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Anesthesiology 250
ANESTHESIOLOGY 250
LEARNING MODULES

AY 2013-2014
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PAIN
Anesthesiology 250
Pain is the main symptom for which patients seek relief and is often a key
clue for diagnosis. Only recently have the mechanisms to pain have been
explained. Several theories are still being unveiled. In the past, the study
of pain and its treatment were of relatively marginal interest to medical
science and limited to anesthesiology, neurology, and a few other
specialties. Now, basic neuroscientists are rapidly expanding the
understanding of pain processing, making it possible for any interested
clinician to translate pain pathophysiology into better diagnosis and
treatment.

Pain is defined by the International Association for the Study of Pain as “an
unpleasant sensory and emotional experience associated with actual or
potential tissue damage, or described in terms of such damage.”

Types of pain
Acute pain
Pain elicited by the injury of body tissues and activation of
nociceptive transducers at the site of local tissue damage. The local injury
alters the response characteristics of the nociceptors and perhaps their
central connections and the autonomic nervous system in the region. In
general, the state of acute pain lasts for a relatively limited time and
generally remits when the underlying pathology resolves. This type of pain
is often a reason to seek health care, and it occurs after trauma, surgical
interventions, and some disease processes.

Chronic pain
It is usually elicited by an injury but may be perpetuated by factors
that are both pathogenetically and physically remote from the originating
cause. Pain extends for a long period of time, represents low levels of
underlying pathology that does not explain the presence and extent of
pain, or both. This type of pain prompts patients frequently to seek health
care, and it is rarely effectively treated. Because the pain persists, it is
likely that environmental and affective factors eventually interact with the
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tissue damage, contributing to the persistence of pain and illness

behaviors. It is also possible that, just as the brain is modified by
experience, especially in early life, the rain may alter the way noxious
information is processed to reduce or augment its effect on subjective
Anesthesiology 250
awareness.

Classification of pain
Pain can be classified based on physiologic mechanisms: visceral, somatic,
nociceptive and neuropathic.

Visceral pain
This form of pain is due to a disease process or abnormal function
of an internal organ or its covering (e.g. parietal pleura, pericardium,
peritoneum). Four subtypes are described: (1) true localized visceral pain,
(2) localized parietal pain, (3) referred visceral pain, and (4) referred
parietal pain. True visceral pain is dull, diffuse, and usually midline. It is
frequently associated with either abnormal sympathetic or
parasympathetic activity causing nausea, vomiting, sweating, and changes
in blood pressure and heart rate. Parietal pain is typically sharp and often
described as a stabbing sensation that is either localized to the area
around the organ or referred to a distant site. The phenomenon of
visceral or parietal pain referred to cutaneous areas result from patterns of
embryologic development and migration of tissues, and the convergence
of visceral and somatic afferent input into the central nervous system.
Thus, pain associated with disease processes involving the peritoneum or
pleura over the central diaphragm is frequently referred to the neck and
shoulder, whereas disease affecting the parietal surfaces of the peripheral
diaphragm is referred to the chest or upper abdominal wall.

Somatic pain
Somatic pain can be further classified as superficial or deep.
Superficial somatic pain is due to nociceptive input arising from skin,
subcutaneous tissues, and mucous membranes. It is characteristically
well-localized and described as sharp, pricking, throbbing, or burning
sensation. Deep somatic pain arises from muscles, tendons, joints, or
bones. In contrast to superficial somatic pain, it usually has a dull, aching
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quality and is less well-localized. An additional feature is that both the

intensity and duration of the stimulus affect the degree of localization.

Nociceptive Pain
Anesthesiology 250
Nociceptive pain is generally transitory in response to nociceptive
stimuli that could be mechanical, thermal, or chemical. Nociceptive pain
plays an important role and is normally present for as long as the
protection of the organism is necessary. However, in certain situations the
pain will persist even after healing of the initial injury. Clinicians are
currently unable to predict which patients will develop a persistent pain
following an acute pain, such as in the case of postsurgical pain, and
several factors are implicated. It is for this reason that early treatment of
acute pain is so important in the prevention of chronic pain.

The recommended treatments for nociceptive pain are analgesic,

NSAIDs, and sodium channel blockers. Opioids also have an important
place in the treatment of acute pain, as peripheral opioid receptors are up-
regulated following an inflammatory response. Persistent acute pain that
may have a nociceptive origin may require treatment strategies similar to
those used for neuropathic pain to prevent central sensitization.

It is important to differentiate somatogenic versus viscerogenic

nociceptive pain that can, in certain cases, present a comparable clinical
picture. It is known that referred pain from the internal organs, such as
the gut, liver, ovaries, or bladder will induce a pain perception localizing in
somatic territories, giving the impression of a purely somatic pain. For
example, pain arising in the abdominal cavity can mimic low back pain.
Appropriate diagnosis and management is dependent upon understanding
the concept of referred.

