Perioperative Acute and Chronic Pain Management


Fiber class

Diameter (μm)

Myelin

Conduction velocity (m/s)

Innervation

Function

A alpha

12–20

+++

75–120

Afferent to skeletal muscle

Motor and reflexes

A beta

5–12

+++

30–75

Afferent from cutaneous mechanoreceptors

Vibration, light touch and pressure

A gamma

3–6

++

12–35

Efferent to muscle spindles

Muscle tone

A delta

1–5

++

5–30

Afferent pain and thermoreceptors

“Fast”, sharp, intense, lancinating pain, touch and temperature

B

<3

+

3–15

Preganglionic sympathetic efferent

Autonomic function

C

0.2–1.5


0.4–2.0

Afferent pain and thermoreceptors

“Slow”, dull, burning, achy pain, touch, pressure, temperature, postganglionic autonomic



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Figure 27.1
Gross anatomy of pain pathways (From Sorkin et al. [5]. Used with permission)


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, while 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.



General Pain Definitions


When discussing acute and chronic pain, it is important to have a basic battery of definitions to express the type and description of pain a patient is experiencing.


Acute Versus Chronic Pain


The clinical definition of acute versus chronic pain is determined in a temporal fashion with an arbitrary timeframe of 3–6 months defining the cutoff point between acute versus 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 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 will 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 (Table 27.2). 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.


Table 27.2
General pain types















Nociceptive pain

Normal, acute pain perception evoked by short-lasting noxious stimuli in intact tissue, in the absence of peripheral or central sensitization

Inflammatory pain

Pain following tissue injury but with no neural injury

Neuropathic pain

Pathophysiologic state of pain after neural injury resulting in peripheral and central reorganization

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, hyperalagesia) 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.


Treatment of Pain



Acute Pain


Pain is often treated utilizing a multimodal approach, meaning multiple treatment methods may be combined to provide analgesia, with the hope of decreasing pain and opioid usage. The treatment of acute pain can often begin prior to the initial surgical insult. In the preoperative period, preemptive analgesia is often utilized to decrease or stop nociceptive input. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as celecoxib (PO), ketorolac (IV), and ibuprofen (PO) or acetaminophen can be used preoperatively in combination with other medications such as gabapentin to prevent central sensitization. The main advantage of celecoxib and other cyclooxygenase-2 (COX-2) inhibitors over other NSAIDs include the decreased risk of gastrointestinal bleeding, but other adverse events such as myocardial infarction, stroke, allergic reaction to sulfa, and renal issues may be seen with the use of COX-2 inhibitors.

Preemptive analgesia can also be obtained through neuraxial and regional techniques, such as peripheral nerve blocks of the femoral nerve, and brachial plexus. In those patients with moderate to severe pain, opioid analgesics such as hydromorphone or morphine may be used in combination with acetaminophen or NSAIDs for analgesia. Surgeons may aid in providing pain relief through infiltration of local anesthetics such as lidocaine or bupivacaine at the surgical site (Table 27.3).


Table 27.3
Abnormal pain descriptor definitions


















Allodynia

The perception of pain by a stimulus that is not normally painful

Hyperalgesia

The enhanced perception of pain by a normally painful stimulus

Dysesthesia

Abnormal sensations experienced in the absence of stimulation

Paresthesia

An abnormal sensation (e.g. burning, pricking, tickling, or tingling)

In those patients not able to take oral medications postoperatively, patient controlled analgesia (PCA) devices allow patients to deliver pain medication through the pressing of a button which allows the medication to be delivered via an intravenous route or an epidural catheter. These devices typically allow patients to deliver a predetermined amount of pain medicine at specific time intervals. There is a lockout period in which the patient can attempt to deliver pain medication, however, none will be given to prevent overdosing on opioid pain medication. A continuous (basal) rate may also be added to provide a baseline level of analgesia without the patient needing to administer the medication.

When assessing postoperative pain, a verbal numeric scale is typically used. The scale typically ranges from 0 to 10 with 0 representing no pain and 10 representing the worst pain imaginable. Important qualitative descriptors of pain to assess are the location, radiation, and the quality (sharp or dull) of the pain.


Chronic Pain


Treatment methods for chronic pain patients are multimodal and include the use of non-narcotic pain medications such as NSAIDs, opioid analgesics, antidepressants, anticonvulsants, and multiple interventional pain procedures. The most common interventional pain procedures are listed in Table 27.4. Additionally, physical therapy, psychiatric evaluation and treatment, and surgical intervention are often coordinated through the pain clinic. Pain physicians are also involved in end-of-life care issues.
Sep 18, 2016 | Posted by in ANESTHESIA | Comments Off on Perioperative Acute and Chronic Pain Management

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