Chapter 2: Anesthesia and Analgesia

The relief of pain and suffering is one of the most important acts that a physician undertakes. Pain relief following orthopedic injuries should be provided universally and promptly, with rare exception. In addition, throughout this book there are descriptions of fracture and dislocation reductions as well as soft-tissue repairs that will require significant anesthesia in order to perform successfully and compassionately. As such, this chapter serves as a reference for the safe and effective use of pain medications, procedural sedation, local anesthesia, and regional anesthesia used in emergency orthopedics. Finally, the clinical use of heat and cold is reviewed in patients with orthopedic injuries.

The largest study to date of patients with closed fractures of the extremities or clavicle revealed that one-third of these patients did not receive pain medications while in the emergency department (ED).¹ Underuse of analgesics after orthopedic injuries is well documented in the literature.^2–7 Groups at risk for “oligoanesthesia” include pediatric patients,⁴ minority ethnic groups,⁵ and women.⁸ Children younger than 2 years of age seem to be at higher risk than school-age children.⁴

Despite the frequent underuse of analgesics by physicians, there is evidence that practice habits can change. One study documented that physicians prescribed pain medications following orthopedic injuries with a 95% compliance rate when an aggressive educational program was instituted.⁹

Once the decision has been made to give an analgesic agent, the next question is which analgesic to provide. Nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided in patients with healing fractures, as these agents have been shown to diminish bone formation, healing, and remodeling.¹⁰

The evidence for the use of nonsteroidal agents in patients with soft-tissue injuries is not as clear. NSAID use in blunt muscle trauma (especially the quadriceps) will decrease the incidence of heterotopic ossification. The majority of randomized controlled studies have shown a benefit for the use of a NSAID after various sprains and strains, although the positive effect is not universally noted. The use of a NSAID after exercise-induced muscle injury may also be beneficial for short-term recovery of muscle function.¹¹ In general, the use of a NSAID in soft-tissue injury is recommended for its potential to stimulate collagen synthesis and the early phases of skin and ligament repair.¹⁰

Of the opioid analgesics, codeine is the weakest agent and in one study it was no better than a placebo.¹² Other oral narcotic medications include hydromorphone (Dilaudid), hydrocodone (Vicodin, Lorcet), and oxycodone (Percodan, Percocet). Complications include constipation, nausea, and vomiting. Patients should be instructed not to drive while taking these medications, although up to 7% of patients admit to doing just the same, despite warnings.²

Procedural sedation and analgesia (PSA) is something that the physician treating emergent orthopedic injuries will use frequently. It is not without significant complications, especially when it is performed hastily or without understanding the pharmacology of the medications involved. However, there is a substantial body of literature supporting the safe use of PSA by emergency physicians.^13–15

The goal of PSA is to induce a state of tolerance to emergency procedures while preserving airway reflexes. This is usually accomplished by administering a sedative or dissociative agent, as well as an analgesic agent. However, certain fundamental principles must be adhered to well before the first agent is used. Requirements include appropriate personnel, thorough patient assessment and consent, adequate equipment, patient monitoring, and documentation.¹⁶ It is only after these requirements are satisfied that the physician can begin to consider drug administration.

PSA should only be performed by an individual who possesses an understanding of the medications used, an ability to monitor the patient’s response, and the skills necessary to address any airway or cardiovascular complications that may occur. In general, this requires a second clinician, other than the physician performing the procedure.

Patient assessment should begin with a past medical history, including anesthetic history, medications, and allergies. PSA in individuals with an American Society of Anesthesiology Physical Status Class III (severe systemic disease with definite functional limitation) or higher should be avoided. Specific fasting periods before procedural sedation are not supported by the available medical literature and the traditional guideline of 2 hours after clear liquids and 6 hours after solids and other liquids is not always practical in the ED, as often the procedure in question cannot be delayed.^17–19 A prospective, observational study of 1014 children identified no difference in airway complications, emesis, or other adverse events between patients who met and did not meet the fasting guidelines. Moreover, no aspiration events were noted in either group. However, the authors did note that the study was underpowered to fully detect differences in rates of emesis due to the extremely rare nature of such events.²⁰ Therefore, while recent food intake is not a contraindication to administering procedural sedation, it should be considered in targeting the depth of sedation.¹⁶

