Control of acute pain in oral and maxillofacial surgery is important for patient care and comfort. Oral surgical procedures are associated with tissue injury and inflammation. Acute pain can arise directly from a surgical procedure or from problems such as dental caries, infection, perforation of maxillary sinus, pericoronitis, and jaw fractures. The major factor in acute pain management is deciding on an appropriate intervention and/or analgesics that will provide the best pain relief. Multimodal pain control has taken a leading role in effectively managing acute pain. This article covers the different options available to dental clinicians.
Notably, current public attention and perception have been directed to the widespread misuse and abuse of opioid medications. Dentists were found to be the most common prescriber of opioid analgesics to patients between 10 and 19 years old for postoperative pain management.
Acute pain is a physiologic response to insult or injury. The pain may be secondary to surgical intervention or part of an infectious or pathologic process. Acute pain stimulation can be divided into 2 main mechanisms: peripheral and central stimulatory responses.
The concept of multimodal or balanced analgesia in acute pain management recommends that combined analgesic regimens are much more effective in achieving postoperative pain control and avoiding untoward side effects. The method takes advantage of synergistic and additive effects of medications at a lower dose.
Pharmacologic treatment modalities of pain control include acetaminophen, ibuprofen, anticonvulsants, opioids, gamma-aminobutyric acid agonists, and local anesthetics. Nonpharmacologic pain control includes application of ice, which is effective by reducing local inflammation.
Acute pain is usually associated with tissue injury, inflammation, a surgical procedure, trauma, or a short-term disease process. In oral and maxillofacial surgery, acute pain can arise directly from a surgical procedure or from problems such as dental caries, infection, perforation of maxillary sinus, pericoronitis, and jaw fractures. Acute pain is of short duration and gradually improves as the injured tissues heal. Acute pain is always present following any surgical procedure.
The major factor in acute pain management is deciding on an appropriate intervention and/or analgesic that will provide the best pain relief to the patient. Although this article addresses acute pain management in general terms, it must be clear that treatment that is effective for one acute pain condition and patient may not be effective in others and the surgeon should therefore be disease and patient specific. In oral and maxillofacial surgery, acute pain often requires a procedure to relieve the pain (eg, treating of dry socket) in addition to pharmaceutical management. In this article, postoperative pain is presented as the exemplar for acute pain management. Postoperative pain should be addressed as soon as possible after the procedure.
Providing appropriate postoperative pain control can have significant impacts on both the patient and the surgeon. Patient perception and tolerance can differ dramatically from patient to patient. Titrating the appropriate analgesic requirement requires careful consideration of the invasive nature of the procedure and the expected patient response and tolerance of pain. Patient response and experience of pain are often subjective, making assessment difficult. In addition to past experiences, other patient factors that may also play a crucial role in the acute pain management include age, sex, race/ethnicity, and the severity of the pain.
Providing appropriate analgesia requires a depth of experience and knowledge of pain management. Providing the patient with the appropriate level of analgesia following a surgical procedure can have dramatic effects on the provider-patient relationship. The patient’s quality of life can be heavily affected, including psychological effects. Uncontrolled postoperative pain has been documented to lead to the development of depression. There is evidence in the literature to show that mismanagement of acute pain may even lead to central sensitization and the development of chronic pain. , A variety of analgesic options are available to clinicians when considering pain control. It is important to have a depth of understanding with regard to analgesic properties, adverse effects, duration of action, and pharmacology to appropriately control and provide appropriate postoperative acute pain relief. This article presents options for acute pain control and provides guidance and strategies for acute postoperative pain control.
Importance and significance
Appropriate use of analgesic is important in the postoperative care of patients after oral and maxillofacial surgery. Pain can have detrimental effects on the quality of life and postoperative experience of patients. Current standards of practice often involve acute pain management with the use of nonsteroidal antiinflammatory medications used in combination with acetaminophen.
All postsurgical pain is associated with inflammation, and to a great extent the control of acute pain is the control of inflammation. For this reason, nonsteroidal antiinflammatory drugs (NSAIDs) are the first-line analgesics for the control of postoperative dental pain. Opioids are never the first choice for management of acute postsurgical pain in dentistry. Acute pain normally resolves as healing from the surgical procedure occurs and can be managed without the use of opioids. In 2019, the Centers for Disease Control and Prevention (CDC) published a guideline for the use of opioids and advised against the use of opioids for acute pain (available at www.cdc.gov/acute-pain/postsurgical-pain/index.html and www.cdc.gov/drugoverdose/pdf/patients/Opioids-for-Acute-Pain-a.pdf ). ,
Notably, current public attention and perception have been directed to the widespread misuse and abuse of opioid medications. Controlled substance prescriptions have nearly doubled in the time period between 1994 and 2007. Opioids are associated with high rates of abuse. In a study conducted by Volkow and colleagues, the investigators analyzed the prescription practices of health care professionals in the United States. The investigators reviewed data acquired through the national database and focused the study primarily on the youth population. There were 201.9 million prescriptions for opioid analgesics in 2009, with 79.5 million to adolescents (39%). Most prescriptions were for products containing hydrocodone and oxycodone. Of the 201 million prescriptions, 11% (9.3 million) were for patients aged 10 to 29 years. Dentists were found to be the most common prescribers of opioid analgesics to patients between the ages of 10 and 19 years for postoperative pain management. In 2015, the Department of Health and Human Services reported that 12.5 million people misused opioid prescription medication. Two million of those people were in the diagnostic category of prescription opioid use disorder, defined as a condition where psychotropic medications are used without a prescription for a use other than as directed by a physician or more often/longer than normally prescribed. , In addition, dentists were found to be the most likely source of unused prescriptions among high school seniors for nonmedical purposes obtained from previous medications (27% of prescriptions).
