, the cells of lamina V receive input from Aδ and C fibers. Dendritic extensions of these cells project throughout laminae I and II as well as to supraspinal sites, including the brainstem, thalamus, and hypothalamus.

Lamina X is an area around the central canal where cell bodies receive bilateral afferent input from mostly high-threshold (nociceptive) afferent fibers. These cells also receive afferent projections from the viscera.

In addition to differences in anatomic location, the second-order neurons display important functional differences. Functionally, second-order neurons are categorized by whether they produce excitatory responses to noxious stimuli, such as high-intensity mechanical or thermal sensory input, or innocuous stimuli such as vibration. These second-order neurons are typically described as being class 1 (excited by innocuous stimuli), class 2 (excited by both innocuous and noxious stimuli), and class 3 (excited by only noxious stimuli). Often, class 1 neurons are referred to as “low threshold,” class 2 is referred to as “wide dynamic range (WDR),” and class 3 as “nociceptive specific.” Class 3, or nociceptive specific, is typified by second-order neurons that exist within the superficial dorsal horn. These cells receive primary afferent input from Aδ and C fibers and are active only when the incoming stimulus is in the aversive range. As the intensity of the noxious stimulus escalates, the frequency of discharge from these second-order neurons will increase. Class 2 neurons, or WDR, represent most of the second-order neurons present in the deep dorsal horn (laminae IV–VI) but they can also be found in the superficial horn (≈20%). Unlike nociceptive-specific neurons, the WDR neurons can be triggered by innocuous as well as aversive stimuli. As the intensity of the stimulus increases from non-noxious to noxious range, WDR neurons increase their frequency of discharge. WDR neurons are also referred to as “convergence” neurons because of their activation by both somatic and visceral afferents. At a given spinal level, neurons located in the nucleus proprius receive sensory information from a specific area of the body. Information from visceral structures activating the same WDR neuron that is receiving cutaneous somatic information in the nucleus proprius will be referred to that area of the body. The convergence of visceral or deep tissues (joints, bones, and muscle) with cutaneous sites on WDR neurons is the mechanism by which we experience referral patterns and referred pain. The last function that distinguishes WDR neurons from low-threshold and nociceptive-specific neurons is their ability to become sensitized. Persistent C-fiber activation of WDR neurons at a frequency greater than 0.5 Hz produces an increase in the frequency of discharge. During periods of tissue injury or ongoing inflammatory processes, repetitive C-fiber (not A-fiber) activation will result in a facilitated or sensitized state. Repeated stimulation of the WDR neurons results in prolonged partial depolarization that raises the resting membrane potential. In this state, afferent stimulation is much more likely to result in signal transmission. This phenomenon is referred to as “wind up” and has been linked to the activation of NMDA ( N -methyl-D-aspartate) receptors. NMDA receptors are both voltage and ligand gated, and when in an open configuration, they allow for the influx of sodium and calcium. NMDA receptors that are in a closed state possess magnesium ions that intracellularly block their channels. After sustained depolarization of the cell membrane, the magnesium ion will disassociate from the receptor. When active, the cell membrane will experience an extremely prolonged depolarization. Activation of WDR neurons also leads to an increase in the receptive field, meaning that a stimulus that is applied to an area that is adjacent to the injury will cause the patient to experience pain. As mentioned previously, afferent fibers enter the spinal cord at a specific segment; however, they may send projections rostrally and caudally, synapsing in other segments via Lissauer tract. Sensitization of these distal segments produces an area of secondary hyperalgesia that is located near the site of injury. An overall reduction in threshold for these sensitized second-order neurons can lead to their activation by normally non-noxious stimuli. For example, afferent information from Aβ fibers within the zone of secondary hyperalgesia can lead to WDR neuron firing frequencies that signal painful stimulus. To prevent the central phenomenon of wind-up and secondary hyperalgesia, clinicians have tried to use preemptive analgesic strategies. The use of peripheral nerve blockade or combination pharmacotherapy (opioids, NSAIDs, and anticonvulsants) before injury can have a profound effect on reducing these hyperalgesic phenomena. Additionally, the uses of NMDA receptor antagonists such as ketamine and dextromethorphan have shown promise.

Nociceptive information relayed in the spinal cord is transmitted to distal spinal cord segments and supraspinal structures, such as the thalamus, hypothalamus, midbrain, and medulla, through long tract systems. Axons from second-order neurons in the dorsal horn travel within the white matter, forming tracts mainly in the ventrolateral quadrants and, to a lesser extent, the dorsal midline. The tracts of the ventrolateral quadrant include the spinoreticulothalamic, spinomesencephalic, spinoparabrachial, and spinothalamic projections. Cells contributing to the spinoreticulothalamic pathway originated from the deep dorsal horn and ascend to reach multiple nuclei within the reticular formation of the brainstem. These areas are involved with autonomic regulation as well as modulation of nociceptive processing. The spinomesencephalic tract is composed of axons from cell bodies within lamina I and V and project predominately to the nuclei in the midbrain. These include the periaqueductal grey, cuneiform, and collicular nuclei. With projections to the periaqueductal gray, this tract plays a role in integrating motor, autonomic, and antinociceptive responses. Projections from the spinoparabrachial tract make synaptic connections with the parabrachial region, which lies adjacent to the superior cerebellar peduncle at the junction of the pons and midbrain. The parabrachial region serves as a relay to the amygdala, ventral medial nucleus of the thalamus, and hypothalamus. Nociceptive information on this tract reaches higher brain centers that are involved with emotional and hormonal responses to pain. The spinothalamic tract plays a central role in the transmission of nociceptive information. Second-order neurons from lamina I and V send axons across the midline to the lateral spinothalamic tract, where they proceed uninterrupted to the thalamus. Information regarding the location, intensity, and duration of nociceptive stimuli is transmitted via this tract as well as the sensation of temperature. Synaptic targets of this tract include the ventrobasal thalamus, ventral medial nucleus of the thalamus, and the mediodorsalis nucleus. Information to the ventrobasal thalamus is in a strict somatotopic pattern that is preserved as it is relayed to the somatosensory cortex. The ventral medial nucleus and mediodorsalis nucleus project to the insula and anterior cingulate cortex, respectively.

Despite the numerous tracts to supraspinal structures, the pathways can be divided into functionally distinct response systems for simplicity. The first system consists of axonal projections of WDR neurons, and the second pertains to projections of nociceptive-specific neurons. WDR neurons project into the brainstem, thalamus, and hypothalamus. These neurons are able to provide not only information of stimulus intensity over a broad range, but they are also able to preserve spatial localization by their somatotopic arrangement. The nociceptive-specific pathway arises from primarily lamina I cells and encodes high-intensity stimuli. This pathway only provides information regarding location and intensity when the stimulus is in an aversive range. This group projects mainly to the ventral medial and mediodorsal nuclei before continuing to the insula and anterior cingulate cortex. Processing of nociceptive information in these supraspinal structures results in the emotional and motivational components of the pain experience.

Treatment Options

Advancements in pharmacotherapy and regional analgesic techniques have provided clinicians with a vast assortment of treatment options. The goal in developing any treatment strategy should be to provide a plan that is safe, simple, and efficient. Care plans should be individualized to the patient by taking into account his or her past medical history, current illness, and comprehensive physiologic function. By doing so, techniques that may potentially exacerbate already impaired functions, such as hemodynamics or ventilation, can be minimized or avoided. Ultimately, providing individualized treatment plans should help clinicians to mitigate morbidity and mortality.


Systemic opioid therapy has been used for centuries and to this day remains one of the mainstays in treating acute pain. Opioids exert their effects primarily through µ-opioid receptors. Opioids are advantageous in that they have multiple routes of delivery, vary in onset and duration, and theoretically have no analgesic ceiling. Despite these advantages, opioids are usually limited by various side effects such as nausea, vomiting, constipation, sedation, and respiratory depression. A study by Zhao and colleagues suggested that administration of every 3 mg of morphine or its equivalent in a 24-hour period was associated with the development of an additional side effect or hospital-related complication. Long-term administration of opioids is fraught with the potential for serious complications such as the development of tolerance, dependence, and opioid-induced hyperalgesia. Although the use of opioids remains a fundamental part of acute pain management, it should not be viewed as the only treatment available.

Patient-Controlled Analgesia

In the acute phase of pain management, the delivery of intravenous (IV) opioids by patient-controlled analgesia (PCA) systems is quite advantageous. Compared with traditional as needed (PRN) regimens, the use of PCA systems can help eliminate interpatient pharmacokinetic variances and access delays. Deliveries by IV methods also produce more predictable drug serum levels as opposed to traditional intramuscular delivery methods. Safe and effective use of this treatment method occurs when patients adhere to self-administration of medication only when they experience pain. Violation of this premise by the patient, family members, or staff can lead to undesired complications such as oversedation or respiratory depression. Complications related to equipment malfunction have been reported, but the vast majority of problems related to the use of PCA systems stem from user or programming errors.

The initial setup of the PCA is relatively simple but requires the clinician to consider several variables. Among these variables, the clinician should select the drug to be infused, the demand dose, the lockout interval between doses, and the appropriateness of a basal infusion. Selection of these variables should be based on clinical judgment because an optimal setting for demand dose and lockout interval does not exist. After the initiation of the PCA system, its effectiveness should be assessed by reviewing visual analog pain scores with the patient as well as by interrogation of the PCA device itself. By interrogating the PCA device, the clinician can review information such as how often bolus demands were made as well as the number of doses delivered. Whereas demand dosing that is too low can result in inadequate levels of analgesia, demand doses that are too high can produce unwanted side effects such as sedation and respiratory depression. Lockout intervals should be selected so that after the delivery of the demand dose, the patient has the opportunity to evaluate its effectiveness before delivering another dose. Lockout intervals that are too short can lead to stacking of boluses and increases in opioid-related side effects. Intervals that are too long can cause temporal gaps of inadequate analgesia. Opioids that are commonly used in PCAs ( Table 14A-1 ) have onset times around 5 minutes (1–2 minutes for fentanyl) with peak effect occurring between 7 and 15 minutes (5–7 minutes for fentanyl). Based on the onset and peak time for the opioid delivered, lockout times generally vary between 5 to 10 minutes. Adjustment in the lockout interval in this range does not appear to contribute to the generation of side effects nor does it seem to change degree of analgesia. The final element to be considered is the use of a continuous basal rate. Basal rates were initially thought to improve analgesia particularly during sleep. Studies have shown that basal infusions, even if limited to nighttime, do not improve analgesia or sleep patterns. The routine use of basal infusions in opioid-naïve patients has been shown to result in a higher incidence of opioid-related side effects such as oversedation and respiratory depression. Although it is not recommended that all patients receive continuous infusions, some patient populations may benefit. For example, the use of continuous infusions have been shown to improve analgesia in opioid-tolerant patients as well as children.