Inflammatory Pain
Inflammatory pain is associated with the healing process following
a lesion. Inflammation is a natural protective reaction of the organism
following an injury. Inflammatory substances are released into the
periphery by cells in the area of damaged tissue but cal also arise from
hyperactivity of the nociceptive neurons in the CNS, a phenomenon known
as neurogenic inflammation. In that the molecules released during
inflammation are pronociceptive, the use of NSAIDs will reduce this
nociceptive activity. NSAIDs have well-known peripheral effects, but
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inhibition of cyclooxygenase can also occur centrally in the spinal cord and
the brain, and may thereby participate in reducing neurogenic
inflammation.
Anesthesiology 250
Neuropathic Pain
Neuropathic pain is defined by the International Association for
the Study of Pain as pain arising as a direct consequence of diseases
affecting the somatosensory system. The mechanisms involved and
treatments are different depending on whether the pain, even of a
peripheral origin, is frequently associated with sensitization of the CNS.
Pharmacologic approaches to treatment of neuropathic pain aim to
reverse or reduce the hyperactivity of the nociceptive neurons. Commonly
used agents include opioids, anticonvulsants, antiarrhythmics,
antidepressants, and even NMDA receptor antagonists (eg, ketamine).

Functional Neuropathic Pain

Functional neuropathic pain is a subcategory of neuropathic pain
occurring in the absence of a defined anatomic lesion within the nervous
system, but rather representing a dysfunction of pain modulation
mechanisms. This may occur as a result of central activation of
endogenous excitatory systems that will amplify the nociceptive signal or
by a dysfunction of endogenous inhibitory mechanisms.

An example of central hyperactivity is the thalamic syndrome

following a lesion of thalamic nuclei as a result of a cerebral event. This
lesion will produce hyperactivity of thalamic neurons that are normally
inhibited by a complex interneuron network. A small lesion within the
thalamus may result in intense pain over a large body area, frequently
involving almost half of the body. In contrast, another pain syndrome,
namely fibromyalgia, may be at least partly explained by a deficit of
descending endogenous pain inhibitory mechanisms. In this condition the
hyperalgesia is related to lack of inhibition, rather than just hyperactivity
of the nociceptive neurons.

Therefore, strategies for the treatment of functional neuropathic

pain will be either focused toward reduction of nociceptive hyperactivity
or activation of endogenous inhibition. Anticonvulsants will reduce
sensory input by effect on ion channels, whereas antidepressant
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medications will augment inhibition by effect on serotonin and

noradrenergic systems.

Pain pathways and mechanisms

Anesthesiology 250
Transmission
A conscious experience of pain generally requires signaling by two
neurons in sequence. The peripheral nociceptor has specialized tissue
endings that transducer strong mechanical, thermal, or chemical stimuli
into action potentials. This nerve fiber, which is nourished by a cell body in
the dorsal root ganglion in the spinal canal, sends its central process into
the dorsal horn of the spinal cord to synapse on a secondary neuron. The
peripheral neuron releases excitatory neurotransmitters, such as
glutamate and substance P, which cause the secondary neuron t discharge,
sending impulses into its projections to the brain stem and thalamus.
Projection of nociception to this level is sufficient to evoke pain experience
and behavior. Additional processing by projections to the cerebral cortex
contributes to the distinct sensory qualities, mood, and motor responses
associated with the pain experience.

Modulation
There is not a one-to-one correspondence between a peripheral
lesion and the experience of pain. Such reflections led to the hypothesis
that higher brain centers could modulate incoming pain signals. Animal
studies have elucidated systems that descend to the spinal dorsal horn and
can wither inhibit or can amplify pain signals, depending on the
importance of pain to the organism in that situation. Neurophysiologic
studies I nonhuman primates whose state of attention is modified during
painful stimulation suggest mechanisms by which a variety of clinical
interventions, such as reassurance, cognitive-behavioral therapy, and
placebo effects associated with drug treatment, may not only change
patients’ interpretation of incoming pain messages but also markedly
decrease the number of pain impulses arising at the spinal dorsal horn
projection neuron.

