PAIN & IT’S MANAGEMENT

Introduction

After years of neglect, issues of pain assessment and management have captured the attention of both health care professionals and the public. Factors that prompted such attention include the high prevalence of pain, continuing evidence that pain is undertreated, and a growing awareness of the adverse consequences of inadequately managed pain.

Pain is common. About 9 in 10 persons regularly suffer from pain, and pain is the most common reason individuals seek health care. Chronic pain is the most common cause of long-term disability.  The large number of people will need treatment for pain from back disorders, degenerative joint diseases, rheumatologic conditions, visceral diseases, and cancer is expected to rise.

Pain is often undertreated. Safe and effective medical treatment for many types of chronic pain also is available. Yet recent studies, reports, and a position statement suggest that many types of pain (e.g., postoperative pain, cancer pain, chronic non-cancer pain) and patient populations (e.g., elderly patients, children, minorities, and substance abusers) are undertreated. Data from a 1999 survey suggest that only 1 in 4 individuals with pain receive appropriate therapy.

Inadequate pain management has adverse consequences. The adverse consequences of undertreated pain are considerable. Poorly managed acute pain may cause serious medical complications (e.g., pneumonia, deep venous thrombosis), impair recovery from injury or procedures, and/or progress to chronic pain. Undertreated chronic pain can impair an individual’s ability to carry out daily activities and diminish quality of life. In addition to disability, undertreated pain causes significant suffering.

Individuals with poorly controlled pain may experience anxiety, fear, anger, or depression. Pain is also a major cause of work absenteeism, underemployment, and unemployment. Hans, undertreated pain has significant physical, psychological, and financial consequences.

Definitions

In general, pain is a defense mechanism when the normal functioning of the body is threatened by internal or external sources. Pain is protective in nature because it provides warning signal for tissue injury. It helps minimize injury and is often a protective injury-protection mechanism.

Pain is subjective in nature and highly individualizes, only the person experiencing it may describe it that cannot be shared with others.

In 1968, McCaffery defined pain as “whatever the experiencing person says it is, existing whenever s/he says it does”. This definition emphasize that pain is a subjective experience with no objective measures. It also stresses that the patient, not clinician, is the authority on the pain and that his or her self-report is the most reliable indicator of pain.

In 1979, the International Association for the Study of Pain (IASP) introduced the most widely used definition of pain. The IASP defined pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” This definition emphasizes that pain is a complex experience that includes multiple dimensions.

CLASSIFICATION OF PAIN

Pain is classified according to various categories, such as duration, intensity, location, body system involved, origin, and temporal characteristics (intermittent, constant, etc.). But the two categories are important - according to duration and origin.

Biased on the duration the pain is categorized into Acute Pain, Chronic Pain, cancer pain and chronic non-malignant pain.

Acute pain

Acute pain was defined as in terms of duration lasting from seconds to 6 months. It is now defined as a “complex, unpleasant experience with emotional and cognitive, as well as sensory, features that occur in response to tissue trauma.” Usually, recent onset and commonly associated with a specific injury. Acute pain indicates that damage or injury has occurred, such as a skin burn or broken bone, but it may also be a warning of impending damage, such as angina or the pain associated with appendicitis or the body’s attempt to pass a kidney stone. Acute pain is also associated with severe headaches (such as migraines) or muscle cramps. Acute pain usually resolves with healing of the underlying injury or the cause of the pain (stimulus) is removed. Common sources of acute pain include trauma, surgery, labor, medical procedures, and acute disease states.

Chronic pain

Chronic pain was defined as pain that extends 3 or 6 months beyond onset or beyond the expected period of healing. However, chronic pain is now defined as pain that extends beyond the period of healing, with levels of identified pathology that often is low and insufficient to explain the presence and/or extent of the pain. Chronic pain is also defined as a persistent pain that “disrupts sleep and normal living, ceases to serve a protective function, and instead degrades health and functional capability.”

cancer pain

Pain associated with potentially life-threatening conditions such as cancer is often called “Malignant pain” or “cancer pain.” Cancer pain includes pain caused by the disease itself (e.g., tumor invasion of tissue, compression or infiltration of nerves or blood vessels, organ obstruction, infection, inflammation) and/or painful diagnostic procedures or treatments (e.g., biopsy, postoperative pain, toxicities from chemotherapy or radiation treatment).

Chronic Non-cancer Pain

Chronic Non-cancer Pain (CNCP) refers to persistent pain not associated with cancer may last for many years. Causes of CNCP include acute injury that has proceeded to chronic pain (e.g., whiplash) and various chronic conditions Such as Osteoarthritis, Low back pain, Myofascial pain, Fibromyalgia, Headaches (e.g., migrainea, tension-type, cluster), “Central pain” (e.g., spinal cord injury, stroke, multiple sclerosis), Chronic abdominal pain (e.g., chronic pancreatitis, chronic peptic ulcer, Irritable bowel syndrome), Sickle cell disease, CRPS-complex regional pain syndrome- Types I and II, Phantom limb pain, Peripheral neuropathy and Neuralgia (e.g., post-herpetic, trigeminal). In some cases, there is no discernable cause, and the pain is considered the disease. CNCP can affect virtually any body system or region, and pain severity ranges from mild to excruciating. Some types of CNCP have well-defined characteristics and patterns, whereas others do not. Neuropathic and myofascial CNCP can be particularly hard to diagnose, as they may occur in the absence of a known injury or disease process.