Concentration Continuous Demand Dose Demand Interval 4-Hour Lockout
Fentanyl 10 mcg/mL 10 mcg/hr 10 mcg 5–10 min 300 mcg
Hydromorphone 0.2 mg/mL 0.2 mg/hr 0.2 mg 6–15 min 6 mg
Morphine 1 mg/mL 1 mg/hr 1 mg 6–15 min 30 mg
Meperidine (not recommended) 10 mg/mL 10 mg/hr 10 mg 6–15 min 150 mg

Studies have shown that the implementation of PCAs in postoperative settings provides superior postoperative pain control and improved patient satisfaction. Several meta-analyses comparing PCAs with traditional PRN regimens indicated that although opioid consumption was higher in the PCA group, the incidence of opioid-related side effects, with the exception of pruritus, did not differ significantly between groups. The rate of serious complications such as respiratory depression with PCAs is less than 0.5%, but clinicians should be aware of factors that may increase this risk such as advanced age, concomitant use of sedatives, comorbid sleep apnea, and advanced pulmonary disease.


Involving the patient in the pain assessment is crucial because the description of the patient’s pain will enable the practitioner to most effectively treat the patient’s pain appropriately. The use of pain scales has helped objectify a subjective phenomenon. An assessment or rating of the patient’s degree of sedation in conjunction with the pain scale may help avoid excessive sedation and respiratory depression. Both the RASS (Richmond Agitation Sedation Scale) and the POSS (Pasero Opioid-induced Sedation Scale) have been validated as tools to assess for opioid-induced sedation. Institutions use a pain scale that best suits their patient population. Examples of pain scales include numerical (0–10), descriptive (excellent–poor), faces (smiling–sad), and behavioral for cognitively impaired patients (e.g., grimacing, vocalizations, resistance to care). One of the most important questions for the patient is, “How would you describe your pain?” The importance of this question rests on the fact that if a patient has predominantly neuropathic pain (burning, muscle spasms, shooting, stabbing), then adjuvants such as anticonvulsants should be used in conjunction with opioids.

Whether the patient describes mostly somatic pain (aching, throbbing) musculoskeletal pain or visceral (deep, crampy, diffuse) abdominal pain, then acetaminophen, NSAIDs, or opioids are the medications of choice.

Patients sometimes have unrealistic expectations regarding the amount of pain they will have after surgery, saying, “I want to be pain free.” Patient education concerning pain management during the perioperative period is very important. The goal should be to decrease a patient’s pain from excruciating to manageable. It is unrealistic for a patient to expect to have no pain or that the pain will be eliminated immediately after surgery. It is important to review with a patient during preoperative teaching all the options available for pain management during the perioperative period. For patients taking long-acting opioids before surgery, it is important for them to take a dose the morning of surgery (except Suboxone); otherwise, their pain may be more difficult to manage postoperatively.


Nonsteroidal Antiinflammatory Drugs

Before surgery, a thorough medication history needs to be done. Medications that the patient is taking preoperatively may need to be held before surgery. Both aspirin and herbal medications need to be held for 1 week before surgery. Nonselective NSAIDs should be held for 3 to 4 days before surgery because NSAIDs cause platelet dysfunction. If an analgesic is needed, then acetaminophen or celecoxib can be used because they do not have an effect on platelet function. When celecoxib (Celebrex) is part of our analgesic order set, we only give it for 3 days at doses of 200 mg once or twice per day. Doses of celecoxib, 400 to 800 mg/day, along with prolonged therapy seem to have the side effect of increased cardiovascular death.

Using NSAIDs postoperatively for their antiinflammatory effect may decrease the use of postoperative opioids by 20% to 40% while maintaining the same degree of analgesia. The NSAIDs appear to be equally effective when equivalent doses are used. The efficacy of NSAIDs may be patient specific so that if a patient fails to respond to one NSAID, a different one can be tried. It is best to give NSAIDs around the clock (ATC) rather than PRN because NSAIDs inhibit a cascade of cytokine activation. If a patient has constant pain, ATC use of NSAIDs provides more consistent and constant analgesia.

There may be a pharmacodynamic interaction between aspirin and some of the nonselective NSAIDs in terms of affecting platelet function. The inhibition of platelet function is a COX-1–mediated effect. If the nonselective NSAID is given on a consistent basis or before the daily dose of aspirin, the NSAID will occupy the COX-1 site on the platelet, inhibiting the ability of the aspirin to cause an irreversible inhibition of platelet function. Nonselective NSAIDs will only temporarily impair platelet function. The COX-2–selective NSAIDs do not interfere with aspirin’s effect on platelets.

Certain patients should not receive NSAIDs because of the high risk of precipitating congestive heart failure or acute renal failure. Patients at risk have as preexisting conditions congestive heart failure, renal dysfunction, or liver disease with ascites. Short-term use of NSAIDs (<90 days) may cause recurrent atrial fibrillation or recurrent myocardial infarction.

Data in animals suggest that NSAIDs have an effect on bone healing. It may be that short-term (<7 days), moderate-dose, and COX-2 preferential drugs have less of an effect on fracture healing. There is not enough definitive human data published to answer this question. For patients with pain caused by acute fractures, the short-term use of NSAIDs is not detrimental, but long-term use may prevent fractures from fusing. NSAIDs can be given to hip replacement and trauma patients to prevent heterotopic ossification. Naproxen, 500 mg every 12 hours for 2 weeks, has been successful.


Sometimes acetaminophen, 1 g, is given as part of a preemptive analgesic regimen and then continued postoperatively as 1 g four times a day. IV acetaminophen is used in our patients who are NPO (nothing by mouth) or have impaired medication absorption. There is not a large “first-pass” effect, so the doses IV and oral are equivalent—1 g every 6 hours. If a patient weighs less than 50 kg then the IV dose is 15 mg/kg every 6 hours. It is best to give acetaminophen ATC as blood levels over 10 to 15 mcg/mL correlate with analgesia. IV acetaminophen adds to opioid analgesia, is opioid sparing, and overall may decrease opioid side effects in patients. Because 4 g/day is the suggested maximum daily dose of acetaminophen, other acetaminophen-containing products should be avoided. Patients may have a prolongation of the international normalized ratio when acetaminophen 4 g/day is given while they are taking warfarin. Certain patients are at risk for acetaminophen hepatotoxicity if more than 4 g/day is given. Patients who are alcoholic, have liver dysfunction, or are taking enzyme-inducing medications such as rifampin or carbamazepine have a higher potential for hepatotoxicity from acetaminophen.


Patients may be using opioids before surgery. The amount of opioid used before surgery needs to be considered when deciding what medication and what dose should be used for postoperative analgesia. If a patient is using opioids before surgery, then giving just PRN opioids for postoperative pain control may result in poor analgesia, adverse effects, overdosing or underdosing, dosing intervals that are too long, or conflicts between patients and provider willingness to give pain medication. In an effort to resolve some of these issues, PCA has become popular. With this method of administering opioids, a continuous amount of opioid may be given as well as providing the patient with access to a “demand” dose of analgesic available at a specific interval, usually every 6 to 15 minutes. Currently, only morphine and meperidine are approved by the Food and Drug Administration and available in prefilled PCA syringes. We rarely use meperidine PCA because of its potential for metabolite (normeperidine) accumulation. Normeperidine accumulation, especially with renal dysfunction, may cause agitation, myoclonus, and seizures. Empty PCA syringes are available that can be filled with morphine at high concentrations, or other opioids may be used (fentanyl, hydromorphone, buprenorphine). Patients who are obese, have sleep apnea, elderly, or opioid naïve should be started on demand-only PCA. The literature suggests that demand-only dosing is just as effective and safer than continuous plus demand dosing in patients who are opioid naïve.

Some patients take significant doses of opioids before surgery. If these patients are started on the “usual” doses of PCA analgesics, they will have poor pain control or opioid withdrawal. Patients using PCA can have their long-acting ATC analgesics continued, but the PCA should be used in demand mode only. These patients will require higher than usual demand dosing. Use of both the patient’s own opioid and the continuous opioid from the PCA could result in side effects. What we usually do is discontinue the patient’s long-acting opioid and increase the continuous dose of PCA to compensate for the long-acting opioid that has been discontinued.

Part of the education regarding PCA should include the fact that only the patient should push the demand button and not the nurse or family. Allowing family members or friends to push the demand button may cause excessive sedation.

The option exists to convert all of a patient’s preoperative opioids into the PCA opioid. Table 14A-2 is the opioid equivalence table that is used at Hartford Hospital. All the doses listed are equivalent to one another, both orally and parenterally. A patient’s 24-hour opioid use should be totaled and converted to the equivalent opioid that will be used in the PCA. This dose should then be divided by 24 to determine the hourly continuous rate on the PCA. The demand dose is usually set at 50% to 100% of the hourly rate. Sometimes for slower onset analgesics (hydromorphone, morphine), the demand interval is set at 10 to 15 minutes to allow those analgesics to reach their peak effect before another demand dose is potentially available. Table 14A-3 lists the suggested starting doses for PCA when patients have been on long-acting opioids.



Chemical Class Drug Parenteral Oral
Buprenorphine 0.3 mg
Codeine 120 mg 180 mg
Hydrocodone 30 mg
Hydromorphone 2 mg 8 mg
Levorphanol 2 mg 4 mg
Morphine 10 mg 20–30 mg
Oxycodone 20 mg
Oxymorphone 1 mg 10 mg
Fentanyl 100 mcg
Meperidine 100 mg 300 mg
Methadone 1–2.5 mg 2–5 mg
Tapentadol 100 mg



Opioid Dose per 24 Hours Hydromorphone Morphine Fentanyl

  • Fentanyl 25 mcg/hr

  • Morphine SR 60–90 mg

  • Oxycodone SR 20–40 mg

  • 0.2 mg/mL: 30 mL

  • Continuous: 0.3 mg/hr

  • Demand: 0.3 mg q10min

  • 4-hr lockout: 6 mg

  • 1 mg/mL: 30 mL

  • Continuous: 1.5 mg/hr

  • Demand: 1.5 mg q10min

  • 4-hr lockout: 30 mg

  • 10 mcg/mL: 30 mL

  • Continuous: 15 mcg/hr

  • Demand: 15 mcg q10min

  • 4-hr lockout: 300 mcg

  • Fentanyl 50 mcg/hr

  • Morphine SR 120–180 mg

  • Oxycodone SR 60–80 mg

  • 0.5 mg/mL: 30 mL

  • Continuous: 0.4 mg/hr

  • Demand: 0.4 mg q15min

  • 4-hr lockout: 10 mg

  • 2 mg/mL: 30 mL

  • Continuous: 2 mg/hr

  • Demand: 2 mg q15min

  • 4-hr lockout: 50 mg

  • 25 mcg/mL: 30 mL

  • Continuous: 20 mcg/hr

  • Demand: 20 mcg q10min

  • 4-hr lockout: 500 mcg

  • Fentanyl 100–125 mcg/hr

  • Morphine SR 240–320 mg

  • Oxycodone SR 100–160 mg

  • 0.5 mg/mL: 30 mL

  • Continuous: 0.6 mg/hr

  • Demand: 0.6 mg q15min

  • 4-hr lockout: 15 mg

  • 3 mg/mL: 30 mL

  • Continuous: 3 mg/hr

  • Demand: 3 mg q15min

  • 4-hr lockout: 75 mg

  • 25 mcg/mL: 30 mL

  • Continuous: 30 mcg/hr

  • Demand: 30 mcg q10min

  • 4-hr lockout: 750 mcg

  • Fentanyl 150–200 mcg/hr

  • Morphine SR 360–480 mg

  • Oxycodone SR 180–240 mg

  • 1 mg/mL: 30 mL

  • Continuous: 1 mg/hr

  • Demand: 1 mg q15min

  • 4 hr lockout: 20 mg

  • 5 mg/mL: 30 mL

  • Continuous: 5 mg/hr

  • Demand: 5 mg q15min

  • 4 hr lockout: 100 mg

  • 50 mcg/mL: 30 mL

  • Continuous: 50 mcg/hr

  • Demand: 50 mcg q10min

  • 4 hr lockout: 1000 mcg

q, Every.

