Acute Pain: Mechanisms, Management, and Treatment Options

Acute Pain: Mechanisms, Management, and Treatment Options
Acute Pain
Mechanisms, Management,
and Treatment Options
Overview
Pain: Definition and Features
Physiologic Consequences of Acute Pain
JCAHO and Pain Management
Characteristics of Acute, Chronic, Peripheral
Neuropathic Pain
Assessment of Pain and Pain Relief
Pain Mechanisms
Role of Prostanoids in Pain
Treatment Options for Acute Pain
Other Approaches
Acute Pain Services
Pain
Definition and Features
Definition
Pain is an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage or described in terms of such damage.
International Association for the Study of Pain. Pain. 1979;6:249.
Features of Acute Pain

Onset
Intensity
Somatic vs visceral
May be referred
Siddall PJ, Cousins MJ. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia
and Management of Pain. 3rd ed; 1998:675713.
General stress response/neuroendocrine

Respiratory
Cardiovascular
Gastrointestinal/urinary
Musculoskeletal
Bonica JJ. The Management of Pain. 2nd ed. Vol. 1; 1990.
General Stress Response

Endocrine/Metabolic
ACTH, cortisol, catecholamines, interleukin-1
insulin
Water/Electrolyte Flux
H2O, Na+ retention
ACTH = adrenocorticotropic hormone

Kehlet H. Reg Anesth.1996;21(6S):3537.
Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447491.
Respiratory Effects
Acute
Pain
Tidal
volume
Vital
capacity
FRC
Alveolar
ventilation
Mobility
Atelectasis
Hypostatic pneumonia
V/Q inequality
FRC = functional residual capacity; V/Q = ratio ventilation:perfusion of the lung
Craig DB. Anesth Analg. 1981;60:46.
Respiratory Effects (Contd)

Acute
Pain
Muscle spasm
Impaired
ventilation
Muscle splinting
Cough suppression
Lobular collapse
Infection/pneumonia
Hypoxemia
Cardiovascular Effects
Acute
Pain
Coronary
vasoconstriction
Anxiety, pain
Ischemia
Sympathetic
overactivity
HR, PVR, BP, cardiac output
Angina
MI
Ischemia
MI = myocardial infarction; HR = heart rate; PVR = peripheral vascular resistance; BP = blood

pressure
Bowler DB, et al. In: Cousins MJ, Phillips GD, eds. Acute Pain Management; 1986:187236.
Effects on Peripheral Circulation

Acute
Pain
Limb blood flow1
Venous emptying2
Venous thrombosis/embolism3
1. Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447491.
2. Modig J, et al. Acta Anaesth Scand. 1980;24:305309.
3. Modig J, et al. Anesth Analg. 1983;62:174180.
Gastrointestinal and Urinary Effects
Gastrointestinal
Acute
Pain
Urinary
Intestinal secretions
Smooth muscle
sphincter tone
Sympathetic
overactivity
Urinary sphincter
activity
Intestinal motility
Urinary retention
Nimmo WS. Br J Anaesth. 1984.56:2937.
Musculoskeletal Effects
Acute
Pain
Muscle
spasm
Sympathetic
overactivity
Sensitivity of peripheral
nociceptors
Musculoskeletal Effects (Contd)

Acute
Pain
Mobility
Reflex
vasoconstriction
Impaired muscle
metabolism
Muscle atrophy
Delayed normal
muscle function
Effects on Pain-Signaling Systems

Acute
Pain
Peripheral nociception
Nerve excitability
Hyperalgesia (1 + 2)
Prolonged pain
Chronic pain
Allodynia
Damaged spinal
pain-signaling systems
Psychologic Effects
Acute
Pain
Anxiety
Sleep deprivation
Depression
Other Effects of Acute Pain

Wound repair
Impaired immunocompetence
Hypercoagulable state
Drucker W, et al. J Trauma. 1996;40(3):S116122.