Plasticity of Pain-Processing Circuits

Injuries to peripheral tissues of nerve and the resulting input alter
subsequent pain processing. In the uninjured state, noxious and
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innocuous stimuli trigger modest numbers of impulses in nociceptors and

A mechanoreceptors. Only the noxious stimuli result in pain. After injury
to any kind of tissue, release of inflammatory mediators, such as
Anesthesiology 250
prostaglandins, cytokines, bradykinin, and protons, sensitizes nociceptors
so that light touch can trigger impulses in these fibers, and noxious stimuli
cause higher rates of firing than before. If nerve is injured, new sodium
channels at sites of repair or regeneration give rise to spontaneous
discharges, which can lead to steady or episodic pain in the absence of
peripheral stimulation. In some cases, adrenoreceptors at the injury site
trigger pain when activated by norepinephrine released by local
sympathetic nerves or by circulating catecholamines. A barrage of painful
impulses from injured nerve or tissue can sensitize the central neuron so
that light touch signals carried by A fibers can trigger a central discharge
can trigger a central discharge sufficient to generate pain. Additional
mechanisms have been described in animal to explain the development of
pain with light touch. One day or more after tissue injury, A
mechanoreceptors may begin to make a neurotransmitter, substance P,
that is otherwise confined to pain-signaling fibers and excites central pain
projection neurons. After nerve injury, A mechanoreceptors, which
normally synapse in a deep layer of the spinal cord that processes light
touch, may grow new sprouts that synapse on pain projection neurons in
the superficial dorsal spinal cord.

Overlapping Inputs
Proximal limbs, trunk, and viscera have heavily overlapping input
on a few spinal neurons. Patients’ description of pain arising from many of
these structures may be similar. The nociceptors from the heart,
esophagus, and deep tissues in the left shoulder and chest wall may
synapse on the same spinal dorsal horn neuron. Noxious chemical
stimulation of the heart (by ischemia) or esophagus (acid) may be
described as pain in the left shoulder and proximal arm and the chest,
whereas inflammation of the left chest wall may be perceived as deep
visceral and local musculoskeletal pain. Patients with chest wall or
esophageal inflammation present with sudden overwhelming chest pain
indistinguishable from that described by patients with myocardial
infarction and require hospitalization until electrocardiograms, caridiac
enzymes and other test results exclude cardiac ischemia. Similar
interactions among noxious stimuli may occur in pelvic disease. In women
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with chronic renal stones, attacks of colic severe enough to require

hospitalization tend to occur near the time of menses. Sensory studies
show sensitization to stimulation of muscle fibers whose afferents feed
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into the same spinal segment as those that subserve uterine and renal
pain. Disease in proximal body parts may refer to other parts of a limb.
Bone and soft tissue disease in the spine often refers pain to the buttock
or hip, and disease in the hip often refers pain to the knee.

GUIDE TO CLINICAL ASSESSMENT OF PAIN

1. Believe the patient’s complaint of pain.
2. Assess the characteristics of each pain, including site, referral
pattern, and aggravating and relieving factors.
3. List and prioritize each pain complaint.
4. Evaluate the response to previous and current analgesic therapies.
5. Assess the patient’s current level of functioning in work and family
life, including what his or her priorities are for increasing function.
6. Record the severity of pain and functional impairment with a scale
simple enough for repeated use.
7. Evaluate the psychological state of the patient, asking specifically
about suicidal thoughts.
8. Ask if the patient has a past history of alcohol or drug dependence.
9. Develop a series of diagnosis-related hypotheses.
10. Personally review the diagnostic procedures.
11. In patients with multiple chronic symptoms that are unexplained
despite a full diagnostic evaluation, consider the possibility of
multisomatoform disorder.
12. Reassess the patient’s response to pain therapy
13. In patients with advanced illness, discuss advance directives for
managing pain and other symptoms.
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TREATMENT
PHARMACOLOGIC TREATMENT OF PAIN:
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There are three classes of analgesic drugs:
1. Non-opioid analgesics --- acetaminophen, NSAIDs,
selective cylcooxygenase-2 inhibitors
2. Opioid analgesics
3. Miscellaneous analgesics --- including some antidepressant
and anticonvulsant drugs

Non-opioid analgesics
The chief advantage of non-opioid analgesics is that they do not
cause sedation or other central nervous system side effects. Unless the
patient has contraindications to these drugs or has been shown not to
respond to several of them, any analgesic regimen should include a non-
opioid drug even if pain is severe enough to require the addition of an
opioid. Acetaminophen optimally is prescribed in doses approaching 4000
mg/day. Higher doses, or standard doses in patients who are fasting or
who drink alcohol heavily, may cause hepatic necrosis. Acetaminophen
lacks the antiplatelet or gastric erosive effects of the NSAIDs. NSAIDs and
COX-2 inhibitors often provide better analgesia than acetaminophen,
although the possible cardiovascular risks of COX-2 inhibitors must be
considered.