When patients are able to take oral medication, they can be switched to PRN short-acting opioids or a combination of long-acting ATC opioids plus PRN short-acting opioids. Table 14A-4 lists suggested starting doses for long-acting opioids when transitioning off of a PCA. If sustained-release oxycodone or sustained-release morphine is used, the initial doses can be given and then the PCA discontinued 2 hours later. If a fentanyl patch is used, the patch should be applied and the PCA discontinued 8 to 12 hours later. For some patients, the transition from IV opioids to oral or topical opioids is difficult. To ease the transition, the ATC oral or topical opioid is started; then the PCA is changed to demand only (after 2 or 8 hours depending on long-acting opioid) for the next 24 hours. Appropriate adjustments in the ATC opioid can be made after reviewing the next 24-hour use of the PCA demand doses. The dose conversions in Tables 14A-3 and 14A-4 are estimates, and factors such as age, trajectory for recovery, and incomplete opioid cross-tolerance need to be considered when these calculations are done.



Hydromorphone IV (mg/24 hr) Morphine IV (mg/24 hr) Fentanyl Patch (µg/hr) Oxycodone SR (mg q12hr) Morphine SR (mg q12hr)
0–7 0–35
8–11 36–55 25 20 30
12–16 56–80 50 30 45
17–21 81–105 75 40 60
22–26 106–130 100 60 90

IV, Intravenous; q, every.

Patients in a methadone maintenance program should always have their methadone doses confirmed by the methadone treatment facility and have their dose continued while hospitalized. This is to make certain that the issues of opioid withdrawal, opioid addiction, and pain management are kept separate. Methadone provides little to no analgesia for patients taking this medication once daily for methadone maintenance. In fact, these patients usually have a lower than normal pain tolerance. If the patient cannot be given food by mouth (NPO), the methadone should be converted to IV. The IV dose of methadone is approximately 50% of the oral dose. The total IV dose is divided so that equal amounts are given at 8- or 12-hour intervals. This is so the patient does not receive a large IV bolus of methadone as a single daily dose. Patients in a methadone maintenance program should have both a continuous and demand opioid during PCA treatment. Their initial doses should be at least 50% higher than the doses listed in Table 14A-1 . Patients taking high doses of methadone will require high doses of their analgesic opioid.

Some patients may be treated with the oral film or sublingual tablets of buprenorphine–naloxone (Suboxone) instead of methadone as part of an opioid addiction program. Suboxone is strongly adherent to and is only a partial agonist at the µ-opioid receptor. The pure opioid agonists at their usual doses (e.g., morphine, hydromorphone, fentanyl) may provide some analgesia, but it may be difficult to control a patient’s pain until the Suboxone has been stopped and metabolized (average half-life at least 24 hours). It is probably best to discontinue the Suboxone while aggressively treating the patient’s pain and then restart the Suboxone as the patient’s pain subsides. Oral naltrexone is used to treat alcohol addiction. Naltrexone is a pure µ-receptor antagonist. It will block any of the opioid effects from systemically administered opioids. It should be stopped if the patient is going to have pain and require opioid analgesics. Vivitrol is an intramuscular suspension of sustained-release naltrexone, which is a full opioid antagonist. The injection is given once per month and blocks opioid effects for approximately 30 days. Using all of the nonopioid analgesics (e.g., nerve blocks, epidurals, acetaminophen, NSAIDs, ketamine, anticonvulsants) will be important. Opioid agonists–antagonists (nalbuphine, butorphanol, pentazocine) should not be given to patients taking systemic opioids, methadone maintenance, or Suboxone because analgesia will be reversed and an immediate opioid withdrawal syndrome may be precipitated. Naloxone and nalbuphine may be used to treat pruritus and nausea if a patient is receiving only epidural opioids.

Selection of Opioids

Morphine is still the gold standard for analgesia. It is avail­able in multiple dose forms for ease of administration, including liquids (multiple concentrations), suppositories, injectable (IV, intramuscular [IM], subcutaneous [SC], epidural), immediate-release tablets, and long-acting tablets and capsules (once daily or every 8 to 12 hours). A lipid-based morphine epidural formulation is available (DepoDur) for postoperative pain that provides analgesia for 48 hours.

One drawback with morphine is the production of a metabolite, morphine-6-glucuronide. This metabolite is a more potent analgesic than morphine itself; however, it does accumulate in patients who are elderly or who have renal insufficiency. Accumulation of the metabolite can cause sedation, confusion, and respiratory depression. These adverse effects are immediately reversible with naloxone. It may take 24 to 48 hours for these adverse effects to resolve after the morphine is stopped.

Hydromorphone has become our drug of choice because of its versatility and lack of significant active metabolites at usual doses. It is especially useful in elderly patients and in patients with impaired renal function. It can be given orally (PO), IM, IV, SC, rectally, and epidurally. An oral liquid is available as well as a concentrated injection. One of the issues with hydromorphone is that it has poor oral bioavailability. There is a difference in the equipotent doses between the oral and parenteral products. Oral hydromorphone 4 mg is equipotent to approximately 1 mg of parenteral hydromorphone.

The use of meperidine has dropped dramatically owing to the availability of safer alternatives. Meperidine has a metabolite, normeperidine, that has no analgesic activity but is a potent CNS stimulant. Normeperidine accumulates especially in patients with renal insufficiency. Patients may or may not show the signs of early toxicity (agitation, delirium, myoclonus) before they have the severe toxicity, which is a generalized tonic-clonic seizure. Administration of naloxone should be avoided because it may only precipitate more seizures. A benzodiazepine will stop the seizure, and if the meperidine is stopped, the patient may not have another seizure. The half-life of normeperidine is 12 hours in patients with normal renal function. The half-life can be much longer in patients with renal insufficiency. If the meperidine is stopped, the adverse effects will decrease over the next 24 hours. If parenteral meperidine is used, the dose should be limited to at most 10 mg/kg/day (600–900 mg/day) for 48 hours in patients with normal renal function. IV meperidine is still excellent for treating postoperative and amphotericin B–induced shivering. Oral meperidine is not very potent; 50 mg provides no better analgesia than 1 g of acetaminophen or an NSAID. In fact, oral meperidine generates more normeperidine owing to the first-pass effect in the gastrointestinal (GI) tract.

Fentanyl can be used as a PRN injection or in a PCA when patients develop nausea, confusion, or pruritus from other opioids. Fentanyl does not accumulate in patients with renal insufficiency and has minimally pharmacologically active metabolites. When patients are ready to stop the parenteral fentanyl, a fentanyl patch can be applied that is equal in strength to the hourly use of fentanyl that can be determined from the PCA. The patch is applied to a nonhairy area of skin and held in place for 30 seconds. This facilitates good adherence between the patch and the patient’s skin. The PCA and patch are overlapped for 8 to 12 hours, and then the PCA can be stopped. Patients usually need an oral PRN short-acting opioid such as oxycodone, hydromorphone, or hydrocodone for breakthrough pain. There are available multiple transmucosal immediate-release fentanyl products and a nasal spray, but they are very expensive, and many pharmacies may not carry these items.

Oxycodone should be used cautiously in patients with renal insufficiency or receiving dialysis. Both oxycodone and metabolites accumulate, causing toxicity if doses are titrated upward too quickly or high initial doses are used. Multiple oral dose forms of oxycodone are available, including liquid, liquid concentrate, immediate-release tablets, and sustained-release tablets. OxyContin is now manufactured in an abuse-deterrent dosage form that is very difficult to crush, cut, or dissolve. Various oxycodone–acetaminophen combinations are available. Using the medication with the least amount of acetaminophen, usually 325 mg per tablet, should avoid acetaminophen toxicity. Patients should not ingest more than 4 g/d of acetaminophen on a chronic basis to avoid hepatotoxicity. Also available is an oxycodone–ibuprofen combination product (5 mg/400 mg per tablet).

Hydrocodone immediate release is not available as a stand-alone analgesic. It is combined with either acetaminophen or ibuprofen. A sustained-release hydrocodone, Zohydro, is now available. One of hydrocodone’s metabolites is hydromorphone. Hydrocodone is safe to use in renal insufficiency. The ibuprofen dose is 200 mg per tablet; however, the amount of acetaminophen per tablet is now consistently 325 mg. A liquid formulation is available. Hydrocodone products are currently classified as controlled substance class III (CIII) narcotics, but they are being considered for a change to class II (CII) narcotics.

Tramadol as an analgesic has a dual mechanism of action. Tramadol itself inhibits the reuptake of norepinephrine and serotonin while the major metabolite, desmethyltramadol, binds to the µ-opioid receptor. Tramadol is not a controlled drug. There are two tablets; one is a 50-mg tablet, and the other is 37.5 mg combined with acetaminophen 325 mg. A sustained-release product, which is given once daily, is available in 100-, 200-, and 300-mg strengths. Slow upward titration prevents the side effects of sedation, nausea, and dizziness from being problematic. The combination of tramadol and antidepressants may cause seizures or the serotonin syndrome; however, the incidence is low.

Methadone is a unique analgesic in that it has a long half-life (at least 24 hours) and is inexpensive, and the d -stereoisomer is an NMDA receptor antagonist, which means it may have an effect on neuropathic pain. It is available as an injection (IV, IM), tablets, and liquids. Despite the long pharmacokinetic half-life, the analgesic action persists for only 6 to 8 hours, so methadone for analgesia needs to be dosed every 6 to 8 hours. When methadone is initiated, a fixed initial dose should be started and not changed for 4 to 7 days, allowing the methadone to accumulate. Patients should have short-acting opioids for breakthrough pain. What should happen after methadone is started is that over the ensuing 3 to 4 days, the use of the PRN opioids should decrease. The conversion from other opioids to methadone can be difficult. The long half-life and the equivalency change depend on the amount of daily prior opioid use. Usually the equivalency is in the range of 5% (for high-dose prior use) to 25% (for low-dose prior opioid use) of the morphine equivalent dose.