Jorgensen L, et al. Br J Anaesth. 1991;66:812.
Advantages of Effective Pain Management

Patient comfort and satisfaction1,2,3
Earlier mobilization4
hospital stay3,4
costs4
1. Eisenach JC, et al. Anesthesiology. 1988;68:444448.

2. Harrison DM, et al. Anesthesiology. 1988;68:454457.
3. Miaskowski C, et al. Pain. 1999;80:2329.
4. Finley RJ, et al. Pain. 1984;2:S397.
JCAHO and Pain Management
Joint Commission on Accreditation

of Healthcare Organizations
New standards in 20002001; scoring begins in 2001
Record pain as the 5th vital sign
Interdisciplinary management with needs assessment
Patients right to pain assessment
Monitor pain intervention responses
Provide pain management education
Joint Commission on Accreditation of Healthcare Organizations. Jt Comm Perspect. 1999;19(5):68.
Sklar DP. Ann Emerg Med. 1996;27:412413.
Pain: The Fifth Vital Sign

Pain should be considered the fifth vital sign
Patients should be assessed for pain every time pulse,
blood pressure, core temperature, and respiration are
measured
Healthcare professionals should recognize a report of
unrelieved pain as a red flag
American Pain Society Quality Improvement Committee. JAMA. 1995;18471880.
JCAHO Revised Standards: The Patients Rights

Patients have the right to appropriate assessment and
management of pain
The patients right to pain management is respected and
supported
Patients are involved in all aspects of their care,
including pain management
A Team Approach to Implementing the JCAHO

Revised Standards for Pain Management
Others
Nursing
Medical
Pharmacy
Managers
Dietetic
Rehabilitation
Characteristics of Acute, Chronic,

and Peripheral Neuropathic Pain
Characteristics of Acute Pain

Sudden, sharp, intense, localized
Usually self-limited
May be associated with physiologic changes, eg,
sweating, HR, BP
Siddall PJ, et al. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and
Management of Pain; 1998:675713.
Characteristics of Chronic Pain

Gnawing, aching, diffuse
No definite beginning or end
Varies in intensity; may remit briefly
Associated with psychological and social difficulties
Acute pain may be superimposed
Siddall PJ, et al. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and
Management of Pain; 1998:675713.
Characteristics of Peripheral Neuropathic Pain

Caused by pathologic changes in peripheral nerves
Spontaneous pain
Burning, tingling, numbness
Allodynia, hyperalgesia
Rathmell JP. Katz JA. In: Benzon H, et al, eds. Essentials of Pain Medicine and Regional Anesthesia;
1999:288294.
Assessment of Pain and Pain Relief
Patients Perception of Pain

Pain is subjective and may be influenced by:
Age1,2
Gender1
Culture2
Communication/language skills
Previous experience
1. Burns JW, et al. Anaesthesia. 1989;44:26.
2. Preble L, Sinatra R. In: Sinatra RS, et al, eds. Acute Pain Mechanisms and Management. St. Louis:
Mosby-Year Book; 1992:140150.
Benefits of Patient Preparation
Less postoperative pain1

Fewer postoperative analgesic medications
Reduced hospitalization2
1. Croog SH, et al. J Am Dent Assoc. 1994;125:13531359.

2. Boeke S, et al. Pain. 1991;45:293297.
Example of Measurement Tool for Assessing Pain

Visual Analog Scale (VAS)
No pain Pain as bad
Carr DB, et al. AHCPR Pub. No. 920032. 1992.
as it could
possibly be
Frequency of Pain Assessment

and Documentation
Preoperatively
Routinely at regular intervals postoperatively
With each new report of pain
At suitable intervals after each analgesic intervention
Carr DB, et al. AHCPR Pub. No. 92-0032. 1992.
Pain Mechanisms
The Somatosensory System