Biology of acute pain
Acute pain is a physiologic response to insult or injury. The pain may be secondary to surgical intervention or part of an infectious or pathologic process. Acute pain stimulation can be divided into 2 main mechanisms: peripheral and central stimulatory responses. Sensory information is transmitted to the brain using a complex network of neurons within the spinothalamic tract ( Figs. 1 and 2 ). , Understanding the chemical mediators and neurophysiologic pathways allows clinicians to have a better understanding and administer targeted therapies to control pain.
Acute insult (eg, surgery or trauma) results in the activation of neurons commonly referred to as nociceptors. These afferent neurons, which project from the tissues to the central nervous system tissues, include but are not limited to skin, muscle, joints, and viscera (see Fig. 1 ). These nociceptors have direct contact with the central nervous system and their cell bodies located in the dorsal rood ganglion. , Also termed the first-order or primary afferent neuron, these neurons are divided into 3 classes based on their diameter and myelination. The 3 peripheral somatosensory classes are termed Aβ, Aδ, and C fibers ( Table 1 ). The A class fibers Aβ and Aδ are rapidly conducting fibers with large diameter and are myelinated. The Aβ is a large myelinated fiber that is primarily responsible for touch but has modulatory effects on the function of the remaining Aδ and C fibers. The Aδ fibers, which are smaller and slower conducting, are responsible for pain stimulation along with the unmyelinated C fibers. Sharp sensation and pain perception are transmitted by Aδ fibers. The unmyelinated C fibers are thought to be the major players in pain perception and respond in a multimodal fashion. The nerve class responds to noxious mechanical, thermal, and chemical stimuli.
|Classification||Diameter (μm)||Myelin||Conduction Velocity (m/s)||Sensory Function|
|Aβ||Large (6–12 )||Yes||>35||Touch|
|Aδ||Medium (1–5)||Thin||5–35||Fast pain|
|C||Small (0.2–1.5)||No||<2.0||Slow pain|
Insult and injury result in nociception through the release of inflammatory mediators. Excitatory neurotransmitters transfer information from the peripheral nervous system to the central nervous system through the actions of glutamate, an inflammatory neurotransmitter. Local modulation is achieved by the actions of chemical mediators, which include bradykinin (peptides), nerve growth factor (neurotrophins), and prostaglandins (lipids). The combined actions of local modulation sensitizes peripheral nociceptors by lowering their activation thresholds. The action of local nociception is further compounded by the release of neurotransmitter substance P. Substance P contributes to local injury via vasodilation, which results in leakage of proteins and fluids into the extracellular space. The combined action of the multimodal stimulants makes up the bases for nociceptive transmission of pain and activation of the peripheral nervous system. Of particular importance in acute pain control is the release of arachidonic acid metabolites. Prostaglandin, which is a metabolite of arachidonic acid produced by the cyclooxygenase (COX) enzyme, acts to block potassium efflux from nociceptors and lowers the activation threshold. Prostaglandin synthesis depends on the activities of COX-1 and COX-2. COX-1 has a primary activity in the peripheral tissues, whereas COX-2 acts within the gut and promotes mucus production. Prostaglandin additionally reserves the ability to modulate vasodilation of peripheral tissues as well as viscera such as the glomerular apparatus of the kidney. This action further contributes to local inflammation and pain. Another important player in nerve sensitization is histamine. Histamine is released through stimulation of mast cells. Similarly to prostaglandin, histamine has stimulatory effects on nociceptors that cause pain with additional effects on vasodilation and local lymphocyte stimulation. Multimodal analgesic strategies target these local inflammatory mediators to modulate pain.