Hydroxyzine has been used as a “potentiator” of opioid analgesia for a number of years. In reality, the studies that demonstrated this effect were poorly designed as analgesic trials. These studies used high doses of hydroxyzine (100 mg IM), but today the typical dose is 25 to 50 mg. It is true that hydroxyzine is an antihistamine, mild antiemetic, and sedative. It is very painful as an IM injection and has a long half-life (≈24 hours). For the most part, now we avoid using hydroxyzine so that there are fewer problems with sedation.

Opioids commonly cause side effects; however, if these are promptly recognized and treated the side effects are manageable. Nausea and vomiting should be treated with antiemetics (haloperidol, metoclopramide, prochlorperazine, promethazine), and if these side effects occur frequently during treatment, the antiemetics should be scheduled ATC. Patients will develop a tolerance to nausea and vomiting, but it may take 1 to 2 weeks. Reducing the dose of the opioid, changing the route of administration, increasing the time of infusion, or changing the opioid may all have a significant effect. Constipation is a side effect to which tolerance does not develop. Patients need to be started on a laxative that is both a softener and a stimulant. The laxatives need to be given daily so that if the patient is eating well there should be a bowel movement daily or every other day. Senokot-S, MiraLax, Amitiza, and lactulose can all be effective. An ileus can occur from opioids or surgery. For a postoperative ileus, if the patient is not taking opioids chronically, using buprenorphine may provide effective analgesia without aggravating the ileus. Buprenorphine is a partial µ-receptor agonist. It has very little effect on smooth muscle and does not cause spasm of the sphincter of Oddi. It may precipitate opioid withdrawal in patients on methadone maintenance or in patients taking opioids chronically. For analgesic use, it is available as Butrans, a sustained-release patch dosed at 5 mcg/hr, 10 mcg/hr, 15 mcg/hr, and 20 mcg/hr changed every 7 days. A 10-mcg/hr patch is equal to 30 mg of oral morphine per day or a 12-mcg/hr fentanyl patch. Buprenorphine as an injection can be given IM or IV or via PCA. The Butrans patch should be removed 24 hours before surgery so that the opioid analgesics can be most effective.

Pruritus does not necessarily indicate a true allergy unless hives and a rash accompany it. Most opioids cause histamine release, which causes pruritus. Both oral and parenteral opioids cause pruritus. It is thought that the least potent opioids (meperidine) cause more pruritus than the most potent (fentanyl). One of the treatments is to switch to a more potent opioid to relieve the pruritus. Antihistamines are somewhat effective for the pruritus.

If a patient becomes sedated, it is time to reassess the opioid therapy. Opioids cause a decrease in respiratory rate, hypoventilation, and hypoxia. They do not cause dyspnea or tachypnea. Other causes of sedation need to be ruled out such as other medications (benzodiazepines), metabolic abnormalities, and so on. Was the opioid dose titrated up too quickly? Is the patient on morphine and now has developed renal insufficiency? Is the patient elderly or opioid naïve or have a history of sleep apnea? Unless the patient is apneic, naloxone (Narcan) should be given slowly and in a low dose to avoid a rebound in pain or opioid withdrawal. Naloxone 0.4 mg (1 mL) should be mixed with 9 mL of saline with 1 to 2 mL given by IV push every 1 to 2 minutes until the patient is awake or a satisfactory respiratory rate has been achieved. Naloxone’s duration of action is short (30–60 minutes), so the patient will need to be monitored carefully for a few hours.

Myoclonus is seen most often with meperidine, than with morphine, or than with hydromorphone. These involuntary, symmetrical muscle spasms occur while the patient is awake or asleep. Myoclonus occurs when the patient is being treated with high doses of opioids or the dose has been titrated up rapidly. Some adjuvants (gabapentin and pregabalin) also cause myoclonus. Sometimes the muscle spasms are painful, and other times the family is bothered by the myoclonus. Decreasing the opioid dose or switching to a different opioid (methadone) will eliminate the myoclonus. A benzodiazepine or valproic acid will effectively decrease the number or intensity of the spasms.

Neuropathic pain is sometimes difficult to identify. It is important to ask patients how they would describe their pain. Words such as burning, stabbing, shooting, aching, throbbing, and electricity-like may indicate the presence of neuropathic pain. Procedures done to bone may affect the nerves that supply the periosteum and endosteum; therefore, neuropathic pain should be considered a component of bone pain. Typically, this pain is described as being opioid resistant or insensitive. What usually happens when a patient is given an opioid for this pain is that the patient has some analgesia but it is of short duration. Patients also frequently have severe side effects at low doses of opioids. These are the patients who are sedated, awaken, and ask for analgesics and then fall back asleep before the analgesic is administered. Typically, opioids alone are only fairly effective for neuropathic pain. When opioids alone are used for neuropathic pain, patients tend to complain about poor pain control despite what we would consider adequate doses of opioid analgesics. The patient may then be labeled as an “addict” or as “drug seeking” when in reality, if an adjuvant such as gabapentin or baclofen is introduced early in therapy, the patient’s pain control may be better with the combination of an opioid and gabapentin–baclofen, a “multimodal analgesia.” When treating difficult neuropathic pain, multiple adjuvants may be needed, and it is best to use agents from different pharmacologic classes, for example, an anticonvulsant plus a muscle relaxant rather than an anticonvulsant plus an anticonvulsant. The anticonvulsants are usually added first (gabapentin, oxcarbazepine, pregablin) because of their fast onset of action and their lack of significant drug interactions. A patient may have effective pain relief within 24 to 48 hours of initiation of therapy. If a patient has muscle spasms, opioids are not effective at relieving the spasm. Medications such as baclofen, lorazepam, and tizanidine are effective at relieving spasms. Diazepam is the classic muscle relaxant, but lorazepam will work just as well. Antidepressants are effective; however, they require a titration process, so their efficacy may be delayed. Usually when patients try an antidepressant, they respond in a shorter time and at a lower dose compared with that which is needed for an antidepressant effect. Lidocaine patch 5% (Lidoderm) is effective for topical pain syndromes. The lidocaine penetrates a few millimeters into the epidermis and dermis, so it is usually not effective for severe bone pain. The systemic blood levels are approximately one-tenth of those needed to treat an arrhythmia. Table 14A-5 lists the most commonly used adjuvants for neuropathic pain.



Drug Class Starting Dose Dose Range Side Effects and Comments
Amitriptyline (Elavil) Tricyclic antidepressant 10–25 mg PO at bedtime
Titrate dose up every 3 days
25–150 mg at bedtime Sedation, anticholinergic effects, prolongation of QTc
Baclofen Muscle relaxant 5–10 mg PO tid
Titrate dose up every 2–3 days
10–30 mg tid
5 mg bid–tid with decrease in GFR or in elderly adults
Sedation, delirium, muscle weakness, withdrawal seizures
Carbamazepine (Tegretol) Anticonvulsant 100 mg PO bid
Titrate dose up every 3 days
200–600 mg bid Sedation, SIADH, enzyme induction, bone marrow suppression; monitor serum levels for efficacy
Desipramine (Norpramin) Tricyclic antidepressant 10–25 mg PO at bedtime
Titrate dose up every 3 days
25–150 mg at bedtime Less sedation and anticholinergic effects than amitriptyline, prolongation of QTc
Duloxetine (Cymbalta) Antidepressant (SNRI) 20–30 mg PO daily
Titrate up every 3 days
30–60 mg bid
30–60 mg daily with decrease in GFR
Nausea, insomnia, headache, diarrhea, constipation; taper off to avoid withdrawal
Gabapentin (Neurontin) Anticonvulsant 100–300 mg PO tid.
Titrate up every 24 hours
300–800 mg tid
300 mg daily or bid with decrease in GFR
Sedation, confusion, myoclonus, dizziness, diplopia, peripheral edema
Lidocaine patch 5% (Lidoderm) Topical anesthetic One patch daily; on for 12 hr and off for 12 hr One to three patches per day depending on area needing analgesia, cut to fit Skin irritation; apply to site of pain; effective for postherpetic neuralgia
Mexiletine Antiarrhythmic 150 mg PO bid–tid
Titrate up every 3 days
200–250 mg tid Nausea, insomnia, delirium; no effect on ECG; not proarrhythmic
Oxcarbazepine (Trileptal) Anticonvulsant 150 mg PO bid
Titrate up every 2 days
150–600 mg bid
75–150 mg bid with decrease in GFR
Sedation, SIADH
Pregabalin (Lyrica) Anticonvulsant 50 mg PO bid
Titrate up every 24 hr
50–300 mg bid
25–50 mg bid–tid with decrease in GFR
Sedation, confusion, dizziness, diplopia, peripheral edema, myoclonus
Tizanidine (Zanaflex) Muscle relaxant 2 mg PO bid–tid
Titrate up every 3 days
4–8 mg tid
1–2 mg tid with decrease in GFR
Sedation, hypotension, dry mouth
Valproic acid (Depakote) Anticonvulsant 250–500 mg PO bid
Titrate up every 3 days
500 mg–1 g bid
Use same dose IV
Mild sedation, tremor, increased LFT results; monitor serum level
Milnacipran (Savella) Antidepressant (SNRI) 12.5–25 mg bid 50–100 mg bid
25–50 mg bid with ↓ in GFR
Nausea, headache, hypertension; taper off to avoid withdrawal; FDA approval for fibromyalgia

bid, Twice a day; ECG, electrocardiogram; FDA, Food and Drug Administration; GFR, glomerular filtration rate; IV, intravenous; LFT, liver function test; PO, oral; tid, three times a day; SIADH, syndrome of inappropriate antidiuretic hormone secretion; SNRI, serotonin–norepinephrine reuptake inhibitor.

Appropriate and Inappropriate Use of Opioids

The use of opioid medications in the treatment of orthopaedic patients has been performed countless times for many decades. Opioids offer an effective way to reduce pain in this population and usually pose little risk of addiction. In certain circumstances, some patients do display behaviors of addiction when treated with opioids. The challenge we have as health care providers is to stop the abuse of opioids while ensuring the continued availability of these medications for patients who benefit from their use.

Approaching the use of opioid medications to treat pain should be approached like any other condition we encounter.

Diagnosis and Differential

Treatable causes of pain should be identified through a history, physical examination, and testing. The treatment should be directed at the pain generator(s). Comorbid conditions need to be taken into consideration when assessing the use of opioid medications. Included in these conditions is a personal or family history of alcohol or drug abuse. The presence of psychological conditions, a history of sexual abuse, and a younger age (18–45 years) are also associated with aberrant drug-related behaviors in some studies.

Risk assessment screening tools are helpful for stratification of risk; however, more validation of the outcomes are needed to understand the effects on clinical outcomes. Tests that appear to have good content, face, and construct validity include the Screener and Opioid Assessment for Patient with Pain (SOAPP), Version 1; the revised SOAPP (SOAPP-R); the Opioid Intractability Risk Tool (ORT); and the Diagnosis, Intractability, Risk, Efficacy (DIRE) instrument. DIRE is clinician administered, and the others are patient self-reporting.