Somatosensory cortex
Frontal
cortex
Thalamus
Hypothalamus
Descending
pathway
Periaqueductal
gray matter
Ascending tracts
Midbrain
Medulla
Dorsal horn area

Noxious stimuli activate receptors in periphery
Spinal cord
Peripheral Sensitization
Cell Damage
Inflammation
Sympathetic
Terminals
Release of pain and inflammatory mediators

eg, bradykinin, H+, prostaglandins
High Threshold
Nociceptor
Low Threshold
Spinal cord
Central
sensitization
Hyperalgesia
Allodynia
Central Sensitization
Peripheral
Sensitization
Tissue Injury
Spinal cord
C-fiber output
Hyperalgesia (1, 2)
Allodynia
Activation of NMDA
receptors
Hyperalgesia
Primary
Sensitization of primary neurons threshold to noxious stimuli
within site of injury
May include response to innocuous stimuli
pain from suprathreshold stimuli
Spontaneous pain
Secondary
Sensitization of primary neurons in surrounding uninjured areas
May involve:
Peripheral sensitization
Central sensitization
Raja SN, et al. In: Wall PB, Melzack R, eds. Textbook of Pain. 4th ed; 1999:1157.
Allodynia
Pain evoked by innocuous stimuli
Central sensitization pain produced by A fibers1
Possibly mediated by spinal NMDA receptors2
1. Woolf CJ. Drugs. 1994;47(suppl 5):19.

2. Dolan S, Nolan AM. Neuroreport. 1999;10(3):449452.
Pain Mediators
Cell Damage
Aa
K+
BK
Brain
PG
Nociceptor
Spinal cord
HISTAMINE
Peptides, eg, SUBSTANCE P
Mast Cell
SEROTONIN
Aa = arachidonic acid; BK = bradykinin; PG = prostaglandin
Platelet
Role of Neurotransmitters
Excitatory
Glutamate, aspartate, ATP
Mediate afferent synaptic transmission
Inhibitory
GABA, glycine, norepinephrine, 5-HT, adenosine, Ach
Analgesia at spinal and higher levels
Altered function hyperalgesia, neuropathic or chronic
pain
GABA = -aminobutyric acid; 5-HT = 5-hydroxytryptamine (serotonin); Ach = acetylcholine
Dougherty PM, Raja SN. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional Anesthesia;
1999:79.
Role of Neuropeptides
Excitatory
Substance P, neurokinin A
Ca2+, induce sensitization, hyperalgesia
Transsynaptic transmitters
Inhibitory
Somatostatin, enkephalins, endorphins, dynorphins (?)
Modulate intracellular cAMP, K+
Act at , , opioid receptors
cAMP = cyclic adenosine monophosphate
Dougherty PM, Raja SN. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional Anesthesia;
1999:79.
Role of Prostanoids in Pain
Prostanoid Production by Cyclooxygenase (COX)

Arachidonic acid
Cyclooxygenase activity of COX
PGG2
Peroxidase activity of COX
PGH2
PGD2
PGF2
PGE2
PG = prostaglandin; TX = thromboxane
PGI2
TXA2
Prostanoids and Their Physiologic Activities

Prostanoid
PGE2
Activities/Properties
Produced in many organs, (eg, kidney,
intestinal tract)
GI mucosal protection/repair
Vasodilates
Diuresis and natriuresis
Inhibits inflammatory/ allergic cells
Thromboxane A2
Prostacyclin (PGI2)
platelet activation
intravascular platelet aggregation
smooth muscle contraction in arteries and bronchi
platelet aggregation
Vasodilates
renin release in kidney
Treatment Options for Acute Pain
WHO Analgesic Ladder

Fre
ed
can om fr
Op
om
ioid
cer
pai
to s for m
n
N evere odera
o
p
t
A n-opi ain e
dju oid
van
t
Pa
in
or pers
Op
inc
i
ioid
rea sting
f
sin
mo or m
g
i
l
N derat d to
e
o
A n-op pain
dju ioid
van
Pa
t
in
or per
inc sis
rea tin
sin g
g
No
A n-op
dju ioid
va
nt
1
World Health Organization, 1990. Used with permission.
Analgesic Options for Acute Pain Management