Because of its chronicity and impact on daily activities, patients with CNCP may experience vocational, interpersonal, and/or psychological problems. If the symptoms of CNCP consume the attention of and incapacitate the patient, he or she may suffer from a psychosocial disorder known as “chronic pain syndrome” (CPS). The pain experienced by these patients is real, and not all patients with CNCP develop this syndrome. Appropriate management of both CNCP and CPS requires an interdisciplinary approach that addresses the complex interaction of physical, psychological, and social factors that contribute to the ongoing pain.

Biased on the origin the pain is categorized into somatogenic Pain and psychogenic pain.

Somatogenic pain

Somatogenic Pain means pain arising from a perturbation of the body. It is further categorized as nociceptive and neuropathic pain on the basis of underlying pathophysiology.

Nociceptive Pain

Nociceptive pain is caused by the ongoing activation of A- d and C-nociceptors in response to a noxious stimulus (e.g., injury, disease, inflammation). Pain arising from visceral organs is called visceral pain, whereas that arising from tissues such as skin, muscle, joint capsules, and bone is called somatic pain. Somatic pain may be further categorized as superficial (cutaneous) or deep somatic pain.

characteristics	Superficial Somatic Pain	Deep Somatic Pain	Visceral Pain
Nociceptor location	Skin, subcutaneous tissue, and mucous membranes	Muscles, tendons, joints fasciae, and bones	Visceral organs*
Potential stimuli	External mechanical chemical, or thermal events Dermatologic disorders	Overuse strain, mechanical injury, cramping, ischemia, inflammation	Organ distension, muscle spasm, traction, ischemia, inflammation
Localization	Well localized	Localized or diffuse and radiating	Well or poorly localized
Quality	Sharp, pricking, or burning sensation	Usually dull or aching cramping	Deep aching or sharp stabbing pain, which is often referred to cutaneous sites
Associated symptoms and signs	Cutaneous tenderness, hyperalgesia hyperesthesia, allodynia	Tenderness, reflex muscle spasm, and sympathetic hyperactivity**	Malaise, nausea, vomiting sweating, tenderness, reflex muscle spasm
Clinical examples	Sunburn, chemical or thermal burns, cuts and contusions of the skin	Arthritis pain, tendonitis myofascial pain	Colic, appendicitis, pancreatitis peptic ulcer disease, bladder distension
* - Visceral organs include the heart, lungs, gastrointestinal tract, pancreas, liver, gallbladder, kidneys, and bladder. ** - Symptoms and signs of sympathetic (autonomic) nervous system hyperactivity include increased heart rate, blood pressure, and respiratory rate; sweating; pallor; dilated pupils; nausea; vomiting; dry mouth; and increased muscle tension.

Neuropathic Pain                                  

Neuropathic pain is caused by aberrant signal processing in the peripheral or central nervous system. In other words, neuropathic pain reflects nervous system injury or impairment. Common causes of neuropathic pain include trauma, inflammation, metabolic diseases (e.g., diabetes), infections (e.g., herpes zoster), tumors, toxins, and primary neurological diseases. Neuropathic pain can be broadly categorized as peripheral or central in origin. Painful peripheral mono-neuropathy and poly-neuropathy, deafferentation pain, sympathetically maintained pain, and central pain are subdivisions of these categories. Neuropathic pain may be continuous or episodic and is perceived in many ways (e.g., burning, tingling, prickling, shooting, electric shock-like, jabbing, squeezing, deep aching, spasm, or cold).

Psychogenic pain

Psychogenic pain, also called psychalgia, is physical pain that is caused, increased, or prolonged by mental, emotional, or behavioral factors.

Headache, back pain, or stomach pain are some of the most common types of psychogenic pain. It may occur, rarely, in persons with a mental disorder, but more commonly it accompanies or is induced by social rejection, broken heart, grief, love sickness, or other such emotional events.