Informed Consent

Health care providers need to thoroughly explain the entire treatment plan with the patient and the use of opioids in that complete plan. The risks and benefits associated with the use of opioids need to be understood, and issues about physical dependence, addiction, abuse, tolerance, and withdrawal need to be explored.


Abuse is use of any substance for a nontherapeutic purpose or for what it is not prescribed.


Addiction is a chronic neurobiologic disease characterized by impaired control over drug use, compulsive drug use, and continued drug use despite harm and because of craving.

Physical Dependence

Physical dependence is a physiologic state characterized by withdrawal symptoms if treatment is stopped or decreased abruptly. It does not equal addiction.


Tolerance is a physiologic state caused by the regular use of an opioid in which increased doses are needed to maintain the same effect

Withdrawal (Abstinence)

Withdrawal is characterized by sweating, tremors, vomiting, anxiety, insomnia, and muscle pain.

Opioid Agreements

Expectations and obligations of the patient and physician are understood. The plan should explain the course of treatment and the goals of therapy. It should set limits on the use of opioid therapy and expectations about follow-up care and monitoring of the therapy. It also should include indications for tapering, changing, or discontinuing opioids as part of the entire treatment plan.

Initiation and Assessment of Therapy

Opioid selection, initial dosing, and titration should be individualized according to the patient’s health status, previous exposure to opioids, attainment of therapeutic goals, and predicted or observed harms. The four As of opioid prescribing should be followed.


The goal for the use of opioid medications is to decrease pain. A baseline pain score using a standard visual analog scale (VAS) or any of the other pain tracking ways is adequate. You need to use the same system every time the patient’s pain is reevaluated for consistency. Failure to make progress in the reduction of pain may cause the health care provider to change, taper, or discontinue current course of treatment because of lack of efficacy.


The goal for the use of opioid medications is to improve activities of daily living and quality of life.

Adverse Effects

Side effects, including nausea, constipation, alterations in cognitive function, and respiratory depression, all need to be monitored throughout the use of opioid medications. Appropriate adjustments in the treatment algorithm may need to occur if adverse effects are not tolerated or correctable.

Aberrant Behavior

An aberrant behavior is any drug-related deviation from the medical plan. This can include unauthorized dose escalations, prescription forgery, using opioids to achieve euphoria or relief of anxiety, abnormal urine test screening results, and request for early refills or requesting refill instead of an appointment with the health care provider, to name a few.

Regimens need to be tailored to the patient based on subjective, objective, and clinical findings. The goal is a stable therapeutic platform. The need for regular follow-up care to assess the outcome of therapy initiated is crucial for success. Look for warning signs of adverse effects and aberrant behavior. This will help with the rationale to continue or modify treatment.

At each visit, review the patient’s diagnosis, comorbid conditions, and addictive disorders, if any. The treatment goals may need to be amended because illnesses evolve and diagnostic tests can change with time.

The management of pain in orthopaedic patients can range from the very acute to chronic, lifelong management. Maintaining safe prescribing habits, reevaluating the continued need for opioids, and monitoring the effectiveness of therapy and the possible development of aberrant behaviors are key to effective use of this class of medications.

Neuraxial Delivery Systems: Subarachnoid Injections

The delivery of opioids or local anesthetics to the intrathecal or epidural space can provide profound analgesia in patients experiencing moderate to severe acute pain. Injection of opioids into the subarachnoid space results in the selective decrease in nociceptive transmission from C polymodal and Aδ afferents with no effect on motor, sensory, or autonomic function. Acting on µ and κ receptors within the spinal cord, opioids exhibit a greater affinity to C fibers than Aδ fibers, the consequence of which is a greater reduction of dull versus sharp pain.

With respect to opioids, the single biggest determinant of onset and duration is the drug’s lipophilicity. Lipophilic opioids such as fentanyl are rapidly cleared from the cerebrospinal fluid (CSF), producing rapid onset but a short duration of action. Clearance from the CSF is so rapid that the primary analgesic effects of these opioids are probably produced by systemic and supraspinal mechanisms. Hydrophilic (lipophobic) agents such as morphine tend to remain in the CSF after neuraxial administration, resulting in a delayed onset but extended duration of effect. Bulk flow of hydrophilic opioids within the CSF produces analgesic effects at locations that are further away from the injection site. Thus, injection of morphine into the subarachnoid space in the lumbar area can produce analgesic effects in the upper abdomen and thoracic regions. This cephalad migration may also contribute to the development of side effects commonly seen with subarachnoid injection of opioids.

Side effects from neuraxial opioids are typically dose dependent and may or may not result from interactions with specific opioid receptors. Far and away the most commonly reported side effect is the development of non–histamine release pruritus. Up to 60% of patients can experience pruritus, which is thought to develop from the activation of “itch centers” in the medulla and trigeminal nucleus. Pruritus often develops in the upper thorax, neck, and face and is not associated with a rash. Patients generally respond to treatment with low-dose naloxone, nalbuphine, droperidol, or naltrexone, further supporting that histamine release is not the underlying cause.

Nausea and vomiting are other common side effects of subarachnoid opioid administration with an incidence greater than 30%. The development of nausea and vomiting generally occurs within 4 hours of opioid administration in susceptible patients. Nausea and vomiting can occur in a dose-dependent fashion and primarily occur because of bulk flow and cephalad migration of opioids within the CSF. Dispersion of opioids within the CSF results in activation of opioid receptors within the area postrema of the medulla. Other mechanisms, including the sensitization of vestibular system to motion as well as decreased gastric motility, may also play a role. Patients who develop nausea and vomiting can be successfully treated with low-dose naloxone, transdermal scopolamine, dexamethasone, metoclopramide, or droperidol.

Urinary retention may also develop among patients receiving subarachnoid opiates. The development of this side effect does not appear to be dose dependent, and its incidence can vary widely but occurs more commonly in young males. Opioid receptors activated in the sacral spinal cord (S2–S4) cause a reduction in parasympathetic outflow, leading to detrusor muscle relaxation and an increase in bladder capacity. Neuraxial administration of morphine has effects on the bladder within 15 minutes and can last as long as 16 hours.

Perhaps the most concerning side effect of subarachnoid opioids is the development of respiratory depression. Clinical studies have shown that when appropriate doses of subarachnoid opiates are given, the incidence of respiratory depression does not vary greatly from systemic administration. Respiratory depression requiring intervention occurs in a dose-dependent fashion with an overall incidence of 1%. Unlike most systemic routes, subarachnoid opiates may result in both early and delayed respiratory effects. Clinically relevant early respiratory depression has been linked to epidural injection of lipophilic opioids and is exceedingly rare with subarachnoid injections. Opioids such as fentanyl and sufentanil can produce respiratory depression within 2 hours of epidural injection, which is likely the result of systemic absorption. Delayed respiratory depression results from the activation of opioid receptors within the ventral medulla following the cephalad migration of hydrophilic opioids. The ventral medulla contains a large number of opioid receptors, and even small concentrations can produce significant effects. Respiratory depression typically occurs between 6 and 12 hours after neuraxial injection of morphine but can persist up to 24 hours. It has been suggested that patients receiving neuraxial lipophilic opioids be monitored for signs of respiratory depression for 4 to 6 hours after treatment and those receiving hydrophilic opioids (morphine) be monitored for 18 to 24 hours after their administration. The earliest signs of respiratory depression include changes in mental status as well as bradypnea with resultant hypercarbia rather than frank apnea. Airway management is the initial step in treatment followed by the use of naloxone. Bolus doses in increments of 0.1 to 0.4 mg of naloxone are given until the respiratory rate recovers. This should then be followed by an infusion of naloxone at 0.5 to 5 µg/kg/hr because respiratory depression may reoccur when the initial dose of naloxone wears off.

Neuraxial Delivery Systems: Continuous Epidural Catheters

The use of continuous epidural catheters has proven to be an effective tool in the management of acute pain by providing analgesia that is superior to systemic opioids. Unlike the one-time neuraxial injections that provide a short duration of relief (4–6 hours for fentanyl, 24 hours for morphine, 48 hours for liposomal morphine), continuous epidural catheters can be left in situ for several days during the recovery period. Infusions can consist of local anesthetics, opioids, or a combination of both. Selection of the drug(s) to be infused should be based on the clinical needs of the patient.

Patients who experience traumatic injuries may experience pain in multiple locations on the body. When it is not possible to cover all painful areas, an epidural infusion of local anesthetic only may be appropriate. The epidural may be placed in an anatomic location that is most beneficial to the patient while secondary areas of pain are addressed through systemic opioids and multimodal pharmacology. Typically, agents such as bupivacaine or ropivacaine are selected for infusion because of their preferential sensory blockade and long duration of action. With increasing doses of local anesthetics, patients may develop unwelcomed side effects. The development of motor blockade can prevent proper assessment of peripheral nerve function, and sympathetic blockade from epidurals placed in the thoracic region can result in hypotension.

When the aforementioned side effects are undesirable, patients may benefit from opioid-only infusions. Although lipophilic agents such as fentanyl and sufentanil can be used, they are not considered ideal because several randomized clinical trials have suggested a primarily systemic rather than spinal site of action. As such, infusions of lipophilic agents produce equivalent levels of analgesia and similar rates of side effects to their IV counterparts. Studies comparing epidural lipophilic opioids with IV opioids have shown either only a modest benefit with epidural administration or no difference. Given its lack of clear benefit over parenteral routes, it makes little sense to expose the patient to the risk of epidural placement for the infusion of lipophilic opioids. On the other hand, the use of hydrophilic opioids may be useful because studies have shown better pain control with hydrophilic opioids than with traditional PRN regimens. Unlike lipophilic agents, hydrophilic agents such as morphine exert their primary analgesic effect by binding to opioid receptors within the spinal cord. Because of its relative lack of vascular uptake, bulk flow within the CSF allows for the distal spread of the medication. This characteristic is particularly useful when the catheter is placed at a site distant to spinal roots carrying the pertinent nociceptive information.

Continuous epidural analgesia is at its most effective when infusions that combine both local anesthetics and opioids are used. Combination therapy has been shown to provide superior analgesia and patient satisfaction compared with IV PCA usage and single-agent epidural infusions. By combining agents, patients report improved sensory block and better dynamic pain relief. Additionally, combination infusions require less of both agents (opioids and local anesthetics) compared with epidural infusions that only contain opioids or local anesthetics. This is advantageous because side effects that occur in a dose-dependent fashion are reduced. Agent selection is similar to single-agent infusions. Typical regimens use local anesthetics that are long acting and provide preferential sensory over motor blockade such as low-concentration bupivacaine or ropivacaine. Lipophilic opioids can be used because they allow for rapid titration of analgesia. Although combinations that include lipophilic agents produce better analgesia than local anesthetics alone, this is probably due to primarily systemic effects. The addition of hydrophilic opioids to local anesthetic infusions also improves analgesia over standard IV regimens. Although neuraxially administered hydrophilic opioids exert their primary analgesic effects at the spinal cord, their addition to local anesthetic solutions confers no additional benefit compared with local anesthetic-only solutions containing lipophilic opioids.

