Sensation of pain can be divided into four steps: transduction, transmission, modulation, and perception. In transduction, the ability of the body to sense noxious stimuli (nociception) depends on the activation of nociceptors (pain receptors). These receptors are divided into thermal, mechanical, and polymodal nociceptors. Thermal receptors are excited by extremes of temperature; mechanical receptors respond to sharp objects that penetrate, squeeze, or pinch; whereas polymodal receptors respond to the destructive mediators of thermal, mechanical, and chemical stimuli such as potassium, serotonin, bradykinin, histamine, prostaglandins, leukotrienes, or substance P. Following transduction, the nociceptor signal is translated into an electrical signal
that allows for transmission of the stimuli via the peripheral nerves. Pain pathways are typically mediated through A delta and C fibers via the dorsal root ganglion and then transmitted through one of three major ascending nociceptive pathways (spinothalamic, spinoreticular, or spinomesencephalic). Modulation of pain (suppression or worsening of a painful stimulus) occurs either peripherally at the receptor, at the level of the spinal cord, or in supraspinal structures (i.e., the brain stem, thalamus, or cortex). Finally, the perception of pain takes place at the level of the thalamus, somatosensory cortex, anterior cingulate gyrus, insula, cerebellum, and frontal cortex. The thalamus and somatosensory cortex are thought to allow for the localization of pain, whereas the anterior cingulate gyrus is involved in the emotional response to the stimulus. The insula, cerebellum, and frontal cortex allow for one to remember and to learn from a painful experience and to develop avoidance behavior.

The clinical definition of acute versus chronic pain is determined in a temporal fashion with an arbitrary timeframe of 3 to 6 months defining the cutoff point between acute and chronic.

Acute pain can be defined as a noxious stimulus caused by injury or abnormal functioning of viscera or musculature. It is usually noted following posttraumatic, postoperative, obstetrical, and acute medical illnesses (i.e., myocardial infarction or nephrolithiasis). It is typically classified as somatic or visceral in nature. Somatic pain is caused by the activation of nociceptors in the skin, subcutaneous tissues, and mucous membranes. This pain is typically well localized and is described as a sharp, throbbing, or burning sensation. Visceral pain arises from injury of the organs and is typically described as dull, distention, achy, and is poorly localized. Acute pain follows the pathways listed above and may resolve within seconds to weeks following resolution of the insult.

Chronic pain can be secondary to lesions of peripheral nerves, the spinal cord, or supraspinal structures. Chronic pain can be complicated by many psychological factors such as attention-seeking behavior, and emotional stresses that can precipitate pain (cluster headaches), and pure psychogenic mechanisms.

The types of acute and chronic pain are subdivided into four categories: nociceptive, inflammatory, neuropathic, and dysfunctional. Nociceptive pain occurs through suprathreshold stimulation of pain receptors and typically serves as a protective mechanism. Typically, no injury or changes to the nervous system are seen in nociceptive pain. This type of pain is typically seen in the acute setting of trauma or following surgery. The pain type works as an adaptive mechanism to allow for protection of the injured body part. Nociceptive pain can be chronic in nature, as is seen in certain pathologic states such as osteoarthritis where destruction of the joint can lead to stimulation of the nociceptors with movement.

Inflammatory pain is secondary to mediators (e.g., bradykinin, serotonin) released by injured tissues and inflammatory cells. These mediators lead to a decreased threshold for the perception of pain secondary to changes in the peripheral and central nervous system.

This pain can be either acute following trauma or surgery or chronic in the setting of cancer or osteoarthritis and as nociceptive pain. Upon the removal of inflammation, the hypersensitivity will typically resolve.

Neuropathic pain is secondary to a lesion of the peripheral or central nervous system.

These pathologic states can include diabetic neuropathy, thalamic strokes, and postherpetic neuralgia. All neuropathic pain syndromes have positive signs and symptoms (e.g., allodynia, hyperalgesia) and negative symptoms (i.e., weakness, sensory loss, and decreased reflexes). As opposed
to inflammatory pain, neuropathic pain will remain long after the resolution of the inciting insult. Dysfunctional pain is a diagnosis of exclusion where no noxious stimuli, inflammation, or pathologic lesion can be elucidated. Common diseases included under this heading include fibromyalgia and irritable bowel syndrome.

Effective postoperative pain management starts with a preoperative assessment and plan, especially in opioid-tolerant patients or patients with preexisting chronic pain. Opioid-induced hyperalgesia and/or opioid tolerance may result in higher doses of opioids and the addition of nonopioid analgesics for adequate pain control. A preoperative assessment prior to surgery may be warranted to allow for an opioid wean prior to surgery to reduce the patient’s tolerance and hyperalgesia. A preoperative assessment may also be utilized to discuss other pain management options including regional and neuraxial analgesia, along with postoperative expectations for pain management with the patient. A thorough evaluation and assessment of the patient’s pain is necessary to elucidate prior chronic pain history, baseline (preoperative) pain scores, prior medication trials, addiction history, aberrant behavior, and worsening pain suggestive of an acute process that may require intervention. Many states now have prescription monitoring programs available to allow clinicians to review patients’ opioid and benzodiazepine prescriptions from other providers to assess for compliance and/or aberrant, drug-seeking behavior.

Laboratory results including renal function (opioid and NSAID use), liver function tests (acetaminophen), urine or blood toxicology (opioids), coagulation studies (neuraxial and regional anesthesia), and white blood cell and platelet counts (neuraxial and regional anesthesia) may be helpful in formulating a plan for the management of postoperative pain. A thorough review of the patient’s medications is necessary prior to regional or neuraxial anesthesia to rule out anticoagulant use.