	Painful Mononeuropathies and Polyneuropathies	Deafferentation Pain	Sympathetically Maintained Pain*	Central Pain
Definition	·   Pain along the distribution of one or multiple peripheral nerve(s) caused by damage to the affected nerve(s)	·   Pain that is due to a loss of afferent input	·   Pain that is maintained by sympathetic nervous system activity	·   Pain caused by a primary lesion or dysfunction of the CNS
Pain characteristics and associated symptoms	·   Three main types: ·   Continuous, deep, burning, aching or bruised pain ·   Paroxysmal lancinating (shock-like) pain ·   Abnormal skin sensitivity	·   Quality: burning, cramping, crushing, aching, stabbing, or shooting ·   Hyperalgesia ·   Hyperpathia ·   Dysesthesia ·   Other abnormal sensations	·   Quality: burning, throbbing, pressing, or shooting ·   Allodynia ·   Hyperalgesia ·   Associated ANS dysregulation and trophic changes**	·   Quality: burning, numbing, tingling, shooting ·   Spontaneous and steady or evoked ·   +/- sensory loss ·   Allodynia ·   Hyperalgesia
Sources	·   Metabolic disorders (e.g., diabetes) ·   Toxins (e.g., alcohol chemotherapy agents) ·   Infection (e.g., HIV, herpes zoster) ·   Trauma ·   Compressive (nerve entrapment) ·   Autoimmune and hereditary diseases	·   Damage to a peripheral nerve, ganglion, or plexus ·   CNS disease or injury (occasional)	·   Peripheral nerve damage (e.g., CRPS II) ·   Sympathetic efferent (motor) innervation ·   Stimulation of nerves by circulating catecholamines	·   Ischemia (e.g., stroke) ·   Tumors ·   Trauma (e.g., spinal cord injury) ·   Syrinx ·   Demyelination
Clinical examples	·   Diabetic neuropathy ·   Alcoholic neuropathy ·   Postherpetic neuralgia ·   Carpal tunnel syndrome	·   Phantom limb pain ·   Post-mastectomy pain	·   CRPS ·   Phantom limb pain ·   Postherpetic neuralgia ·   Some metabolic neuropathies	·   Post-stroke pain ·   Some cancer pain ·   Pain associated with multiple sclerosis
*- Sympathetically maintained pain is a pain mechanism, not a diagnosis. It is associated with several types of pain, but it also may exist as a single entity. ** - Focal autonomic dysregulation can manifest with signs and symptoms such as swelling, pallor, erythema (redness), sweating, and temperature changes. Trophic changes include thinning of the skin, abnormal hair or nail growth, and bone changes. ANS: autonomic nervous system; CNS: central nervous system; CRPS: complex regional pain syndrome types I and II; CRPS II: complex regional pain syndrome type II; HIV: human immunodeficiency virus.

Pathophysiology of Pain

Nociception refers to the process by which information about tissue damage is conveyed to the central nervous system (CNS). The experience of pain involves a complex sequence of biochemical and electrical events or processes beginning with tissue damage, followed by transduction, transmission, perception, and modulation.

·        Transduction: the conversion of the energy from a noxious thermal, mechanical, or chemical stimulus into electrical energy (nerve impulses) by sensory receptors called nociceptors

·        Transmission: the transmission of these neural signals from the site of transduction (periphery) to the spinal cord and brain

·        Perception: the appreciation of signals arriving in higher structures as pain

·        Modulation: descending inhibitory and facilitory input from the brain that influences (modulates) nociceptive transmission at the level of the spinal cord.

Transduction

a. Nociceptor activation and sensitization

Nociceptors are sensory receptors that are preferentially sensitive to tissue trauma or a stimulus that would damage tissue if prolonged. These receptors are the free endings of (primary afferent) nerve fibers distributed throughout the periphery. Signals from these nociceptors travel primarily along two fiber types: slowly conducting unmyelinated C-fibers and small, myelinated, and more rapidly conducting A-d fibers.

Injury to tissue causes cells to break down and release various tissue byproducts and mediators of inflammation (e.g., prostaglandins, substance P, bradykinin, histamine, serotonin, cytokines). Some of these substances activate nociceptors (i.e., cause them to generate nerve impulses) and most sensitize nociceptors (i.e., increase their excitability and discharge frequency). Ongoing activation of nociceptors may cause nociceptive pain. Peripheral (nociceptor) sensitization amplifies signal transmission and thereby contributes to central sensitization and clinical pain states.

b. Peripheral neuropathic pain

Not all pain that originates in the periphery is nociceptive pain. Some neuropathic pain is caused by injury or dysfunction of the peripheral nervous system (i.e., peripheral nerves, ganglia, and nerve plexi).

c. Clinical implications

Some analgesics target the inflammatory process that produces sensitization. For example, non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX), thus decreasing the synthesis of prostaglandins. Other analgesics (e.g., antiepileptic drugs, local anesthetics) block or modulate channels, thus inhibiting the generation of nerve impulses.

Transmission

Nerve impulses generated in the periphery are transmitted to the spinal cord and brain in several phases:

a. Periphery to the spinal cord

Most sensory nerve impulses travel via the nerve processes (axons) of primary afferent neurons to the dorsal horn (DH) of the spinal cord. There, primary afferent neurons propagate nerve impulses to DH neurons through the release of excitatory amino acids (EAAs) (e.g., glutamate, aspartate) and neuropeptides (e.g., substance P) at synapses (connections) between cells. Activated DH projection neurons forward nociceptive impulses toward the brain. However, not all events in the DH facilitate nociception. Spinal interneurons release inhibitory amino acids (e.g.,  g-aminobutyric acid [GABA]) and neuropeptides (endogenous opioids) that bind to receptors on primary afferent and DH neurons and inhibit nociceptive transmission by presynaptic and postsynaptic mechanisms.