In addition to providing superior analgesia to systemic opioids, the use of epidural catheters for acute pain management in perioperative settings has been associated with a reduction in morbidity and mortality. Pain control and inhibition of sympathetic outflow aids in diminishing the stress response, which can have beneficial effects on a variety of physiologic processes. The placement of an epidural catheter in the thoracic region for pain related to chest wall injuries, thoracotomies, and upper abdominal surgical procedures has been shown to decrease the risk of pulmonary complications. Better analgesia in these situations allows for better pulmonary toilet and use of incentive spirometry, resulting in preservation of preoperative or preinjury pulmonary function. After thoracotomies or upper abdominal surgical procedures, there is impairment of diaphragmatic function. This phenomenon is due to reflex inhibition of phrenic nerve activity and does not improve with analgesia. The addition of local anesthetics to thoracic epidural infusions suppresses the reflex, thereby improving pulmonary function. Mitigation of the stress response by thoracic epidurals has also been shown to decrease the incidence of myocardial infarction. Sympathetic blockade results in small reductions in heart rate, blood pressure, and cardiac output, thereby decreasing myocardial oxygen demand. The supply side of the equation is also altered. Sympathetically mediated vasoconstriction at sites that are distal to preexisting coronary artery stenosis are abolished, and myocardial blood flow undergoes redistribution, resulting in improved endocardial to epicardial blood flow ratios. Limiting a patient’s exposure to opioids coupled with decreased sympathetic output has also been shown to favor the return of GI motility, improve blood flow to the bowel, and prevent the reduction of intramucosal gastric pH. The restoration of normal GI function allows for a faster return to PO intake so that nutritional goals can be met. As stated previously, patients who experience significant acute pain are subject to a significant neuroendocrine response that often leads to hypermetabolic and catabolic states. By meeting nutritional goals early, it may be possible to limit negative nitrogen balance and protein catabolism that can delay wound healing and impede patient recovery.

The use of epidural catheters provides a myriad of benefits that make it an attractive option for the management of acute pain. Although studies conflict as to whether combined local anesthetics and opioid infusions exhibit a synergistic or an additive effect, it is clear that they can improve analgesia and decrease side effects when used together. Additionally, it has been proposed that the use of epidural analgesia may help at-risk patients from developing chronic pain syndromes. Reduction or blockade of nociceptive input into the dorsal horn may prevent the development of chronic pain states by decreasing C-fiber activation of WDR neurons, which have been linked to wind-up and central sensitization.

Despite the numerous advantages of epidural analgesia, there are potential risks to consider. Although the placement of an epidural catheter has inherent risks, the presence of an indwelling catheter represents ongoing risk to the patient. Serious complications such as epidural abscess and epidural hematoma are uncommon yet potentially devastating complications for the patient. With the introduction of low-molecular-weight heparin in North America in 1993, there was a dramatic increase in the incidence of spinal hematoma. Before this time, the incidence of spinal hematoma was estimated to be one in 220,000 for spinal techniques and one in 150,000 for epidural access. From 1993 to 1998, the frequency of spinal hematoma increased precipitously with incidences of one in 6600 for spinal techniques and one in 40,800 for epidural access. The dramatic rise in these events resulted in an increasing focus on the use of thromboprophylactic and anticoagulation medications. The American Society of Regional Anesthesia and the European Society of Anesthesiology have developed consensus statements regarding the use of hemostasis-modifying agents and the timing of neuraxial techniques (access, catheter placement, and catheter withdrawal). These statements reflect that different agents have different pharmacokinetic properties that should be considered. In general, the consensus statements suggest that two half-lives of the medication should pass before performing neuraxial procedures. Special consideration should be taken for elderly patients and those with renal impairments. The consensus statements also highlight the need for continued assessment of neurologic function and warn that patients on regimens of multiple anticoagulants are at higher risk of bleeding complications. Based on these consensus statements, most institutions have developed guidelines for the provision of neuraxial techniques. Clinicians should check with their institutions regarding their specific guidelines.

Peripheral Nerve Blocks

In the management of acute pain, it is clear that methods that provide safe and efficient analgesia can have profound effects on patient outcomes and satisfaction. The use of regional anesthetic techniques has undergone a renaissance over the past decade. In particular, the utilization of ultrasonography has given practitioners the ability to perform fast, reliable blocks. Additionally, it has provided clinicians the confidence to pursue novel techniques that confer greater selectivity and decreased motor blockade. As techniques have advanced, the implementation of indwelling peripheral nerve catheters (PNCs) has provided a means of extending the benefits of regional anesthesia.

The utilization of regional techniques has also changed the way we approach acute pain management in both civilian and war trauma patients. Under the right circumstances, simple effective blocks that do not compromise hemodynamics or respiratory function can be provided in prehospital settings to provide fast analgesia. The use of regional anesthesia in these settings should only be considered after conducting a baseline neurologic examination to rule out potential contraindications. Additionally, regional anesthesia techniques should only be used after proper stabilization of the patient and should not delay transport to higher care facilities. In France, the implementation of femoral nerve blocks has become common before transporting patients with femur fractures. On the battlefield, regional anesthesia plays a vital role in providing effective analgesia in triage areas so that patients can be transported to tertiary care centers without the need for advanced airway management. Victims of traumatic injuries often present with a full stomach. Additionally, they may require cervical spine stabilization from injury; it is also possible that one cannot reliably rule out injury. These circumstances place the patients at higher risk of aspiration and make it difficult for the clinician to properly secure the airway. Using regional techniques mitigates some of these risks and provides superior analgesia over systemic and oral opioids.

The use of regional anesthesia is also an invaluable part of perioperative pain management. Increasing institutional demands to reduce length of stays or provide same-day discharges coupled with societal demands to provide effective pain management underscore the need for regional techniques. Strategies that incorporate regional anesthesia combined with anesthetic management with propofol have been shown to provide rapid recovery and decrease the incidence of postoperative nausea and vomiting (PONV). Studies also suggest that avoidance of volatile anesthetic agents has reduced incidences of unplanned admissions secondary to uncontrolled pain.

Recent trends in regional anesthesia have seen the implementation of indwelling PNCs. As opposed to single-injection blocks that provide 12 to 24 hours of analgesia, indwelling catheters extend the benefits of the block by providing constant infusions of low-concentration local anesthetics. As opposed to epidural analgesia and IV PCA use that requires hospitalization, patients can be discharged home with PNCs in place. This practice has been shown to be very effective for select procedures by providing superior analgesia, reducing opioid side effects, and providing high levels of patient satisfaction. A meta-analysis of randomized controlled trials comparing postoperative analgesia among PNCs with opioids found PNCs to confer significant benefits. In addition to providing superior analgesia and reduced opioid side effects, PNCs were associated with improved physical therapy, better sleep patterns, shorter lengths of stay, and better patient satisfaction. Perhaps the area where PNCs have had the most dramatic impact has been in their use in the treatment of military-related traumas. Early placement of PNCs allows for improved evacuation conditions, and their continued use in tertiary care settings facilitates anesthesia and analgesia for patients who may require multiple procedures, including operations to dressing changes. Continued use throughout the recovery period aids in rehabilitation efforts. PNCs have been proven to be extremely versatile; they can be used to achieve surgical anesthesia or maintain analgesia through continuous infusions or even be temporarily stopped to assess peripheral nerve functions.

Upper Extremity Blocks

Severe acute pain of the upper extremity from surgeries or injuries can be managed by performing peripheral nerve blocks at various locations along the brachial plexus. The brachial plexus is the network of nerve fibers that is responsible for most sensory and motor function of the upper extremity. The exceptions are the spinal accessory nerve (cranial nerve XI), which innervates the trapezius, and the intercostobrachial nerve, which supplies sensation to the upper half of the medial and posterior aspect of the arm. The brachial plexus is formed by the ventral rami of the fifth to eighth cervical and the first thoracic nerves. The fourth cervical and second thoracic nerves can also make small contributions to the brachial plexus. As the brachial plexus emerges from the cervical roots in the neck through the upper extremity, it divides to form trunks, divisions, cords, and terminal branches ( Fig. 14A-2 ). Sensory information can be interrupted at each of these locations along the plexus through the application of local anesthetics.

Figure 14A-2

Nervous system of the brachial plexus. n, Nerve.

Interscalene Block

Halsted performed the first brachial plexus block in 1885 through direct surgical exposure by applying cocaine. It was not until the 1900s that percutaneous approaches were described. In 1970, Winnie described a percutaneous approach between the anterior and middle scalene muscle at the level of the cricoid cartilage that produced consistent and effective results. The interscalene block (ISB) is performed at the level of the roots and trunks yielding the most proximal approach to the brachial plexus. This approach is effective in providing analgesia to the shoulder and proximal humerus from surgeries or traumatic injuries. Although the brachial plexus is responsible for all motor function of the shoulder, it is not entirely responsible for all sensory function. The cephalad–cutaneous portions of the shoulder are supplied by the supraclavicular nerves that emanate from the lower portion of the superficial cervical plexus (C3–C4) ( Fig. 14A-3 ). The interscalene approach offers superior analgesia to the shoulder because it reliably blocks the upper (C5–C6) and middle trunk (C7) as well as the cervical plexus (C3-4). It is common for this approach to spare the lower trunk (C8–T1), thus making it unsuitable for treating acute pain in the forearm or hand.

Figure 14A-3

Supraventricular nerves in the shoulder. n, Nerve.

Interscalene blocks have been used extensively for procedures involving the shoulder, demonstrating analgesia that is far superior to IV opioids. Additionally, studies have found that the use of ISB in shoulder surgeries dramatically reduces VAS pain scores as well as total opioid requirement, decreases the incidence of PONV, improves sleep patterns, shortens lengths of stay, and improves patient satisfaction. Continuous ISBs by placement of an indwelling catheter have also been used with a high rate of success. Compared with one-time ISB injections and IV opioids for postoperative pain management, continuous blocks have demonstrated improved VAS scores, reduced opioid consumption, and improved rehabilitation. The use of continuous interscalene catheters has also allowed previously inpatient procedures, such as total shoulder arthroplasties, to be performed in ambulatory settings. Early studies have shown that a subset of patients who do not have significant comorbidities may be eligible for same-day total shoulder arthroplasties if continuous interscalene catheters are a part of their multimodal pain management regimen.