Necessary equipment includes oxygen, suction, advanced life support equipment, and appropriate reversal agents (when applicable). Intravenous access should be established and the patient should be placed on a monitor with continuous pulse oximetry and capnometry, if available. Supplemental oxygen via a nasal cannula, though controversial in the literature, is generally recommended. A departmentally developed checklist will help ensure compliance and will improve documentation.²¹

There are a numerous options for PSA in the ED, which include midazolam, fentanyl, ketamine, etomidate, propofol, and various combinations of these medications. The ideal agent varies depending upon the clinical circumstances. Whichever agents are used, a key to safe administration involves slow titration of the drug until the desired effect is achieved.^16,22 Rapid administration may lead to a higher rate of complications including hypotension and respiratory depression. A review of the most commonly used agents as well as reversal agents is provided in Table 2–1.

Commonly Used Agents

Midazolam (Versed)

This agent should be dosed in increments of 0.05 mg/kg (up to 1–2 mg increments in adults) every 3 to 5 minutes to get the desired effect. A dose of 0.1 mg/kg will usually produce sedation within 2 to 3 minutes. This agent is the ideal benzodiazepine for procedural sedation due to its amnestic properties, as well as its short duration of action (30–60 minutes). The most important complication from midazolam use is respiratory depression. This effect appears to be augmented in patients receiving concomitant opioids or who have underlying pulmonary disease. Other adverse reactions include hypotension, vomiting, hallucinations, and hiccups. Of note, 1% of children under the age of 5 may experience paradoxical excitation which can be reversed with flumazenil.²³

Fentanyl (Sublimaze)

This agent is the preferred opioid for procedural sedation due to its rapid onset and short duration of action. Peak analgesia is accomplished in 2 to 3 minutes and the duration of action is only 20 to 30 minutes. It is recommended to use incremental doses of 1 μg/kg IV in adults and children, given slowly to a total dose of 2 to 3 μg/kg. Fentanyl is contraindicated in children younger than 6 months because of the risk of severe laryngospasm. In addition to respiratory depression and hypotension, fentanyl is also associated with chest wall rigidity. Rigid chest syndrome appears to occur at very high doses (>15 μg/kg) when the drug is administered rapidly.

Ketamine (Ketalar)

This agent has dissociative properties and is one of the most commonly used anesthetic agents for procedural sedation. Patients who have been administered this drug have blunted sensory perceptions and no memory of the events. Ketamine is advantageous for procedural sedation because it is not associated with a loss of protective airway reflexes and is the only sedative that also has analgesic properties. The recommended dose is 1 to 2 mg/kg intravenously. The onset of action is 1 minute with duration of 45 minutes. Contraindications include age less than 3 months, increased intraocular pressure, cardiovascular disease, or active respiratory infections. Adverse reactions include increased respiratory secretions, emergence reactions, and laryngospasm. Administering atropine or glycopyrrolate at 0.01 mg/kg 10 minutes before giving ketamine can decrease the respiratory secretions. Emergence reactions are hallucinations that occur during the recovery period. They are seen in up to 50% of adults and 10% of children. They are rare in children younger than 10 years. Concurrent administration of midazolam is sometimes given with the hope of decreasing the frequency of emergence reactions, although one randomized controlled trial refuted its effectiveness.²⁴ Laryngospasm is a rare complication of ketamine administration that can often be treated with positive pressure ventilation. Rarely, succinylcholine is required for adequate ventilation if laryngospasm is severe or persists. Post-recovery nausea and vomiting may occur and can generally be treated with antiemetics, such as ondansetron.