Descending inhibitory input from the brain also modulates DH nociceptive transmission. Thus, nociceptive traffic in the DH is not merely relayed to higher centers but rather is heavily modulated. These inhibitory events are part of a natural nociceptive-modulating system that counterbalances the activity of the nociceptive-signaling system.

b. Spinal cord to the brain

The nerve processes of DH projection neurons project to the brain in bundles called ascending tracts. Projection neurons from some DH regions transmit nociceptive signals to the thalamus via the spinothalamic tract (STT). Others transmit nociceptive information to the reticular formation, mesencephalon, and hypothalamus via the spinoreticular, spinomesencephalic, and spinohypothalamic tracts.

c. Clinical implications

Some analgesics inhibit nociception in the DH. For example, opioid analgesics bind to opioid receptors on primary afferent and DH neurons and mimic the inhibitory effects of endogenous opioids. They also bind to opioid receptors in the brain and activate descending pathways that further inhibit DH nociceptive transmission. Baclofen, a GABA agonist, binds to GABAB receptors and mimics the inhibitory effects of GABA on nociceptive transmission.

Perception

The perception of pain is an uncomfortable awareness of some part of the body, characterized by a distinctly unpleasant sensation and negative emotion best described as threat. Both cortical and limbic system structures are involved. Nociceptive information from some DH projection neurons travels via the thalamus to the contralateral somatosensory cortex where input is somatotopically mapped to pre- serve information about the location, intensity, and quality of the pain. The thalamus relays other nociceptive input to the limbic system. This input joins input from the spinoreticular and spinomesencephalic tracts to mediate affective aspects of pain. Immediate social and environmental context influences the perception of pain, as do past experience and culture. Consequently, a standard cause of pain (e.g., surgery) can generate enormous individual differences in pain perception.

Modulation

a. Descending pathways

Modulation of nociceptive transmission occurs at multiple (peripheral, spinal, supraspinal) levels. Yet, historically, modulation has been viewed as the attenuation of DH transmission by descending inhibitory input from the brain. Melzack and Wall’s Gate Control Theory brought this notion to the forefront in 1965. Models of descending pain systems now include both inhibitory and facilitory descending pathways. Multiple brain regions contribute to descending inhibitory pathways. Nerve fibers from these pathways release inhibitory substances (e.g., endogenous opioids, serotonin, norepinephrine, GABA) at synapses with other neurons in the DH. These substances bind to receptors on primary afferent and/or DH neurons and inhibit nociceptive transmission. Such endogenous modulation may contribute to the wide variations in pain perception observed among patients with similar injuries.

b. Clinical implications

Some analgesics enhance the effects of descending inhibitory input. For example, some antidepressants interfere with the reuptake of serotonin and norepinephrine at synapses, increasing their relative interstitial concentration (availability) and the activity of endogenous pain-modulating pathways. Thus, some, but not all, antidepressants are used to treat some types of chronic pain.

CONSEQUENCES, AND COSTS OF PAIN

Pain is common, and inadequately managed pain is associated with many adverse consequences. These consequences affect patients, their families, and society as a whole and can be broadly categorized as physiological, psychosocial (quality of life), and financial.

Physiological consequences

Acute tissue injury triggers physiological “stress” responses intended to protect the body. Yet these responses can have adverse effects if allowed to persist unchecked.

Functional Domain	Stress Responses to Pain	Examples of Clinical Manifestations
Endocrine/metabolic	·   Altered release of multiple hormones (e.g., ACTH, cortisol, catecholamines, insulin) with associated metabolic disturbances	·   Weight loss ·   Fever ·   Increased respiratory and heart rate ·   Shock
Cardiovascular	·   Increased heart rate ·   Increased vascular resistance ·   Increased blood pressure ·   Increased myocardial oxygen demand ·   Hypercoagulation	·   Unstable angina (chest pain) Myocardial infarction (heart attack) ·   Deep vein thrombosis (blood clot)
Respiratory	·   Decreased air flow due to involuntary (reflex muscle spasm) and voluntary (“splinting”) mechanisms that limit respiratory effort	·   Atelectasis ·   Pneumonia
Gastrointestinal	·   Decreased rate of gastric emptying ·   Decreased intestinal motility	·   Delayed gastric emptying, constipation, anorexia, ileus*
Musculoskeletal	·   Muscle spasm Impaired muscle mobility and function	·   Immobility ·   Weakness ·   Fatigue
Immune	·   Impaired immune function	·   Infection
Genitourinary	·   Abnormal release of hormones that affect urine output, fluid volume, and electrolyte balance	·   Decreased urine output ·   Hypertension (fluid retention) ·   Electrolyte disturbances
* - Mechanical, dynamic, or adynamic obstruction of bowel often manifests as colicky pain, distension, vomiting, and absence of the passage of stool. ACTH: adrenocorticotrophic hormone.

