Treatment of Acute Pain in the Orthopedic Patient
Acute pain after orthopedic surgery should be anticipated and its treatment should be a part of every anesthetic plan. Analgesic approaches have changed in recent years in part due to patient expectations, the shift toward ambulatory surgery, and shorter hospital stays. Further, analgesic options have increased with new drugs and modes of delivery. Some of the improvement in management of acute pain is based on a greater understanding of the neural pathways and mechanisms involved in the stages of acute pain. There is also increasing interest in the strategy of preventing pain before it is perceived — “pre-emptive analgesia.” Non-steroidal anti-inflammatory drugs, local anesthetics, adrenergic agents, and novel methods of applying opioids have been added to conventional parenteral analgesics, and thus increasing the options for acute pain control. Using more than one analgesic option (multi-modal analgesia) — ideally with different mechanisms — may achieve improved pain control with decreased side-effects.
Management of acute pain after orthopedic surgery has changed significantly during the last decade. Formerly a task relegated to residents and ward nurses, analgesia is now being managed by increasingly large numbers of Anesthesiologists and members of surgical teams. This change is driven, in part, by increasing expectations from patients who hear from the lay press that excellent control of pain is possible and should be considered in selecting physicians and health care facilities.1 Also there is increasing evidence that acute pain may cause postoperative complications and that excellent analgesia may improve outcome after surgery as measured by a variety of factors.2 Acute pain results in hemodynamic changes, such as hypertension, tachycardia, and increased tissue oxygen demand, which can cause myocardial ischemia. Acute pain can decrease ventilation, prevent effective pulmonary toilet, and predispose the patient to pulmonary complications. Severe acute pain causes metabolic and hormonal changes that inhibit fibrinolysis. This inhibition of fibrinolysis may increase thrombotic complications, such as deep venous thrombosis and pulmonary embolism, which are the leading causes of morbidity after elective reconstructive orthopedic surgery.
The development of devices such as patient controlled analgesia (PCA) pumps have increased options for effectively treating acute pain. The traditional, on-demand parenteral opiate strategy accomplishes analgesia but has some limitations. Severe pain motivates the patient to request analgesia. The lag period that follows between demand and delivery allows the pain to become excruciating. Experienced surgeons recognize that pain is often extreme by the time that treatment is finally administered, so they order larger doses that have a potent analgesic effect. However, as the dose increases, so does the potential for sedation and respiratory depression. These limitations have led to the development of (PCA) for opioid delivery. The risk of respiratory depression with large doses of on-demand opioids has increased use of non-opioid analgesics and regional anesthesia for acute pain control in orthopedic patients. Combinations of these options are also being prescribed, to achieve the optimal analgesia with the lowest side-effect profile. The level of pain control and the incidence of sedation that occurs with traditional, on-demand opiate treatment has been compared to PCA approaches, and the PCA patients have superior analgesia with less variability and less total opioid than demand patients.3 The further observation that patients medicated with parenteral opiates before surgery exhibited less acute postoperative pain led to the question of whether analgesics — given before the establishment of acute pain — decreased postoperative pain. This approach has been called “pre-emptive” and considerable work has been performed to determine the clinical relevance of various pre-emptive analgesia strategies.
It is the purpose of this review to discuss the mechanisms of acute, postoperative pain in orthopedic patients, to discuss strategies for treatment, and explore the potential role for a strategy of pre-emptive analgesia.
Mechanisms of Acute Pain
Acute pain after orthopedic surgery is the result of tissue injury from the procedure. The link between a surgical incision and the pain experienced by the patient is mediated by distinct neural pathways. The surgical intervention activates receptors (nociceptors), which send a signal from the site of surgery via slow conducting A delta and C fibers within peripheral nerves, which are geographically integrated in the dorsal column of the spinal cord, and transmitted rostrally to the brain. The signal is transmitted up the spinal cord in the lateral spinothalamic tracts into the lateral thalamus and is projected geographically onto the sensory cortex. Further modulation is possible at any of the upward transmission sites. An understanding of the anatomy and biochemistry involved in such transmission is essential to the treatment and prevention of acute pain.
Peripheral Receptors and Nerve Transmission
The receptors activated by tissue injury (nociceptors) are the specialized terminal ends of small nerve fibers in the tissue. Although a few nociceptors are highly specialized and respond only to very limited types of stimuli, most are activated by almost any chemical, thermal or mechanical disruption. The A delta and C fibers conduct 5 to 10 times slower compared to those that control motor activity and fine sensory discrimination. However, A delta and C fibers are the most common peripheral nerve fibers, and stimulation causes a nociceptive signal to be conducted centrally.
Tissue injury also causes nociceptors to release a number of chemical mediators, such as bradykinin, serotonin, substance P, and histamine. Substance P increases the sensitivity of peripheral receptors such that the threshold for signal conduction decreases (allodynia); consequently, receptors are more frequently activated. This increased activity is termed hypersensitivity.4 In addition, most of these mediators are potent vasodilators and degranulate mast cells, releasing histamine, which is also a potent vasodilator. This sensitization of peripheral nociceptors is further increased by chemical messengers of tissue injury, which leak from damaged cells, such as potassium, serotonin, histamine, bradykinin, leukotrienes and prostaglandin. The combination of edema, vasodilation and the direct effects of tissue-injury mediators maximally stimulates mechanical receptors. The gradually increasing transmission from peripheral nociceptors, and the accompanying perception of increased pain from decreasing levels of stimulation is termed hyperalgesia.