Etomidate (Amidate)

This agent is a nonbarbiturate, imidazole hypnotic that has been gaining popularity for procedural sedation in the ED due to its rapid onset (30–60 seconds), short duration, and low side-effect profile. A dose of 0.1 mg/kg is given slowly with additional doses of 0.05 mg/kg given every 3 to 5 minutes until appropriate sedation is achieved. Ninety-five percent of patients obtain full recovery within 30 minutes of administration.²⁵ Side effects include respiratory depression, myoclonus, vomiting, and pain with injection.^25–27 Myoclonus occurs in up to 20% of patients and is usually mild and self-limited, but occasionally may interfere with the procedure.^14,28 Etomidate has not been shown to produce seizure activity when observed by an electroencephalogram.²⁹ Respiratory depression, as represented by an oxygen saturation of <94%, occurs in 3% to 8% of patients.^22,24–27 Adrenocortical dysfunction is transient and the clinical significance of this finding is unclear.³⁰ Some authors recommend caution when using this agent in patients with septic shock, but it is unlikely to be clinically significant in the ED PSA setting.³¹

Methohexital (Brevital)

Methohexital is an ultrashort-acting barbiturate. One of the advantages of methohexital is that it has a rapid onset with maximal sedation in less than 1 minute in most cases. The initial dose is 1 to 1.5 mg/kg followed by repeat doses of 0.5 mg/kg every 3 to 5 minutes as needed for further sedation. Alteration in hemodynamics is unusual, but respiratory depression is not uncommon. In one study of 76 adult patients, methohexital caused apnea in eight patients (10.5%) for an average duration of 64 seconds. Bag-valve mask ventilation was required in these patients, but none needed intubation.³² In another study, 4 of 52 patients (8%) receiving methohexital required bag-valve mask ventilation.³³

Propofol (Diprivan)

Propofol is a nonopioid, nonbarbiturate, sedative-hypnotic agent that can be administered at an initial dose of 0.5 to 1.0 mg/kg. Others prefer to give smaller initial amounts (10–20 mg intravenous push every 30 seconds until adequate sedation is achieved). This avoids overshooting with your initial bolus. Subsequent maintenance dosing can be as a continuous infusion or with 0.25 to 0.5 mg/kg boluses every 3 minutes as needed.³⁴ Propofol is remarkable because it produces a very rapid onset (approximately 45 seconds) of a deep and effective sedation with a short duration (3–5 minutes). When compared with midazolam/fentanyl, both onset and duration are significantly shorter.³⁵ Additional benefits are its potent antiemetic properties and its ability to reduce intracranial pressure. This must be balanced against the propensity of propofol to cause transient decreases in blood pressure, though the significance in otherwise healthy patients is debatable.

The depth of sedation provided by propofol requires extra vigilance in the observation of the patient to detect early complications, respiratory compromise, and hypotension.^35,36 In one study, the rate of oxygen desaturation was 8% and assisted ventilation with bag-valve mask was 4%.³⁶ In the only study to compare propofol with etomidate, rates of bag-valve mask use, airway repositioning, and stimulation to induce breathing were the same.³⁶ Intravenous fluids should be available to administer if the patient becomes hypotensive during the use of propofol.³⁷ Despite these potential problems, multiple studies looking at the use of propofol in the ED have shown it to be safe and cost effective for both adults and children when compared with other agents.^38–45

Propofol is a potent amnestic agent that lacks intrinsic analgesic properties. For this reason, it is frequently used with fentanyl, although a lower dose of ketamine (0.3 mg/kg) appears to reduce the rate of adverse events fivefold.^46,47 Other authors have noted that because patients who receive only propofol without an analgesic generally have no recollection of the procedure and high satisfaction scores that an accompanying analgesic may not be necessary.⁴⁰

Ketofol

Ketofol is a newer procedural agent composed of equal amounts of ketamine and propofol. The initial dose ranges from 0.375 to 0.7 mg/kg each of ketamine and propofol, which can either be given individually or mixed together in the same syringe.^48–51 The concept behind this mixture was to balance the hypotensive, respiratory depressant, and antiemetic components of propofol with the hypertensive, respiratory drive preserving, emetogenic, and analgesic components of ketamine. When compared with ketamine, there were decreased episodes of vomiting, decreased emergence reactions, greater patient satisfaction, and decreased sedation and recovery times.⁴⁸ However, when compared with propofol, there appeared to be little difference in respiratory events or patient satisfaction.⁴⁹ At this time, further studies are needed, but this combination may be utilized more frequently in the future.

Reversal Agents

Naloxone (Narcan)

This agent will reverse the effects of opioids. An intravenous dose of 1 to 2 mg (0.1 mg/kg in children) will reverse respiratory depression in most situations. Onset is rapid, but duration of action is relatively short (20–40 minutes), so resedation may occur if longer-acting opioids were used.