QUALITY OF LIFE

Inadequate control of pain interferes with the pain sufferer’s ability to carry out activities of daily living (e.g., work, relationships, hobbies, sex). It also has adverse psychological consequences. Patients with inadequately managed pain may experience anxiety, fear, anger, depression, or cognitive dysfunction, and family members report varying levels of helplessness, frustration, and “heartbreak.”

These consequences are especially likely to occur in patients with chronic pain. These individuals report impairments on multiple measures of physical, social, and psychological well-being, and many experience psychological symptoms (e.g., depression, anxiety) that adversely influence health care. Left unchecked, these symptoms can contribute to more serious consequences. In one study, about half of the patients with CNCP reported that they had considered suicide despite the availability of resources and coping strategies.

FINANCIAL CONSEQUENCES

Patients with chronic pain are five times as likely as those without chronic pain to use health care services. In addition, medical complications associated with inadequately controlled acute pain can increase length of stay, rehospitalization rates, and outpatient visits. Results from some studies suggest that adequate management of acute (postoperative) pain can reduce length of stay and costs.

Pain is also costly in terms of lost productivity and income. It is a leading cause of medically related work absenteeism and Individuals with chronic pain often face long-term or permanent unemployment or underemployment.

Common terminologies:

1.      Radiating pain—perceived at the source of the pain and extends to the nearby tissues

2.      Referred pain— pain is felt in a part of the body that is considerably removed from the tissues causing the pain

3.      Intractable pain—pain that is highly resistant to relief

4.      Phantom pain—painful perception perceived in a missing body part or in a body part paralyzed from a spinal cord injury

5.      Phantom sensation—feeling that the missing body part is still present

6.      Hyperalgesia—excessive sensitivity to pain

7.      Pain threshold—is the amount of pain stimulation a person requires in order to feel pain

8.      Pain sensation—can be considered the same as pain threshold

9.      Pain reaction—includes the autonomic nervous system and behavioral responses to pain

10. Pain tolerance—maximum amount and duration of pain that an individual is willing to endure

11. Nociceptors—pain receptors

12. Pain perception—the point which the person becomes aware of the pain

Assessment of Pain

Assessment is an essential, but challenging, component of any pain management plan, because Pain is highly subjective in nature. The report of pain is a social transaction; therefore, assessment and management of pain require a good rapport with the person in pain. Pain is also multidimensional, so the clinician must consider multiple aspects (sensory, affective, and cognitive) of the pain experience. Finally, the nature of the assessment varies with multiple factors (e.g., purpose of the assessment, the setting, patient population, and clinician), so no single approach is appropriate for all patients or settings.

Principles of Pain Assessment and Management

1)     Patients have the right to appropriate assessment and management of pain and Pain (should be) is assessed in all patients.

2)     Pain is always subjective. Therefore, the patient’s self-report of pain is the single most reliable indicator of pain. A clinician needs to accept and respect this self-report, absent clear reasons for doubt.

3)     Physiological and behavioral (objective) signs of pain (e.g., tachycardia, grimacing) are neither sensitive nor specific for pain. Such observations should not replace patient self-report unless the patient is unable to communicate.

4)     Assessment approaches, including tools, must be appropriate for the patient population. Special considerations are needed for patients with difficulty communicating. Family members should be included in the assessment process, when possible.

5)     Pain can exist even when no physical cause can be found. Thus, pain without an identifiable cause should not be routinely attributed to psychological causes.

6)     Different patients experience different levels of pain in response to comparable stimuli. That is, a uniform pain threshold does not exist.

7)     Pain tolerance varies among and within individuals depending on factors including heredity, energy level, coping skills, and prior experiences with pain.

8)     Patients with chronic pain may be more sensitive to pain and other stimuli.

9)     Unrelieved pain has adverse physical and psychological consequences. Therefore, clinicians should encourage the reporting of pain by patients who are reluctant to discuss pain, deny pain when it is likely present, or fail to follow through on prescribed treatments.

10) Pain is an unpleasant sensory and emotional experience, so assessment should address physical and psychological aspects of pain.

Goals of the pain Assessment

Goals of the assessment of pain include –

1.      Establishing rapport with the patient

2.      Providing an overview of the assessment process

3.      Obtain information about pain

Elements of the Pain Assessment

Elements of the Pain Assessment include –

1.      Patient history,

2.      Physical examination, and

3.      Diagnostic studies

PATIENT HISTORY

The patient’s self-report of pain is the most reliable indicator of pain. Physiological and behavioral signs of pain (e.g., tachycardia, grimacing) are neither sensitive nor specific for pain and should not replace patient self-report unless the patient is unable to communicate.