Opioid analgesics
The  receptor opioid agonists include morphine, codeine,
oxycodone, hydrocodone, fentanyl, hydromorphone, methadone, and
meperidine. More than a century of research has failed to reveal
significant differences in the relative ratios of analgesia to side effects
offered by different members of this class, although clinical anecdote
suggests that individual patients may responds to one drug better than to
another. The one exception is meperidine, which has a toxic metabolite
that accumulates after several days of treatment and causes myoclonus,
anxiety, and with higher doses, confusion and seizures. The key
differences among the available opioids are in speed of onset and duration
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of action. Tramadol is an opioid-like drug that has weak opioid analgesic

properties and opioid-like side effects of sedation and nausea, but it is less
constipating and has less risk of abuse than the  receptor agonists.
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CLASSIFICATION OF OPIOIDS
Naturally occuring Morphine
Papaverine
Codeine
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Thebaine
Semisynthetic Heroin
Hydromorphone
Buprenorphine
Oxycodone
Synthetic Morphinan series (levorphanol, butorphanol)
Diphenylpropylamine series (methadone)
Benzomorphinan series (pentazocine)
Phenylpiperidine series (meperidine, fentanyl,
sulfentanil, alfentanil)

ALTERNATIVE CLASSIFICATION OF OPIOIDS

CLASS DEFINITION EXAMPLE
A drug that, when bound to the Morphine
receptor, stimulates the
Agonist receptor to the maximum level;
by definition, the intrinsic
activity of a full agonist is unity.
A drug that, when bound to the Naloxone
receptor, fails to completely
produce any stimulation of that
Antagonist
receptor; by definition, the
intrinsic activity of a pure
antagonist is zero.
A drug that, when bound to the Buprenorphine
receptor, stimulates the (partial  agonist)
receptor to a level below the
Partial agonist maximum level; by definition,
the intrinsic activity of a partial
agonist lies between zero and
unity.
A drug that acts simultaneously Nalbuphine (partial 
Mixed agonist-
on different subtypes, with the agonist,  agonist, 
potential for agonist action on antagonist)
antagonist
one or more subtypes and
antagonist action on another.
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Adjuvant drugs:

1. Anticonvulsants
Anesthesiology 250
In chronic nerve injury, there is redistribution and alteration of subunit
compositions of sodium and calcium channels resulting in spontaneous
firing at ectopic sites along the sensory pathway. Sodium channel blockers
inhibit spontaneous activities at neuromas, dorsal root ganglia, and at the
dorsal horn of the spinal cord. The anticonvulsants block sodium channels,
explaining their efficacy in convulsions and in neuropathic pain syndromes.
Other drugs directly block calcium channels. Randomized controlled
studies showed the efficacy of anticonvulsants in the following
neuropathic pain syndromes: a) trigeminal neuralgia – carbamazepine and
lamotrigine; b) postherpetic neuralgia (PHN) – gabapentin and pregabalin;
c) diabetic painful neuropathy (DPN) – gabapanetin, pregabalin,
topiramate; d HIV polyneuropathy – lamotrigine; e) phantom limb pain –
gabapaentin; f) spinal cord injury pain – gabapanetin; g) central poststroke
pain – lamotrigine; h) Guillain-Barre Syndrome – gabapentin; and, i) mixed
neuropathic pain – gabapentin, valproic acid.

2. Selective Serotonin Reuptake Inhibitors (SSRIs)

The antinociceptive effect of SSRIs appears to involve serotonergic as well
as opioidergic (e.g. paroxetine) systems. In diabetic painful neuropathy,
SSRIs, especially fluoxetine, appears to be less effective than amitriptyline
or desipramine. SSRIs appear to be of little benefit in fibromyalgia.
Although their side effects are less, SSRIs are less effective than TCAs in the
management of pain.

3. Serotonin-Norepinephrine Reuptake Inhibitors

(SNRIs)
SNRIs block the reuptake of serotonin and norepinephrine, with duloxetine
and venlaflaxine having increased selectivity for serotonin. Venlafaxine
and duloxetine have been shown to have an analgesic affect in the nerve
constriction model of neuropathic pain. Duloxetine is effective in diabetic
painful neuropathy and in fibromyalgia and have a good safety profile for
long term use. Venlafaxine is also effective in fibromyalgia.
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NERVE BLOCKS:
Anesthesiology 250
Nerve blocks useful for pain include somatic peripheral nerve blocks,
intravertebral central neural blocks, and sympathetic blocks. They can be
spectacularly effective in acute pain relief, they are used to interrupt the
transmission of nociceptive stimuli from the peripheral to the central
nervous system. Because mechanisms of chronic pain are frequently
different from those of acute pain, nerve blocks may be less affective in
chronic pain states. Nevertheless, they still have an important part to play
in the diagnosis, prognosis, and sometimes therapy of chronic pain.
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TREATMENT GUIDELINES
The following principles may be used as a guide in tailoring of a treatment
Anesthesiology 250
regimen to the needs of an individual patient.

Individualize the route, dosage, and schedule

Routes of administration

Intravenous (IV) bolus

IV bolus provides the most rapid onset of effect and clarity of
titration. Time to peak effect varies with drug lipid solubility, ranging
from 1 to 5 minutes for fentanyl to 15 to 30 minutes for morphine.
Although morphine is the traditional treatment for the pain of acute
syndromes, its slow penetration into the brain may delay the onset of
pain relief and predispose toward relative overdosage 1 to 2 hours
later. Opioids with long elimination half-lives, such as methadone and
levorphanol, are not recommended for rapid opioid titration because
drug levels remain elevated for many hours if too high a dose is given.