Flumazenil (Romazicon)

This agent will reverse the effects of benzodiazepine administration. The intravenous dose in an adult is 0.2 mg over 15 seconds (0.02 mg/kg in a child) that can be repeated at 1-minute intervals until the desired effect is achieved. In a manner similar to naloxone, resedation may occur if the effects of the benzodiazepine outlast the 20- to 40-minute duration of action of flumazenil. It is recommended to use this agent with caution, as it is known to lower the seizure threshold and can produce refractory seizures in chronic benzodiazepine users.

Postprocedure Monitoring

Monitoring in the postprocedure period is still important, as complications may occur following the removal of noxious stimuli. In children, the risk for adverse events is greatest within the first 10 minutes after the administration of a medication and in the immediate postrecovery phase.⁵² Discharge criteria should include a patient who is conscious and responding appropriately, has normal vital signs, normal respiratory status, and is able to tolerate oral liquids.¹⁶

Local anesthetic agents are used for abscess drainage, acute wounds, and for regional anesthesia. The advantages of using local anesthesia are that it is often quicker, safer, and provides better hemostasis (via direct distension of tissue and concurrent use of epinephrine) than regional or general anesthesia. The disadvantages include the relatively larger amount of anesthetic required and the potential tissue distortion.

These agents are classified as esters or amides on the basis of their intermediate chain. Lidocaine, mepivacaine, and bupivacaine are amide anesthetics, whereas procaine is the prototypical ester local anesthetic agent. Their mechanism of action is based on blockage of sodium channels, thus inhibiting nerve cell depolarization. Longer-acting agents bind to sodium channels for prolonged periods of time. The addition of epinephrine increases the duration of action by causing vasoconstriction and a subsequent decrease in the absorption of the agent into the systemic circulation. To reduce the pain associated with anesthetic infiltration, it has been recommended to buffer the solution with 8.4% sodium bicarbonate, warm the solution to room temperature, inject slowly with a small-gauge needle, and infiltrate through wound edges.⁵³

Contraindications to the use of a local anesthetic include an allergy to the agent. A true IgE-mediated allergy to a local anesthetic is rare and it is important to realize that there is no cross-reactivity between esters and amides, though the reaction may be due to a preservative in the vial. In such cases, avoid using multi-dose vials. In patients with a history of an allergic reaction to an unknown local anesthetic, 1% diphenhydramine solution can be used as a substitute agent. To create this, dilute 1 mL of the standard 5% parenteral solution into 4 mL of normal saline.

It is important to avoid systemic toxicity by being aware of maximal recommended doses of local anesthetic agents. Maximum doses as well as other properties of the most commonly used local anesthetic agents are listed in Table 2–2. It is important to remember when calculating the maximum dose that 1% lidocaine contains 10 mg/mL and 2% lidocaine contains 20 mg/mL. Therefore, in a 100 kg individual, for example, the maximum dose of 1% lidocaine without epinephrine is 450 mg or 45 mL.

Regional anesthesia offers many advantages over procedural sedation for fracture and dislocation reduction. In general, a successful block will provide complete anesthesia within the desired nerve distribution without the potential complications of procedural sedation. In addition, regional anesthesia does not require a prolonged postprocedural observation period following reduction, thus shortening ED length of stays and decreasing the requirement for nursing care.

The supplies needed for regional anesthesia include a local anesthetic agent, a syringe, a 25- or 27-gauge needle, an alcohol swab, a sterile drape, and a healthy knowledge of anatomy. Ultrasound is currently used for a variety of applications, including nerve blocks, and will be briefly discussed below where applicable. Please refer to an ultrasound textbook for further discussion of ultrasound-guided nerve blocks.

Epinephrine can be added to the local anesthetic for most blocks to increase their duration of action. Epinephrine injection is classically avoided in the hand and digit due to the potential fear of digital ischemia, although the concentrations used with local anesthetic agents are low and unlikely to cause ischemia. In fact, no long-term complications or necrosis have been reported after injection of as much as 0.3 mg of epinephrine into a digit. Obvious contraindications to regional anesthesia include a bleeding disorder or the need to traverse infected tissue. Nerve function should be properly tested and documented before and after the procedure.