The pain history is obtained as part of the patient history, which includes the patient’s past medical history, medications, habits (e.g., smoking, alcohol intake), family history, and psychosocial history. Information to be elicited during the initial assessment of pain includes:

1.      Characteristics of the pain (e.g., duration, location, intensity, quality, exacerbating / alleviating factors)

2.      Present and past pain management strategies and their outcomes

3.      Past and present medical problems that may influence the pain and/or its management

4.      Relevant family history

5.      Current and past psychosocial issues or factors that may influence the pain and its management

6.      The impact of the pain on the patient’s daily life and functioning

7.      The patient’s and family’s knowledge of, expectations about, and goals for pain management

Parameter	Information to Be Obtained
Pain characteristics	·    Onset and duration ·    Location(s) ·    Quality ·    Intensity (severity) ·    Exacerbating or alleviating factors
Management strategies	Past and current: ·    Medications ( “natural,” nonprescription, and prescription) ·    Nonpharmacologic treatments ·    Coping strategies (e.g., prayer, distraction)
Relevant medical history	·    Prior illnesses (including psychiatric illnesses and chemical dependence), surgeries, and accidents ·    Coexisting acute or chronic illnesses ·    Prior problems with pain and treatment outcomes
Relevant family history	·    Health of family members ·    Family history of chronic pain or illnesses
Psychosocial history	Past or current: ·    Developmental, marital, or vocational problems ·    Stressors or depressive symptoms ·    “Reinforcers” of the pain (e.g., compensation-litigation issues)
Impact of the pain on the patient’s daily life	Impact of the pain on the patient’s: ·    Work ·    Other daily activities (e.g., chores, hobbies) ·    Personal relationships ·    Sleep, appetite, emotional state
Patient’s expectations and goals	·    Expectations and goals for pain management in regard to pain intensity, daily activities, and quality of life

PHYSICAL EXAMINATION

The initial assessment of a patient with pain includes a physical examination. The clinician uses this examination to help identify the underlying cause of the pain and reassure the patient that his or her complaints of pain are taken seriously. During this examination, the clinician appraises the patient’s general physical condition, with special attention to the musculoskeletal and neurological systems and site(s) of pain.

GENERAL

Observe and/or identify:

§  Patient’s general appearance and vital signs

§  Evidence of overt abnormalities (e.g., weight loss, muscle atrophy, deformities, and trophic changes)

§  Any subjective manifestations of pain (e.g., grimacing, splinting)

SITE OF PAIN

§  Inspect the pain site(s) for abnormal appearance or color of overlying skin or visible muscle spasm

§  Palpate the site(s) to assess for tenderness and correlate tenderness with any associated subjective or objective findings

§  Use percussion (or jarring) to elicit, reproduce, or evaluate the pain and any tenderness on palpation

§  Use the brush, pinch, pin prick, and/or scratch tests to assess for allodynia, hyperalgesia, or hyperesthesia

§  Determine the effects of physical factors (e.g., motion, applied heat or cold, deep breathing, changes in position) on pain

OTHER REGIONS

Examine other regions as directed by the patient history or assessment of pain site

NEUROLOGICAL SYSTEM

At minimum, perform a screening neurological examination (i.e., assess cranial nerves, spinal nerves, sympathetic nervous system function, coordination, and mental status) to screen for:

§  Sensory deficits (e.g., impaired vision or hearing) or abnormal sensations (e.g., paresthesia, dysesthesia, allodynia, hyperpathia)

§  Motor abnormalities or deficits (e.g., weakness, exaggerated or diminished reflexes)

§  Lack of coordination

§  Evidence of sympathetic nervous system dysfunction (e.g., skin flushing, unusual sweating)

§  Abnormalities or deficits in orientation, recent or remote memory, parietal sensory function, language function, and mood

MUSCULOSKELETAL SYSTEM

Observe and/or identify:

§  Body type, posture, and overall symmetry

§  Abnormal spine curvature or limb alignment and other deformities

§  Abnormal movements and/or irregular gait during walking

§  Range of motion (spine, extremities)

§  For muscles in neck, upper extremities, trunk, and lower extremities:

§  Assess multiple parameters (e.g., tone, volume, contour, strength and power, range of motion)

§  Observe for any abnormalities (e.g., weakness, atrophy, hypertrophy, irritability, tenderness, trigger points)

Diagnostic Tests

The need for and type of diagnostic studies are determined by characteristics of the pain and suspected underlying condition. Appropriately selected tests can lead to accurate diagnosis and improve outcomes (e.g., reduce pain and adverse effects of therapy; improve function and quality of life). Diagnostic tests those are used in patients with pain, include -

1)     Screening laboratory tests {Screen for illnesses, organ dysfunction}: - Includes CBC, chemistry profile (e.g., electrolytes, liver enzymes, BUN, Creatinine), urinalysis, ESR

2)     Disease-specific laboratory tests {for autoimmune disorders, sickle cell disease}: - Includes autoantibodies, sickle cell test

3)     Imaging studies {for Detection of tumors, other structural abnormalities}: - Includes radiographs (x-rays), CT, MRI, USG, myelography

4)     Diagnostic procedures {for Detection of various illnesses}: - Includes lumbar puncture, thoracentesis, paracentesis, biopsy etc.

5)     Electrodiagnostic {for Detection of myopathies, some neuropathies, Multiple Sclerosis}: - Include EMG (electromyography) - (direct examination of tests skeletal muscle via needle electrodes) and NCS (nerve conduction studies) (examination of conduction along peripheral sensory and motor nerves or plexuses)

6)     Diagnostic nerve block: - Nerve block (injection of a local anesthetic to determine the source/ mechanism of the pain). Uses of nerve block, including: - Identification of structures responsible for the pain (e.g., sacroiliac or facet joint blocks); Differentiation between types of pain etc.