Opioid analgesics
Nonopioid analgesics
acetaminophen
tramadol
anti-inflammatory agents
Combination analgesic products
Local anesthetics, nerve, neuraxial blocks
Opioid Analgesics
Binding at , , receptors
Highly efficacious
May be combined with anti-inflammatory agents
Effects may be reversed
Side effects common
Pain recurrence
Fishman SM, Borsook D. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional
Anesthesia; 1999:5154.
Adverse Effects of Opioids

CNS depression, sedation
Respiratory depression
GI motility, nausea, vomiting
Urinary retention
Pruritus
Nonopioid Analgesics
Acetaminophen
Tramadol
Mechanism
of action
pain threshold
-receptor binding
inhibits re-uptake of
norepinephrine and
serotonin (5-HT3)
Adverse effects
Hepatotoxic
Opioid-like effects
Sisson CB. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional Anesthesia; 1999:5962.
Anti-inflammatory Agents
Inhibit cyclooxygenase (COX), key enzyme in
prostaglandin synthesis
Conventional anti-inflammatory analgesics inhibit
both COX-1 and COX-2 isoenzymes
COX-1 inhibition gastrotoxicity, platelet
aggregation
Some newer agents target COX-2 but do not inhibit
COX-1 at full therapeutic doses
Combination Analgesic Products

Usually two or more agents with different yet
complementary mechanisms of action
Severity of dose-related side effects may be reduced,
since lower doses of each agent are utilized
Range of side effects increased
Local Anesthetics, Nerve, Neuraxial Blocks

Na+ channel blockade
Possible interaction at pre- and postsynaptic
junctions
Tachyphylaxis
Dose-related CNS, cardiovascular toxicity
Nonpharmacologic Treatment Options for Pain

Cognitive-Behavioral
Relaxation
Preparatory information
Imagery
Hypnosis
Biofeedback
Physical Agents
Application of superficial heat and cold
Massage
Exercise
Immobilization (eg, to provide rest and maintain
alignment after musculoskeletal procedures)
Electroanalgesia (eg, TENS)
Chiropractic
Acupuncture
Carr DB, et al. AHCPR Pub. No. 92-0032. 1992.
Other Approaches
Multimodal Analgesia
An Example
Morphine
Reduced doses of each

analgesic
Potentiation
Improved antinociception
due to synergistic/additive
effects
May reduce severity of
side effects of each drug
NSAIDs,
acetaminophen,
nerve blocks
Kehlet H, Dahl JB. Anesth Analg. 1993;77:10481056.
New Approaches to Treatment of Acute Pain

Bradykinin receptor antagonist
COX-2 specific inhibition
Cytokine suppressive anti-inflammatory agents
(CSAIDs)
Neuropeptide inhibitors
Epibatidine analogues
Rang HP, Urban L. Br J Anaesth. 1995;75(2):145156.
Acute Pain Services
Management of Surgical Pain

The Unmet Needs
Pain is undertreated
Inadequate knowledge of pain management
Inadequate pain assessment
Rawal N. Anesth Pain Med. 1999;24(1):6873.

Sinatra R. In: Cousins MJ, Bridenbaugh PO. Neural Blockade in Clinical Anesthesia and Management of
Pain; 1998:793835.
American Pain Society Quality Improvement Committee. JAMA. 1995;18471880.
Acute Pain Services

Goals
Improve management of surgical pain
Promote continuing education and training of healthcare
providers
Increase awareness of importance of effective pain
management
Serve as clinical research center
Chin ML. In: Ashburn MA, Rice LJ, eds. The Management of Pain; 1998:537545.

Acute Pain: Mechanisms, Management, and Treatment Options

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