Anatomic landmarks should be identified and sterile procedure should be maintained. The needle is inserted with care to watch for the presence of paresthesias. If paresthesias are noted, the tip of the needle is likely within the fibrous outer sheath of the nerve. Injection at this point may result in permanent nerve damage and therefore the needle should be withdrawn until paresthesias dissipate. Then, the anesthetic can be injected. Depending on the agent used and the accuracy of the injection, anesthesia will be complete within 10 to 15 minutes. The closer the needle is to the nerve, the faster the onset of anesthesia. When in doubt about the proximity of the needle to the nerve, err on the side of injecting more anesthetic. A comprehensive discussion of regional anesthesia is beyond the scope of this text; however, the most commonly used extremity blocks are described subsequently.

Digital Blocks

Ring and Half-Ring Blocks

These are commonly used blocks to provide anesthesia to fingers or toes. The digits possess two dorsal and two palmar nerves that run along the phalanges in the 2, 4, 8, and 10 o’clock positions. The ring block is successfully performed by blocking these nerves in a circumferential pattern around the base of the digit. The half-ring block is an alternative method with similar success in which anesthetic is injected on either side of the base of the digit. To perform the half-ring block, insert the needle through the dorsal aspect of the hand into the web space just lateral to the corresponding MCP joint. One milliliter of anesthetic is injected in the subdermal area. The needle is advanced until it reaches an equivalent depth on the volar side and another 1 mL is injected. This is then repeated on the medial side (Fig. 2–1 and Video 2–1). For blocking the great toe, a circumferential ring of anesthetic is recommended due to the greater distance between the nerves.

Metacarpal Block

Alternatively, the digit can be anesthetized by blocking the common digital nerves before they divide to innervate the digits. With this block, the needle is inserted on the dorsal aspect of the hand in the web space between the digits. The needle is directed toward the metacarpal heads and the palm of the hand (Video 2–2). For this block to be successful, anesthetic agent should be injected all the way to the palmar aspect of the hand to anesthetize the palmar branches of the nerve. Swelling should be noted on the palm between the metacarpal heads after infiltration. The opposite side of the metacarpal should be injected to anesthetize the entire digit. This method, although favored by some, has some disadvantages. In one study, the digital half-ring block outperformed the metacarpal block in terms of pain scores, failure rate, and time to complete the procedure.⁵⁴

Transthecal Block

An advantage of the transthecal block is that it requires only one injection at a site that avoids proximity to the neurovascular bundle of the digit.⁵⁵ Anesthetic is injected directly into the flexor tendon sheath. In the initial description, the anesthetic was injected into the distal palmar crease of the hand.⁵⁶ This technique was shown to be similar to the digital half-ring block in both pain score and time to anesthesia.⁵⁷ A simpler, but equally efficacious, modified approach has been described that uses the center of the proximal digital crease on the volar surface of the digit as the site of needle insertion (Fig. 2–2).⁵⁸ A 25-gauge needle is inserted to the bone and then withdrawn slowly while applying pressure to the syringe plunger (Video 2–3). The resistance to anesthetic flow decreases when the needle tip is resting within the tendon sheath. At this point, approximately 2 mL of anesthetic agent is injected while proximal pressure is applied to the volar surface to aid distal diffusion.

Wrist Block

The wrist block provides anesthesia to the entire hand and is useful for many soft-tissue procedures and reductions of the bones in the hand. Proper technique requires the deposition of local anesthetic to block the radial, median, and ulnar nerves at the wrist.