Intravenous (IV) infusion

Continuous IV infusions provide steady blood levels, which
should provide the most effective analgesia with the fewest side
effects.

Subcutaneous (SC) infusion and bolus

Subcutaneous infusion is an alternative to IV infusion and
produces equivalent blood levels at steady state. Subcutaneous
boluses have slower onset and offset, and a lower peak effect than IV
boluses.

IV, patient-controlled analgesia

A popular method and effective method for treating severe
acute pain is to titrate the patient to temporary comfort with IV
boluses, then start a patient-controlled analgesia machine. Usual
patient-triggered bolus doses of morphine are 0.5 – 2 mg every 5 -10
minutes.
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Trandermal
Fentanyl is available is a transdermal drug delivery system,
providing a steady opioid infusion without pumps or needles. Several
clinical trials suggest that constipation is reduced by use of the
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transdermal route, which avoids the local slowing effects of opioids in
the gut. There is a 12 – 24 hour lag to analgesia after initial application
of the patch as opioid is transferred to subcutaneous fat and 24-hour
offset after the patch is removed. Temperature higher than 39oF or a
local heating pad accelerates absorption and may cause overdose.

Oral transmucosal
Oral transmucosal fentanyl citrate is absorbed rapidly through
the oral mucosa, giving this route a rapidity of onset comparable to IV
morphine.

Rectal suppositories
Suppositories of hydromorphone, oxymorphone, and
morphine are available and well absorbed but are used rarely because
of patients’ preferences.

Administer analgesic(s) round-the-clock if the pain is present most of the

day.

Clinicians often begin opioid therapy with preparations that

combine acetaminophen or an NSAID with small doses of codeine,
hydrocodone or oxycodone. Data from single-dose postoperative pain
studies suggest that the following doses have similar effects: codeine
60mg, hydrocodone 10mg, oxycodone 7mg, and tramadol 50mg. In pain
too severe to respond to these moderate opoioid doses, treatment may be
started with an immediate-release preparation of one of the opioids.
When the optimal dose requirements for a 24-hour period have been
established by titrating with a short-acting opioid preparation, the
analgesics can be administered on a scheduled around-the-clock asis with
better pain relief and fewer side effects. An as-needed (PRN) order for a
supplementary opioid dose between regular doses is an essential back-up.
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When changing to a new opioid or a different route, first use the

equianalgesic doses to estimate the new dose, then modify the estimate on
the basis of the clinical situation and the specific drug.
Anesthesiology 250
Changing from one opioid to another in patients already receiving
moderate to large doses can be challenging. Estimates must take into
account the wide interindividual variability, any difference in the time
course of absorption and metabolism, the expected course of the pain
condition, and the possibility of incomplete cross-tolerance between
opioids. For this reason, the general recommendation is to convert only
half of the dose of the old opioid to the new opioid at one time, in case the
estimate is too high or too low for that patient.

Anticipate and treat opioid side effects

Sedation, constipation, nausea, itching, and respiratory depression

are the most common side effects, and may be treated by changing the
dosing regimen to provide lower or more steady blood concentrations, by
switching to a different opioid, or by adding a treatment that counteracts
the adverse effect. Sedation may be counteracted partly by adding a
stimulant such as caffeine, dextroamphetamine (2.5 -10 mg PO), or
methylphenidate (5 – 10 mg PO). To prevent constipation, patients should
be given stool softeners and agents to increase bowel motility. A useful
regimen includes dioctyl sodium sulfoccinate (100 – 300 mg/day)
combined with senna (2 – 3 tablets 2x a day), laxative suppositories, or
lactulose. Opioid-related nausea and vomiting often abate after the first
few days of treatment but may be treated with transdermal scopolamine,
hydroxyzine, or phenothiazine antiemetic. Although respiratory
depression is rare in patients receiving opioid treatment long term, even
when doses are increased, it is a risk in the treatment of opioid-naïve
patients who require high opioid doses for severe pain. When pain is
relieved, the patient may fall asleep, which considerably augments the
opioid depressant effect. If an opioid antagonist is required to reverse
respiratory depression or coma in a patient on long-term opioids, the
physician must be aware that these patients are exquisitely sensitive to
antagonists. Expert often start with small doses of naloxone (e.g. one
twentieth of a 0.4mg ampule IV every 2 minutes).
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References:
Anesthesiology 250
Marchand S. Physiology of Pain Mechanisms: From the Periphery to the
Brain. Rheum Dis Clin N Am 34 (2008) 285-309
Bonica J. Management of Pain. 3rd ed
Longnecker D, Brown D, Newman M, Zapol W. Anesthesiology.
Raj P. Pain Medicine: A Comprehensive Review
Benzon H. Pharmacological Treatment of Pain. ASA 2006 Refresher Course
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CANCER PAIN
Introduction
Anesthesiology 250
Pain is one of the most common and dreaded symptoms associated with
cancer. It occurs in one-quarter to one-half of patients with newly
diagnosed malignancies, in one-third of those undergoing treatment, and
in more than three-quarters with advanced disease. Overall, 75% of
patients with cancer experience pain severe enough to require treatment
with opioids during their illness. Unrelieved pain directly affects patients’
daily activities, quality of life, and psychologic status.