Pain management

·        Treatments for pain can be broadly categorized as pharmacologic and non-pharmacologic.

PHARMACOLOGIC TREATMENT

Pharmacologic treatment is the mainstay of pain therapy. Almost half of individuals who suffer from pain choose a nonprescription analgesic as their initial choice for pain relief such as OCT.

Analgesics are broadly categorized as:

·        Non-opioid analgesics (non-opioids): acetaminophen and non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin and other salicylic acid derivatives

·        Opioid analgesics (opioids): mu opioid agonists (i.e., morphine-like agonists) and agonist- antagonist opioids

·        Adjuvant analgesics or co-analgesics: a diverse group of drugs, with primary indications for conditions other than pain, with analgesic properties relevant to some conditions. Commonly used adjuvant analgesics include antiepileptic drugs (AEDs), tricyclic antidepressants (TCAs), and local anesthetics (LAs).

NONNARCOTIC ANALGESICS

Generic Name	Dose	Route	Interval	INDICATION
Acetaminophen	650 Mg	PO	TDS	Mild to moderate pain due to multiple causes including headache, toothache, muscular aches, backache, menstrual cramps, arthritis, common      cold, and flu; fever reduction
NSAIDs
Aspirin	650 Mg	PO	TDS	Mild to moderate pain due to multiple causes including headache, toothache, sinus pain, muscular aches, bursitis, backache, sprains, arthritis, pain due to fever, cold, flu
Ibuprofen	400 Mg	PO	TDS	Mild to moderate pain due to multiple causes including headache, toothache, muscular aches, backache, menstrual cramps, arthritis, common      cold, and flu; fever reduction
Diclofanic	50-75 Mg	PO/IM	BD/TDS	Mild to moderate pain due to multiple causes including headache, toothache, muscular aches, backache, menstrual cramps, arthritis, common      cold, and flu; fever reduction
Naproxen	250–500 Mg	PO	BD/TDS	RA, OA, AS, JA, tendonitis, bursitis, gout, primary dysmenorrhea
Indomethacin	20–50 Mg	PO	BD/QID	Moderate to severe OA, RA, AS; acute gouty arthritis; acute painful shoulder (bursitis and/or tendonitis)
Ketorolac	10-20 Mg	IM/IV	QID	Short term (<5 days) treatment of moderately severe acute pain that requires analgesia at the opioid level (e.g., postoperative pain)
Celecoxib	100–200 Mg	PO	BD	OA, RA, FAP
AS: ankylosing spondylitis; FAP: familial adenomatous polyposis; JA: juvenile arthritis, OA: osteoarthritis; RA: rheumatoid arthritis

Adverse effects of nonselective NSAIDs

·        Gastrointestinal problems (e.g., dyspepsia, ulcers, perforation, bleeding),

·        Liver dysfunction, bleeding due to inhibited platelet aggregation (i.e., “antiplatelet effect”),

·        Kidney problems (e.g., renal insufficiency, acute renal failure), hypersensitivity reactions (i.e., aspirin sensitivity), and

·        CNS effects (e.g., attention and memory deficits, headache, dizziness, drowsiness)

NARCOTIC ANALGESICS

Generic Name	Route & Dose	Interval	INDICATION
Morphine	PO : 10-50 mg IM/SC : 10-50 mg IV : 2-6 mg	BD/TDS	Severe acute pain (e.g., trauma,              postoperative pain, MI), cancer pain, chronic pain
Codeine	PO : 10-30 mg	TDS	Mild to moderately severe pain
Pethidine (Meperidine)	IM/SC : 50-100 mg PO – 200-300  mg	BD/TDS	Moderate to severe pain (e.g., migraine, trauma, postoperative pain, acute abdominal pain)
Fentanyl	Trans dermal patching 25,50,75  mg/hr	For 2- 3 days	Severe acute pain, cancer pain, CNCP. TD fentanyl is only indicated for treatment of chronic pain that requires continuous administration and cannot be managed by lesser means
tramadol	PO/IM 50-100 mg Or slow IV	BD/TDS	Moderate to severe pain Postoperative pain
Common side effects include sedation, nausea, vomiting, constipation, pruritus (itching), and respiratory depression.
Generally contraindicated or need to be used with extreme caution in patients with known hypersensitivity to the drug, head injury or lesion associated with increased intracranial pressure, asthma and other respiratory conditions, or paralytic ileus.

Adjuvant analgesics or co-analgesics

·        Antiepileptic drugs (AEDs) – such as phenytoin, carbamazepine, oxcarbezine, Clonazepam and gabapentin

·        Tricyclic antidepressants (TCAs) – such as Amitriptyline, Nortriptyline

·        Local anesthetics (LAs) – such as Bupivacaine, Lidocaine

·        Corticosteroid – prednisone

NONPHARMACOLOGIC MANAGEMENT

Pharmacologic approaches to pain management are the most powerful tool for the treatment for acute pain and cancer pain and are increasingly being used to manage chronic non-cancer pain (CNCP). However, optimal pain management also includes psychological, physical rehabilitative, and in some cases, invasive treatment strategies.