Radial Nerve

The radial nerve is blocked at the wrist using two injections. The initial injection is made at the proximal wrist crease just lateral to the radial artery. Three milliliters of anesthetic are injected at a depth of approximately 0.5 cm. Because dorsal branches of the radial nerve arise more proximally, a second injection is required. A superficial skin wheal is created on the dorsum of the hand extending from the lateral aspect of the wrist at the dorsal wrist crease to the base of the fourth metacarpal bone. An additional 5 mL of local anesthetic is injected here (Fig. 2–3 and Video 2–4).⁵⁹

Median Nerve

The median nerve is located directly below or slightly lateral to the palmaris longus tendon. The palmaris longus tendon is absent in 10% to 20% of individuals, but if present, can be palpated by having the patient flex the wrist against resistance. To block this nerve, insert the needle perpendicular to the skin and along the radial border of the palmaris longus tendon (or 1 cm medial to the flexor carpi radialis tendon if this is not present) to a depth of 1 cm. A “pop” should be felt when the needle penetrates the flexor retinaculum and the presence of paresthesias signifies that the nerve is located. Withdraw slightly and inject 3 to 5 mL of local anesthetic. If no paresthesias are elicited, redirect slightly in an ulnar direction and inject the full 5 mL (Fig. 2–4 and Video 2–5).⁵⁹

Ulnar Nerve

The ulnar nerve is located between the flexor carpi ulnaris and the ulnar artery in the volar aspect of the wrist. It can be blocked by injecting 3 to 5 mL of local anesthetic agent just lateral to the flexor carpi ulnaris tendon, while remaining medial to the ulnar artery. This block is performed 2 cm proximal to the wrist crease in order to block the dorsal branch before its takeoff. A depth of 0.5 cm is sufficient for the ulnar nerve block (Fig. 2–5 and Video 2–6).⁵⁹

Femoral Nerve Block

This block is useful for relieving pain due to femoral neck fractures, intertrochanteric femur fractures, and femoral shaft fractures.^60–62 The femoral nerve also supplies innervation to the anterior and medial aspect of the thigh and leg. The femoral nerve is located just lateral to the femoral artery and can be blocked using either the landmark or ultrasound-guided approach.

Using the landmark-based approach, locate the femoral artery and insert the needle approximately 1 to 1.5 cm lateral to the artery and 1 to 2 cm distal to the inguinal crease at a 45-degree angle to a depth of about 3 to 4 cm. Two distinct “pops” should be felt as the needle crosses the fascia lata and fascia iliaca. This block usually requires 15 to 25 mL of local anesthetic.

The ultrasound-guided approach is an increasingly popular alternative, wherein a 6 to 18 MHz linear probe is placed in the inguinal crease and slid transversely until the vessels and nerve are located. The needle is inserted in-plane from the lateral aspect of the probe and advanced until the fascia lata and fascia iliaca are punctured. Small, 1 mL boluses are injected to surround the nerve, confirming proper placement under ultrasound visualization. As noted above, a total of 15 to 25 mL of anesthetic is usually required.

Ankle Block

The ankle block is the most challenging of the regional blocks. To provide complete anesthesia to the foot, a total of five nerves must be blocked—the saphenous nerve, the sural nerve, the posterior tibial nerve, the superficial peroneal nerve, and the deep peroneal nerve. To anesthetize the sole of the foot only, the posterior tibial nerve and sural nerve must be blocked. The patient should be positioned prone on the stretcher with the foot dangling off the edge. All of these blocks are performed at a level just superior to the malleoli.

Saphenous Nerve

The saphenous nerve is blocked at the anterior border of the medial malleolus just posterior to the greater saphenous vein. The needle is inserted approximately 1 to 2 cm above the superior aspect of the medial malleolus and 3 to 5 mL of anesthetic solution is injected.

Sural Nerve

The sural nerve is blocked by raising a wheal using 3 to 5 mL of local anesthetic from the lateral border of the Achilles tendon to the fibula at the level of the superior malleoli. Anesthetizing this nerve and the posterior tibial nerve will provide anesthesia to the plantar aspect of the foot (Fig. 2–6 and Video 2–7).

Posterior Tibial Nerve

The posterior tibial nerve is located on the posteromedial ankle between the medial malleolus and the Achilles tendon. Palpate the posterior tibial artery and insert the needle 0.5 to 1 cm posterolateral to a depth of 0.5 to 1 cm. Paresthesias should be elicited during this block. At that time, withdraw the needle approximately 1 mm and inject 3 to 5 mL of anesthetic solution (Fig. 2–7 and Video 2–8).

Superficial Peroneal Nerve

The superficial peroneal nerve is blocked 1 to 2 cm above the malleoli by raising a wheal using 6 to 10 mL of anesthetic from the anterior edge of the tibia to the anterior edge of the fibula. This nerve provides sensory innervation to the dorsum of the foot and toes.