Cancer pain is associated with disease progression as well as treatments

and co-existing diseases. Types of pain the patients may feel depends
largely on the progression of their disease. Therapy is always developed
and adjusted based on patients’ needs.

Classification of Pain
In principle, pain results from stimulation of nociceptors or by lesions of
afferent nerve fibers.

1. Nociceptive Pain – mechanism of pain is related to ongoing tissue

pathology
 Somatic
 Associated with tissue damage and results from
activation of nociceptors in either peripheral or deep
tissues
 Pain transmission is by C and A delta fibers from the
periphery to various parts of the midbrain and neocortex
 Quality of pain is described as well localized, aching, or
gnawing
 Bone pain and post-surgical pain are common examples
 Visceral
 Associated with stretching, compression, invasion, or
distention of visceral structures and visceral nociceptors
are activated
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 Pain is poorly localized because C mediated pain fibers

enter on both sides of the spinal cord through the
autonomic ganglia
 Quality of pain is described as deep, squeezing, crampy,
Anesthesiology 250
and colicky
 Referred pain is a sviscerosomatic pain, eg shoulder
complaint when disphragm is invaded with liver tumor,
which causes nausea and vomiting
2. Neuropathic pain
 Pain that stems from injury to neural tissues and aberrant
somatosensory processing in the peripheral or in the
central nevous system
 Can result from direct injury to neural tissues from tumor
infiltration, erosion, or from cancer therapies
 Described as noxious and intractable pain
 Associated sensory, motor, and autonomic deficits can
accompany symptoms of burning, squeezing, and
paroxysmal sharp pain
 Examples: brachial and lumbar plexopathies and
peripheral neuropathies like post thoracotomy pain
syndrome

Patterns of Cancer Pain

Breakthrough pain refers to sudden increases in the base level of pain or
different but recurring pains. The majority of breakthrough pains are
usually associated with tumor or its treatment.

Incident pain is pain directly related to an event or activity, such as bed

turning, weight bearing, bowel movement, etc. it is often defined and
predictable, and is anticipated by the physician and treated
prophylactically.

End of dose failure is pain that emerges because too much time has
elapsed between medications. This is predictable and readily preventable
by using time-contingent dosing at appropriate intervals.
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Spontaneous pain occurs without relationship to a particular event or

procedure. These pains are more difficult because of their unpredictable
nature and their often fleeting character. In some cases, adjunctive
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analgesics effectively provide relief.

Pyschogenic pain is judges o be a manifestation of a psychiatric disorder –

a somatoform disorder, such as a pain disorder, associated with a
psychological component.

Steps in Cancer Pain Management

Clinical Assessment
 Directly influences success or failure of treatment
 Initial treatment should be based on pain etiology and type of pain
 Detailed analysis of pain condition in each patient should form the
basis of rational therapy
History and Physical Examination
 Include a complete neurological examination
 Elicit site, character, duration of pain
 Review past medical history and previous therapeutic measures
done
 Take into account constitutional symptoms, eg insomnia,
depression, fatigue, anxiety, anger, anorexia, and side-effects of
therapeutic intervention such as nausea, vomiting, dysphoria,
headache, pruritus, constipation, and light-headedness
Diagnostic Testing
 Based on clinical assessment, history, and PE
Set Treatment Goals and Establish Treatment Plan
 Based on patients’ expectations of treatment and physician-
patient agreement
Reassessment of Therapy on Subsequent Visits
 Elicit side effects and potential for abuse
 Re-evaluation of treatment goals

Treatment
Pharmacologic Strategies for the Control of Tumor Pain

1. Select the appropriate analgesic drug

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2. Prescribe the appropriate dose

3. Administer the drug by the appropriate route
4. Schedule the appropriate dosing interval
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5. Prevent persistent pain and treat breakthrough pain
6. Titrate the dose of drugs aggressively
7. Prevent, anticipate, and manage drug side-effects