Psychological Modalities

1.      Relaxation Techniques and Imagery - It used to achieve a state or mental and physical relaxation. Relaxation techniques include simple focused breathing exercises progressive muscle relaxation, meditation and music therapy. Simple relaxation techniques should be used for episodes of brief pain, e.g., during procedures, high level of anxiety. Imagery means Pleasant mental images can be used to aid relaxation, e.g., patient may be encouraged to visualize a peaceful scene of life.

2.      Distraction - Distraction involves focusing the patient's attention on something other than the pain, may be the mechanism responsible for other effective cognitive techniques. The effectiveness of distraction depends on the patient's ability to receive and create sensory input other than pain. Distraction techniques may range from simple activities, such as watching TV or listening to music, to highly complex physical and mental exercises. Pain relief generally increases in direct proportion to the patient's active participation, the number of sensory modalities used, and interest in the stimuli. Therefore, the stimulation of sight, sound, and touch is likely to be more effective in reducing pain than is the stimulation of a single sense. For example - Watching an action-packed movie on a large screen with “Surround Sound” through headphones may be effective (provided the patient finds it acceptable). Others may benefit from games and activities (eg, chess, crossword puzzles) that require concentration. Distraction helps relieve both acute and chronic pain but not all patients obtain pain relief with distraction, especially those in severe pain. Severe pain may prevent patients from concentrating well enough to participate in complex physical or mental activities.

3.      Hypnosis - Hypnosis is a state of heightened awareness and focused concentration that can be used to manipulate the perception of pain and has been effective in relieving pain or decreasing the amount of analgesic agents required in patients with acute and chronic pain.

Physical Modalities

1.      Cutaneous Stimulation and Massage - Rubbing of painful or non-painful adjacent area; that facilitates muscle relaxation and promotes comfort and decreases muscle tension and pain.

2.      Thermal Therapies (Applied heat or cold) - Application of cold (cryotherapy) to decrease pain and swelling and improve function. It produces local analgesia, slows nerve conduction, and promotes tendon flexibility. Application of heat (thermotherapy) to augment performance and diminish pain, by produces local analgesia, dilates (widens) blood vessels, and promotes flexibility.

3.      Transcutaneous Electrical Nerve Stimulation - TENS uses a battery-operated unit with electrodes applied to the skin to produce a tingling, vibrating, or buzzing sensation in the area of pain. It has been used in both acute and chronic pain relief and is thought to decrease pain by stimulating the non-pain receptors in the same area as the fibers that transmit the pain.

Invasive Therapies

Depending on client's condition, prognosis and benefits derived, the interrupt or modification of pain pathways may be considered. The most commonly used interventions are nerve blocks, cordotomy, acupuncture and non-invasive techniques such as Trans Cutaneous Nerve Stimulation.

1.        Nerve Blocks: The procedure involves identifying specific nociceptive or pain pathways and blocking them by rejecting drugs close to nerve.

2.        Chordotomy: it is a surgical procedure that disables selected pain-conducting tracts in the spinal cord, in order to achieve loss of pain and temperature perception. This procedure is commonly performed on patients experiencing severe pain which are currently no cure. Anterolateral cordotomy is effective for relieving unilateral, somatic pain while bilateral cordotomies may be required for visceral or bilateral pain.

(a)     Percutaneous Chordotomy - It is done with fluoroscopic guidance while the patient is under local anesthesia.

(b)     Open Cordotomy – it requires a laminectomy, is often risky for patients with poor medical conditions, but may be required if percutaneous cordotomy is not feasible or an attempt has failed.

3.        Dorsal Rhizotomy: Selective ablation of the dorsal nerve root reduces nociceptive perception in the affected area, and spares motor junction. Procedure can be accomplished by chemical neurolysis with radiographic guidance to place the tip of an infusion catheter at the precise segment within the epidural space.

4.        Acupuncture: Old Chinese healing technique involves insertion of fine needles into the skin at varying depths; application of pressure at acupuncture sites is called acupressure. Acupuncture may cause the secretion of endorphins and interfere with transmission of nociceptive information to relieve pain.

Nursing care

·        Use pain assessment scale to identify intensity of pain.

·        Assess and record pain and its characteristics: location, quality, frequency, and duration.

·        Administer balanced analgesics as prescribed to promote optimal pain relief.

·        Re-administer pain assessment scale.

·        Document severity of patient's pain on chart.

·        Obtain additional prescriptions as needed.

·        Identify and encourage patient to use strategies that have been successful with previous pain.

·        Teach patient additional strategies to relieve pain and discomfort: distraction, relaxation, cutaneous stimulation, etc.

·        Instruct patient and family about potential side effects of analgesics and their prevention and management.

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