Deep Peroneal Nerve

The deep peroneal nerve is located on the anterior and dorsal aspect of the foot, just deep to the extensor hallucis longus tendon. After anesthetizing the superficial peroneal nerve, insert the needle just medial to the extensor hallucis longus 30 degrees laterally until the tibia is encountered. Withdraw 1 mm and inject 1 mL of anesthetic. This nerve provides sensory innervation to the web space between the first and second toe.

This technique is frequently employed for anesthesia during reduction of distal radius (Colles’) fractures, but the principles apply to any type of fracture. The infiltration of local anesthetic agent within a fracture serves to block the nerve fibers of the surrounding soft tissues and periosteum (Fig. 2–8). To perform this procedure, a large bore needle is used to withdraw blood from the fracture and replace it with local anesthetic agent. For a distal radius fracture, a total of 10 to 15 mL of 1% lidocaine is injected directly into the fracture site (Video 2–9). Following the injection, place an elastic bandage around the wrist and allow 10 minutes for proper anesthesia.⁶³ Multiple studies have shown that hematoma blocks result in decreased pain scores when compared with procedural sedation.^64,65 Of note, this technique is only effective during the acute management, when the hematoma has not yet become coagulated.

There are identifiable and measurable physiologic effects produced by heat and cold that are therapeutically desirable. Although both heat and cold are known to reduce muscle spasm and decrease the pain associated with injuries, the mechanisms and indications for each are different.⁶⁶

Superficial application of heat relieves pain through three primary mechanisms. Heat-induced vasodilation increases blood flow, thereby “washing out” the inflammatory cytokines. In addition, heat will relax muscle fibers, thereby relieving muscle spasm. Finally, heat decreases synovial fluid viscosity, which allows for better joint mobility. However, because of the aforementioned vasodilation, heat can also increase initial bleeding and edema in acute injuries. Therefore, heat is predominately used for subacute and chronic injuries.⁶⁷

Cold therapy will decrease the metabolic rate, as well as slow nerve conduction, with a combined effect of decreasing the amount of pain experienced. Moreover, cold therapy will decrease blood flow, thereby decreasing bleeding and edema after acute injuries. This is further supplemented with the use of compression and elevation—hence, the popular RICE (Rest, Ice, Compression, Elevation) therapy commonly recommended after acute orthopedic injuries. Some studies have also shown that cold can decrease muscle spasm, though the mechanism of this is unclear. Consequently, cold therapy may be used for acute, subacute, and chronic injuries.^67,68 In general, during the acute phase after injury, pain relief is best obtained with cold.⁶⁶ Despite this almost universal recommendation, there is little evidence-based medicine beyond observational studies and animal studies to support the use of cold. Even less evidence exists regarding the ideal duration of treatment, frequency, and mode of application.^69–71

Nonetheless, enough of a consensus exists to allow for some recommendations. The goal of therapy is a reduction in tissue temperature of 10 to 15°C while avoiding injury to the superficial layers and skin. This is best performed by using melting iced water applied through a wet towel for a period of 10 to 15 minutes.^69,71 Longer application is appropriate in areas with more subcutaneous fat (20–30 minutes if >2 cm of fat). Using repeated, rather than continuous applications will help sustain reduced muscle temperatures without causing cold-induced tissue injury to the superficial layers (Fig. 2–9). Treatment should continue every 1 to 2 hours initially and continue for a period of 48 to 72 hours.

In the subacute stage, mild superficial heat with hot packs is preferable, though ice may also be used.⁶⁷ As with cold therapy, heat should be applied intermittently for 10 to 30 minutes with care to avoid skin injury, although there is very limited literature to support this. The combined application of heat and passive range of motion may significantly improve the range of motion of patients with hip and shoulder problems.

Of note, neither cold nor heat should be used in combination with topical methyl salicylate/menthol (Bengay^® or Icy Hot^®) or other related products. Topical anesthesia to the skin and superficial layers will blunt the ability of the patient to sense any damaging effects of temperature change (hot or cold) and may produce burns (Fig. 2–10).