Principles of Pharmacotherapy

1. By mouth
 When possible, patient should take analgesics per orem
 Alternative routes such as rectal, transdermal, sublingual,
and parenteral administration may better serve patients
with dysphagia, uncontrolled vomiting, or GI obstruction
2. By the clock
 Patients with continuous pain should take analgesic
medications at fixed intervals of time
 Dose of analgesic drugs should be titrated based on the
patient’s pain
 The patient must take the next dose before the effect of
the previous dose has fully worn off
 Some patients may need to take rescue doses for incident
and breakthrough pain, in addition to regular schedules
3. By the ladder
 WHO
stepladder
for cancer
pain
developed
in 1985
 Use only 1
drug from
each group
at the same time

Treatment modalities include:

1. Pharmacologic therapy:
a. Opioids
 Page 22 of 32

b. NSAIDs
c. Serotonin antagonists
d. Anti-epileptics
e. Antidepressants
Anesthesiology 250
f. Regional Technique
2. Regional Technique
a. Ganglion / Plexus Block
b. Intraspinal therapies
c. Epidural therapies
3. Nonpharmacologic therapy
a. Surgical procedures
4. Alternative Medicine
a. Massage
b. Acupuncture
 Page 23 of 32

Anesthesiology 250 LOW BACK PAIN

Introduction
Low back pain is a common complaint in any nation. It is a major cause of
health care consumption and by far the most common reason for disability
in the working years. It is the most common cause of activity limitation in
the working years. Synonyms include lumbago and lumbalgia.

Lifetime prevalence of low back pain exceeds 70% in industrialized nations.

It occurs in all ages, and about half the population will report back pain
over a 12-month period. Peak prevalence is between 45-59 years, but it is
common in the young and the elderly. The first episode of back pain is
likely to occur between ages 20-40 years.

Characteristics
Back pain is usually due to benign, mechanical causes with acute
symptoms settling within a month in more than 90% of patients.
Indicators or red flags for the presence of a more serious condition include
neurologic deficits, pain that worsens with rest, history of malignancy, or
unexplained systemic symptoms (e.g. weight loss) and/or signs (e.g. fever).
Investigations are only indicated if there is clinical suspicion of underlying
serious pathology, or if the symptoms persist in spite of adequate
treatment for a significant period of time.

There are many different causes of back pain. Back pain due to benign,
mechanical causes often presents with pain in the lumbosacral region that
is aggravated with movement. Radiation of the pain into the buttock or
posterior thigh may be present.

History may include the following:

 Pain in the lumbosacral region
 It is usually in the midline or just off the midline
 The pain may radiate into the buttock, groin, or posterior aspect of
the thigh - often described as sciatica as this is the general course
of the sciatic nerve
 Page 24 of 32

 Often follows an episode of bending, twisting, and lifting

 May have been preceded by a period of aching and stiffness in the
back that lasted a few days

Anesthesiology 250
Often associated with numbness and paresthesias in one of the
lower limbs

Physical examination may reveal the following:

 Limitation of all spinal movements due to pain
 Lateral scoliosis may be present due to spasm of the paraspinal
muscles on one side
 Points of localized tenderness may be detected
 Severe limitation of straight leg raising, more pronounced on the
affected side (the leg is raised passively by the examiner with the
knee extended, with reproduction of symptoms extending below
the knee; this is normally pain free until at least 70°)
 Positive sciatic stretch test (passive dorsiflexion of the foot while
performing straight leg raising reproduces the patient's pain).
 The patient may have dermatomal sensory changes
 Motor weakness due to nerve root compression
 Distended bladder due to urinary retention, saddle anesthesia, and
a lax anal sphincter indicate cauda equina syndrome. If present,
indicates a surgical emergency.

Identification of red flags of potentially dangerous conditions or looking

for neurologic deficits in patients with leg symptoms or identifying a
structural deficit that might require attention before definitive treatment
begins is important. Enumerated below are the red flags:

Possible fracture
 Major trauma, such as from a vehicular accident or fall from a
height
 Minor trauma or even strenuous lifting in an older or potentially
osteoporotic patient
Possible tumor or infection
 Age over 50 or under 20
 History of cancer
 Constitutional symptoms
 Page 25 of 32

 Risk factors for spinal infection: recent bacterial infection, IV drug

abuse, or immune suppression
 Pain that worsens when supine; severe nighttime pain
Anesthesiology 250
Possible Cauda Equina Syndrome
 Saddle anesthesia
 Recent onset of bladder dysfunction, such as urinary retention,
increased frequency, or overflow incontinence
 Severe or progressive neurologic deficit in the lower extremity
 Unexpected laxity of the anal sphincter
 Perianal/perineal sensory loss
 Major motor weakness: quadriceps (knee extension weakness),
ankle plantarflexors, evertors, and dorsiflexors (foot drop)

Diagnosis may be made on history and PE alone, and no special study is

needed in the absence of red flags. Ancillary procedures available include
laboratory studies such as sedimentation rate and urine analysis, bone
scans, EMG, somatosensory evoked
potentials, X-ray, CT scan, MRI, CT-
myelogram, and discogram.