The ISB is a relatively simple procedure to perform and begins with the patient in the supine position with the head of the bed elevated to approximately 45 degrees. The patient’s head is turned slightly away from the side to be blocked, and the level of the cricoid cartilage is identified. Palpating posteriorly along the lateral border of the sternocleidomastoid muscle can identify the interscalene groove. Placement of a linear, low-penetration, high-resolution ultrasound probe allows for rapid identification of the neural structures ( Fig. 14A-4 ). The use of a nerve stimulator may also be used for either primary identification of the brachial plexus (no ultrasound) or as a method of confirmation (with ultrasound). After sterile prep and drape, the patient is typically given light IV sedation to provide anxiolysis and improve the patient experience. A 2-inch short bevel echogenic or stimulating needle is then advanced toward the brachial plexus. When the ultrasound is used, the needle is advanced “in plane” of the ultrasound beam, allowing for easier identification of the tip of the needle ( Fig. 14A-5 ). Local anesthetic is deposited around the neural structures under direct visualization. If ultrasound is not used, the needle is advanced at a 45-degree angle in relation to the skin directed toward the contralateral nipple. The practitioner relies on evoked motor responses at low amplitude (<0.5 mA) as a means of determining the relationship between the tip of the needle and the nervous structures.

Figure 14A-4

Ultrasound image of the interscalene groove. At this level, the roots and trunks of the brachial plexus can be identified as hypoechoic structures (circle) lying between the anterior scalene muscle (ASM) and middle scalene muscle (MSM).

Figure 14A-5

An in-plane approach allows for direct visualization of the block needle as it approaches the trunks of the brachial plexus within the interscalene groove. The local anesthetic (LA) is hypoechoic on ultrasonography and can be seen spreading in a circumferential fashion around the nerve structures.

The injection of local anesthetic in the interscalene groove (between the anterior and middle scalene) invariably results in the diffusion of local anesthetic away from the groove. Although this has some advantages such as blockade of the supraclavicular nerve, it also produces some undesirable side effects. The phrenic nerve runs along the superficial surface of the anterior scalene and is blocked 100% of the time with ISB. Blockade of the phrenic nerve can be undesirable in certain patients with significant pulmonary disease. Similarly, trauma patients with pulmonary injuries or contralateral pneumothorax are poor candidates for ISB. The effect on the phrenic nerve can last, on average, 6 hours. Interestingly, studies that have measured respiratory function in patients undergoing total shoulder repairs found that those who received continuous interscalene catheters versus opioids showed improved respiratory function at 24 and 48 hours postoperatively. The improvement in respiratory function was attributed to better analgesia, resulting in better force diaphragmatic excursion coupled with an absence of respiratory depression often caused by opioids. For patients who require shoulder surgeries but are not candidates for ISB because of pulmonary concerns, it is possible to provide improved analgesia by performing a combined suprascapular and axillary block. Although this technique provides inferior analgesia than ISB for shoulder procedures, it has been shown to be more effective than PCA alone.


The supraclavicular approach to the brachial plexus provides the unique opportunity to provide dense analgesia and anesthesia to most of the upper extremity. Before entering the axilla, almost all of the sensory, motor, and sympathetic innervation of the upper extremity is contained within three neural structures that lie within close proximity to one another. This allows for a rapid, dense block that does not require a high volume of local anesthetic. Kulenkampff described the first supraclavicular approach in 1911, which he reportedly performed on himself. Although his technique offered the ability to provide blockade over a vast majority of the upper extremity, it carried the inherent risk of causing pneumothorax. Kulenkampff’s approach was published in 1928 and was widely used until the first descriptions of the axillary block were published in 1949. The advent of the axillary approach eliminated the risk of pneumothorax, making it a safer choice. Over the past decade, there has been resurgence in the use of supraclavicular blocks mainly because of the use of ultrasound guidance. In experienced hands, the trunks of the brachial plexus can be easily identified as they appear lateral and superior to the subclavian artery ( Fig. 14A-6 ). Direct visualization of the structures and advancing needle allows the block to take place quickly and safely. Although this block confers a high rate of success for procedures involving most of the upper extremity, it may not reliably cover procedures related to the shoulder. As stated previously, patients with pulmonary compromise who would not tolerate phrenic nerve blocks are not candidates for ISBs. As an alternative, supraclavicular blocks have produced moderate success. Studies indicate that the incidence of phrenic nerve blockade with the supraclavicular approach ranges from 0% to 50%. Current literature suggests that the incidence of phrenic nerve blocks is closer to 0% when ultrasound is used; use of nerve stimulator alone results in an incidence closer to 50%. Failure to produce adequate coverage of the shoulder from the supraclavicular approach is due to sparing of the dorsal scapular nerve, which emanates from the root of C5, as well as the supraclavicular nerve arising from the cervical plexus (C3–C4).

Figure 14A-6

The ultrasound probe placed in the supraclavicular fossa allows for quick identification of the brachial plexus. Above both the upper (blue circle) and lower trunks (red circle) of the brachial plexus can be easily identified. In this view, the nerve structures are hypoechoic and appear as a cluster of grapes lying superiorly and laterally to the subclavian artery. This view demonstrates that before entering the axilla, most of the nerve structures of the upper extremity lie within close proximity to each other. This allows for a single-site injection that produces anesthesia and analgesia for most of the upper extremity.

To perform the block, the patient is positioned supine with the head of the bed elevated up to 45 degrees. After sterile preparation and draping of the skin, the patient is given a small amount of sedation for anxiolysis and comfort. The patient’s head is turned slightly away from the side to be blocked, and a linear, low-penetration, high-resolution ultrasound probe is placed with the supraclavicular fossa. The probe is scanned in a coronal and oblique plane to optimize a transverse view of the subclavian artery and neural structures. In this region, the trunks of the brachial plexus will appear as a hypoechoic cluster of grapes lying lateral and posterior to the subclavian artery. A 2-inch echogenic or nerve-stimulating needle is advanced in plane toward the neural structures. The final needle tip position can vary slightly, but it is often advantageous to direct the needle toward the posterolateral aspect of the subclavian artery at about the 7 o’clock position. Positioning the needle at this location allows for more consistent coverage of the lower trunk and ulnar nerve ( Fig. 14A-7 ). To avoid inadvertent puncture of the underlying pleura or subclavian artery, visualization of the needle tip is critical in performing this block.

Figure 14A-7

An ultrasound-guided supraclavicular block using an in-plane technique. With the upper (blue circle) and lower (grey circle) trunks easily identified, the needle is directed toward the 5 o’clock position of the subclavian artery (SA). The initial spread of local anesthetic in this picture can be seen around the lower trunk. As the injection continues, local anesthetic will continue to surround the trunks, allowing for anesthesia and analgesia of most of the upper extremity.


The infraclavicular block disrupts nerve transmission at the level of the cords and divisions of the brachial plexus. Similar to the supraclavicular approach, this approach accesses the brachial plexus at a point where the neural structures are fairly compact. The first descriptions of the infraclavicular block were published by Bazy and colleagues in 1914. The initial technique underwent numerous modifications and was only moderately used up until the 1940s. Similar to the supraclavicular block, a reduction in its popularity most likely stemmed from the increasing popularity of the axillary block. The infraclavicular block was reintroduced by Raj in 1973. and later modified by Whiffler in 1981. Since that time, this block has steadily increased in popularity and use.

The infraclavicular block has been shown to provide effective analgesia and anesthesia for procedures that involve the elbow, wrist, and hand. Additionally, this approach lends itself well to the insertion of indwelling continuous catheters because they can be secured very easily to the chest wall. Positioning of the catheter on the chest wall provides stability, reducing the risk of catheter dislodgement while providing improved comfort to the patient ( Fig. 14A-8 ). Outcome studies of infraclavicular blocks have shown improved postoperative analgesia for patients undergoing wrist and hand procedures. Patients who were randomized to receive general anesthesia with volatile anesthetics, on the other hand, were more likely to have higher pain scores, longer times to ambulation, longer times to discharge, and increased admissions. The use of continuous infraclavicular catheters has been shown to extend the benefits of the block by reducing pain scores while in place, reducing total opioid consumption, and minimizing opioid-related side effects.

Figure 14A-8

A, The infraclavicular approach to the brachial plexus allows for blockade of the brachial plexus at the level of the cords. In this view, the cords appear as small, densely hyperechoic structures lying lateral, posterior, and medial to the axillary artery. The arrow signifies the desired trajectory of the block needle. B, With the needle placed at the 6 o’clock position, the axillary artery injection allows for circumferential spread about the artery. Spread in this distribution allows for blockade of all three cords without further manipulation of the block needle. C, Example of a continuous infraclavicular catheter that has been secured to the chest wall. Catheter placement at this location is less likely to migrate or dislodge than other sites (axillary) and is comfortable for the patient.

To perform the block, the patient is placed in the supine position with the head of the bed slightly elevated. The patient is provided a small amount of IV sedation for anxiolysis and comfort. After sterile prep and drapes are applied, a standard linear high-frequency probe is placed medial to the coracoid process and inferior to the clavicle in a parasagittal orientation. Small adjustments are made with the ultrasound until the view of the axillary vessels and cords of the brachial plexus are optimized. Below the level of the clavicle, the cord structures will appear as small, dense hyperechoic structures that are oriented around the axillary artery. The lateral cord is typically observed superolateral to the artery between the 9 and 12 o’clock positions, and the posterior cord is often identified between the 6 and 9 o’clock positions. The median cord can be harder to visualize but typically resides on the medial aspect of the artery between the 3 and 6 o’clock positions. Using an in-plane technique, a 4-inch echogenic or nerve-stimulating needle is placed inferior to the clavicle and advanced caudally. Individual identification of the cords can be achieved by nerve stimulation with subsequent deposit of local anesthetic at each site. Alternatively, to decrease block time and improve efficiency, the needle may be directed toward the posterior cord. Deposition of the local anesthetic posterior to the artery often results in a U-shaped spread around the artery. This distribution of local anesthetic around the artery confers successful blockade of all three cords.


The axillary approach to the brachial plexus has been the most widely used regional technique since the late 1950s. This has been an attractive approach to the brachial plexus because it is a relatively easy block to perform and has a low side effect profile. The goal of the axillary block is to cover the distal terminal branches of the brachial plexus, which consists of the radial, median, ulnar, and musculocutaneous nerves. Performance of this block produces analgesia and anesthesia for the distal upper extremity but may not be relied on as a sole anesthetic technique when a tourniquet is required. Coverage for cases that involve the use of an upper extremity tourniquet may require additional block supplementation of the intercostobrachial, medial brachial cutaneous, and median antebrachial cutaneous nerves ( Fig. 14A-9 ).

Figure 14A-9

Sensory innervation for the upper extremity.

As with other blocks of the brachial plexus, the axillary block has been shown to be effective in the management of acute pain. Studies have demonstrated a greater than 50% reduction in VAS scores with increased time to requested pain medication, decreased opioid consumption, and decreased opioid-related side effects. As might be expected, benefits are discontinued with the resolution of the block. As a result, continuous indwelling catheters have been advocated. Continuous axillary catheters have been used for outpatient use with varying degrees of success. Because of the catheter’s location in the axilla, it is often difficult to maintain a clean comfortable site. Problems related to infection, failure rate, catheter kinking, and dislodgement have led clinicians to favor other sites for catheter placement (infraclavicular and supraclavicular).