Stimulation and afferent sensory input are transferred from the peripheral to the central nervous system and ultimately to the somatosensory cortex. Transfer of neurosensory signals from the periphery to the central nervous system involves the synapsis and transfer of information from the first-order neurons to the second-order neurons within the spinal cord or brain stem. Activation of the secondary somatosensory neurons is completed via the release of neurochemical agents such as glutamate, vasoactive peptide, somatostatin, calcitonin gene–related peptide, and substance P. Activated second-order neurons project to the somatosensory cortex via the thalamus and the brain stem using third-order neurons. The information is transferred up the spinal cord via the contralateral and ipsilateral spinothalamic tracts. Of these sensory highways, the anterior spinothalamic tract carries sensory information of pain, temperature, and touch (see Fig. 1 ).
Pain from the maxillofacial region is transmitted to the central nervous system by the trigeminal nerve. The trigeminal nerve system is a complex arrangement of nerve transmission fibers and its transmission pathway is slightly different from what was described earlier. Sensory information from the dental and maxillofacial regions first travels to the subnucleus caudalis within the spinal trigeminal nuclear complex. The subnucleus caudalis is located in the medulla, and is the principal brain relay site of nociceptive information arising from the orofacial region. The subnucleus caudalis exhibits considerable similarity with the spinal dorsal horn and thus it is termed the medullary dorsal horn (MDH). Its similar laminar organization to the spinal dorsal horn is what has led to this alternative name. However, despite apparent homology in nociceptive processing, features of trigeminal pain processing in the MDH are distinctly different from that of the spinal dorsal horn. The continuity of the spinal dorsal horn and MDH is collectively termed the trigeminocervical complex. Following injury and noxious stimulation of the dental and maxillofacial region, there is increased excitability and sensitization of trigeminal pain pathways in nonlaminar regions of the spinal trigeminal nuclear complex. The spinal trigeminal nucleus projects to the ventral posteromedial (VPM) nucleus in the contralateral thalamus via the ventral trigeminal tract. This sensory information is relayed from the thalamus to the primary motor cortex via the primary sensory cortex, allowing response to stimuli of the face. Both incoming nociceptive signals to the subnucleus caudalis and projecting nociceptive signals on their way to the thalamus can be modified (modulated) by descending nerve fibers from higher levels of the central nervous system or by drugs.
Psychological effects of pain
Mental distress and anxiety has a significant impact on the outcome of patient pain perception and experience in operative and postoperative pain control. Psychological preparation before surgery can help reduce acute postoperative pain by a variety of mechanisms. Negative emotions, cognitive preparation, behavior, and stress have been found to have a significant impact on postoperative pain experience. , Negative emotions compound postoperative pain by enhancing pain sensations. Cognitive emotions influence behavior when experiencing acute pain by affecting medication dosing and compliance with postoperative instructions.
In a prospective observational study conducted by Maple and colleagues, patients undergoing a hand-assisted laparoscopic donor nephrectomy were asked to complete a perceived stress scale survey before surgery. The study used a high-resolution ultrasonography scan of surgical wounds on the first 3 postoperative days and once following discharge. The wound size and median intensity, which is a marker of tissue fluid that is edema, were measured. Improved median intensity reflected faster wound healing and resolution of tissue edema. The study found that increased emotional stability was associated with faster wound healing. Fifty-eight patients were involved in the study. The investigators concluded that stress had a negative impact on wound healing and that optimism and emotional stability had a positive impact on postoperative outcomes. In 1993, Johnston and Vögele conducted a meta-analysis investigating the benefits of psychological preparation before surgery. The study concluded that psychological preparation was beneficial in reducing use of pain medication, length of hospital stay, behavior recovery, and clinical recovery, and improving patient satisfaction. , A Cochrane Review conducted by Powell and colleagues examined the benefits of psychological preparation before surgery. The investigators highlight the following preoperative interventions as beneficial in reducing postoperative pain: procedural information, sensory information, behavioral instruction, cognitive intervention, relaxation techniques, hypnosis, and emotion-focused interventions. The anxiety of having to see the dentist and the fear of dentistry can activate the pituitary-adrenal axis, leading to an increased experience of pain.
The management of acute pain in the average oral surgical patient is not often affected by central neurophysiologic plasticity from chronic pain but it is important for dentists to screen patients for chronic pain elsewhere in the body; for example, arthritis, back pain, and migraine. Patients with chronic pain problems who have developed central neurophysiologic plasticity do not respond to the treatment of acute pain as would pain-free patients, and they may require adjustments to routine analgesics.
In 1993, Kehlet and Dahl published an article that introduced the concept of multimodal or balanced analgesia in acute pain management. The investigators argued that appropriate pain control cannot be achieved by a single drug or method without significant side effects. The investigators recommended that combined analgesic regimens are much more effective in achieving postoperative pain control and avoiding untoward side effects. The method takes advantage of synergistic and additive effects of medications at a lower doses. This approach offsets side effect profiles. Multimodal analgesic takes advantage of targeting therapy at the peripheral nervous system and central nervous system ( Fig. 3 ).