The axillary block is performed with the patient in the supine position. The patient’s arm to be blocked is abducted 90 degrees, externally rotated with the elbow flexed. Although modifications using a nerve stimulating technique exist, the most common approach is a transarterial method. After sterile prep and drape, the axillary artery is palpated in its most proximal location, usually around the axillary crease. A small, thin needle is advanced toward the pulsation under constant aspiration. When bright red blood is freely aspirated, the needle is further advanced just until aspiration ceases. Half of the volume of local anesthetic to be used is injected, allowing for blockade of the radial nerve. The needle is then slowly withdrawn, again under constant aspiration. Withdrawal of the needle continues until aspiration of blood ceases. With the needle now in a medial and superficial location with respect to the artery, the remaining local anesthetic is injected for blockade of the median and ulnar nerves. This approach is fast and easy but often spares the musculocutaneous nerve, which typically leaves the neurovascular sheath at the level of the coracoid process. The musculocutaneous nerve often needs to be blocked separately and is found within the coracobrachialis muscle. More recently, ultrasound guidance has been used to deliver a fast, reliable block without having to pierce vascular structures. A linear, high-resolution ultrasound probe oriented in the transverse plane of the axillary crease allows for visualization of the vascular and neural structures. Using an in-plane approach, an echogenic or nerve-stimulating needle is advanced to each neural structure and bathed in a local anesthetic solution.

Lower Extremity Blocks

For many years, spinal and epidural infusions have been the treatment of choice for acute pain in the lower extremity from surgical procedures or injuries. Although there is no questioning the effectiveness of these techniques, the use of peripheral nerve blocks and indwelling catheters may provide more flexibility. Patients who require anticoagulation or thromboprophylactic medications may not be candidates for neuraxial procedures. Additionally, peripheral nerve blocks are not associated with the side effects commonly reported with neuraxial techniques, such as urinary retention, bilateral motor weakness, nausea and vomiting, pruritus, and respiratory depression. As the field of regional anesthesia continues to evolve, techniques that focus on providing preferential sensory blocks have the potential to radically improve pain management while facilitating early mobilization and rehabilitation. This emerging trend can be seen in the current use of adductor canal blocks, local infiltrations of anesthesia with liposomal bupivacaine, and motor-sparing knee blocks.

Lumbar Plexus Blocks (Psoas Compartment Block)

The innervation of the lower extremity stems from the lumbar and sacral plexuses. The lumbar plexus is formed from the divisions of the L1–L4 nerve roots with variable contribution from T12 and give rise to peripheral nerves that innervate the anterior lower extremity ( Fig. 14A-10 ). After leaving the intervertebral foramina, the roots of L2–L4 give rise to nerves that run within the body of the psoas muscle. The lateral femoral cutaneous and femoral nerves exist within a fascial sleeve that divides the muscle into an anterior two-thirds and posterior third. More than 50% of the time, the obturator is separated from this sheath by a muscular fold. Winnie and colleagues first described the posterior approach to the lumbar plexus in 1974. and since that time, only small modifications have been made. Because of the complexity of the block, most practitioners prefer to perform a neuraxial technique, which is a proven, fast, and reliable way of providing surgical-grade anesthesia. Additionally, because of the depth of the block, as well as the possibility of entering the neuraxial space, this block should not be used as an alternative for neuraxial blocks when the patient is on anticoagulants. When done successfully, the lumbar plexus block provides anesthesia and analgesia to the lateral femoral cutaneous (L3–L4), femoral (L4–L5), and obturator (L5–S1) nerves.

Figure 14A-10

Lower extremity innervation.

Although lumbar plexus blocks can be performed for a variety of procedures involving the lower extremity, it has been shown to be particularly useful for pain related to the hip. Studies comparing lumbar plexus blocks with general anesthesia for hip surgeries have found reductions in pain scores and opioid consumption with lumbar plexus blocks until block resolution. As with other peripheral nerve blocks, the benefits of the block can be extended by the placement of a continuous catheter. When lumbar plexus catheters were compared with epidural catheters for total hip arthroplasties, the results showed that the plexus group demonstrated less motor block, quicker ambulation, and fewer complications. Although data exist showing the benefit of lumbar plexus blocks in patients undergoing invasive knee procedures, it has not been shown to provide benefits beyond what can be achieved with femoral blocks. Given that femoral blocks are fast and easy and present low risks, they are typically favored over lumbar plexus blocks for invasive knee procedures.

To perform the lumbar plexus block, the patient is placed in the lateral decubitus position with the side to be blocked facing upward. A line connecting the iliac crests (Tuffier line) is drawn as well as a line that connects the spinous processes of the lumbar region. The needle insertion point is located 4 cm lateral to the intersection point of the two lines. Alternatively, a line extending from the posterior superior iliac spine (PSIS) can be drawn parallel to the spinous processes. The needle is inserted at the intersection of the line from the PSIS with the Tuffier line. After sterile preparation of the skin and appropriate drape placement, the patient is given light IV sedation for anxiolysis and comfort. A 10-cm nerve-stimulating needle is inserted at an angle that is perpendicular to the skin. The needle is advanced stimulating at a current between 1.0 and 1.5 mA. Needle location is assumed to be in the right location when contraction of the quadriceps muscles occurs. When the appropriate muscle group is stimulated, the amplitude should be slowly decreased to optimize needle location. When stimulation occurs at low amplitudes (<0.4 mA), the practitioner should be concerned about the possibility of dural sleeve or epidural placement. Because this procedure has the risk of epidural or subarachnoid injection, it is suggested to carefully inject the local anesthetic in small aliquots over a 5- to 10-minute period. During the injection phase, the patient should be frequently assessed for epidural or subarachnoid spread.


The femoral nerve block is a fast, easy block that can provide anesthesia and analgesia to the anterior thigh and medial aspect of the lower leg. The femoral nerve arises from the dorsal divisions of the anterior rami of the L2, L3, and L4 nerve roots. As the nerve emerges from the lateral border of the psoas muscle, it enters the thigh posterior to the inguinal ligament, running a course that is lateral and slightly posterior to the femoral artery. It is the nerves’ relation to the femoral artery, just below the inguinal ligament, that makes it relatively easy to locate. As stated previously, this block is so basic yet effective that it is even being used in prehospital settings to provide fast and effective pain management.

The femoral nerve block has been shown to provide reliable, effective analgesia for procedures or injuries of the anterior thigh and knee. When the femoral block is coupled with a sciatic block, excellent anesthesia and analgesia can be provided for invasive knee procedures. Unlike the lumbar plexus block, the femoral block fails to block the obturator nerve. As a result, a variable percentage of the population will report medial thigh pain despite evidence of adequate femoral block. Modifications of the femoral block to achieve a “three-in-one” block have produced inconsistent results. The use of indwelling femoral catheters has been shown to be advantageous in patients undergoing total knee arthroplasties. Compared with patients with IV PCA or epidural infusions, the femoral catheter patients demonstrated reduced postoperative morphine requirements, earlier ambulation, significant reductions in serious complications, and decreased lengths of hospital stay.

To perform the femoral block, the patient is placed in the supine position, and the femoral pulse is palpated in the inguinal crease on the side to be blocked. After sterile preparation of the skin and appropriate placement of drapes, the patient is given a minimal amount of IV sedation to produce anxiolysis and comfort. A 2-inch nerve-stimulating needle is inserted just lateral to the femoral pulsation in a slightly cephalad orientation and advanced to achieve motor stimulation of the quadriceps muscles. The presence of patellar excursion indicates proper placement of the needle. The stimulating current is slowly decreased to optimize needle position. Current output between 0.3 and 0.5 mA that still produces a consistent quadriceps response suggests adequate placement of the needle. After negative aspiration, the local anesthetic is injected in 2- to 3-mL aliquots over several minutes. The use of a linear high-resolution ultrasound probe allows for the direct visualization of the femoral nerve and artery. The ultrasound probe should be placed in line with the femoral crease and scanned in a cephalad direction to optimize the view of the femoral nerve. An echogenic or nerve-stimulating needle is directed toward the femoral nerve utilizing an in-plane technique ( Fig. 14A-11 ). The ultrasound also aids in the speed and efficiency of placing an indwelling catheter by allowing direct visualization of catheter placement next to the nerve ( Fig. 14A-12 ).

Figure 14A-11

A, View of the ultrasound anatomy in the femoral crease. The femoral nerve (FN) appears as a tear-shaped structure lateral to the femoral artery and vein (FV). The fascia lata and iliaca lie superior to the nerve. B, An in-plane approach to the FN allows for direct visualization of the block needle. In this image, local anesthetic (LA) can be seen surrounding the FN. The local anesthetic stays confined to an area below the fascia iliaca and fascia lata. FA, Femoral artery.

Figure 14A-12

Continuous femoral nerve catheter. In this view, a catheter that has been placed appears as bright, hyperechoic structure lying posterior to the femoral nerve (FN). Local anesthetic that has been injected through the catheter can be seen surrounding the nerve. FA, Femoral artery; LA, local anesthetic.

Adductor Canal Block

Although femoral nerve blocks and continuous femoral nerve catheters have been shown to provide benefits and improved outcomes for patients undergoing total knee arthroplasties, a modification of the femoral nerve block is becoming increasingly popular. Blockade of the femoral nerve within the adductor canal allows for blockade at a location where many of the motor branches to the quadriceps muscles have already departed from the nerve. By preserving muscle strength, patients have better stability (less falls) and are able to ambulate earlier. Initial studies compared the level of muscle sparing among patients receiving either the adductor canal blocks or the traditional femoral blocks. These studies demonstrated that adductor canal blocks reduced motor strength by only 8% from baseline as opposed to 49% for femoral nerve blocks. The additional quadriceps strength allowed for better stability and weight-bearing with a lower risk of patient falls. Recent studies comparing their analgesic effects have shown that adductor canal blocks produce a level of analgesia for patients undergoing total knee arthroplasties that is equivalent to femoral blocks.

To perform an adductor block, the patient is placed in the supine position, and the leg to be blocked is flexed at the knee and externally rotated. After the skin is prepared in a sterile fashion and the appropriate drapes are applied, the patient is given light IV sedation. A linear high-resolution ultrasound probe is placed in a transverse orientation on the medial aspect of the midthigh. In this position, the femoral artery and the roof of the canal (the sartorius muscle) can be easily identified. An echogenic 4-inch needle is advanced toward the neurovascular structures using an in-plane technique so that the tip of the needle can be visualized. The femoral nerve can vary in its location about the artery; injection of local anesthetic should be performed so that spread includes both the medial and lateral sides around the artery ( Fig. 14A-13 ). When a catheter is used, it is optimal to thread the catheter around the 12 o’clock position on the artery to achieve perivascular spread with the infusion.

Jun 11, 2019 | Posted by in ORTHOPEDIC | Comments Off on Medical Management of the Orthopaedic Trauma Patient

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