Pathophysiology
The vertebra has three primary
structures: the body, the neural
arches, and the bony process. The
bodies are connected by inter-
vertebral discs with supporting
anterior and posterior longitudinal
ligaments. The neural arches are
joined by the facet joints. The
stability of the spine not only relies on
the ligamentous structures by also on the extensive muscular structures
surrounding it.

It is important to remember that the cervical nerve roots pass above the
same numbered vertebral body, and the C8 nerve root passing above the
T1 vertebral body, and there after all nerve roots pass below the same
 Page 26 of 32

numbered vertebral body. It should also be noted that the spinal cord
ends at L1 and that from this point on, each nerve root runs as its own
distinct entity with the higher nerve roots being more lateral in the spinal
Anesthesiology 250
canal than the lower nerve roots (ie the L2 nerve root is more lateral than
the L5 nerve root).

The figure depicts the different structures one would expect in the lumbar
spine. However, not all structures would be centers for pain generation.
Impingement and inflammation of any structures may produce low back
pain.

Treatment
Goals for treatment of patients with low back pain include relief of pain
and inflammation and improve functioning and limit impact of pain on
lifestyle. Remember, never start treatment without investigating further if
there is a possibility of the back pain being caused by a potentially serious
condition.

Therapeutic
1. Pharmacologic therapy:
a. Paracetamol/ Acetaminophen
b. Muscle Relaxants
c. NSAIDs
d. Antidepressants and anticonvulsants for the neuropathic
component
e. Opiods for severe pain
2. Nonpharmacologic therapy
a. Exercise and activity - Bed rest provides no benefit to
patients who have acute low back pain with or without
sciatics
3. PT/OT modalities
i. Heat therapy (hot pads or ultrasound)- studies
show no significant improvement
ii. Electrical therapy eg. TENS- controversial
4. Alternative Medicine
a. Massage – few trials done, none showed significant
improvement
b. Acupuncture – no trial showed (+) benefit
 Page 27 of 32

FIBROMYALGIA SYNDROME
Introduction
Anesthesiology 250
Fibromyalgia syndrome (FMS) is a subjective disorder of vague
musculoskeletal pain which the physician could not objectively document
on examination nor confirm with laboratory testing. This is often
characterized as widespread body pain accompanied by remarkably
consistent tenderness to palpation at soft tissue body sites referred to as
tender points (TePs), long duration morning stiffness, and inefficient sleep.
The adult population is most commonly affected, between 18-30 years of
age, with women more commonly affected than men. In children, the
gender distribution is approximately equal.

Characteristics
The most prominent symptom of FMS is chronic, widespread pain in soft
tissue regions such as the muscles, ligaments, bursae, and tendons, but
does not involve the synovial joints directly. The pain has been
characterized as persistent, diffuse, deep, aching, throbbing, sometimes
stabbing pain associated with distal extremity dysesthesia.
Enumeration of the criteria for diagnosis of FMS is as follows:

1. History of widespread pain present for at least 3 months. Pain is

considered widespread when all of the following are present:

 Pain on both sides of the body, above and below the waist
 Axial skeletal pain must be present (cervical spine, anterior
chest, thoracic spine, or low back)
 Pain in 11 of 18 tender point sites on digital palpation
 Patient must state that the palpation is 'painful'; 'tender'
does not qualify

2. Presence of 11 out of 18 anatomically defined TePs which are

paired and bilateral as delineated by the American College of
Rheumatology:

 Occiput: at the suboccipital muscle insertion

 Page 28 of 32

 Low cervical: at the anterior aspects of the intertransverse

spaces at C5-7
 Trapezius: at the midpoint of the upper border
Anesthesiology 250
 Supraspinatus: originating above the scapula spine near
the medial border
 Second rib: at the second costochondral junctions
 Lateral epicondyle: 2 cms distal to the epicondyles
 Gluteal: in upper outer quadrants in anterior fold of
muscles
 Greater trochanter: posterior to the trochanteric
prominence
 Knee: at the medial fat pad proximal to the joint line
The pathognomonic physical finding of multiple TePs in FMS can be elicited
by pressing applying 4kg of pressure on an area of approximately 1 cm2.
TePs are distinctly different from trigger points. TePs hurt locally when
pressed and do not refer pain. Trigger point is a regional phenomenon
which refers pain to a symptomatic zone of reference, which is usually
more distal.

Pathophysiology
The exact pathophysiology of FMS is still unknown. Theories regarding its
etiology have undergone a transition from a psychiatric process, as it is
sometimes viewed, to a muscle disorder, as it is currently classified in the
Medline index, to a genetically determined CNS disorder of nociception
and neuroendocrine dysfunction as it probably should be considered.
Hypothesis include the following:
 Changes in muscle tissue at the cellular level, including
changes in blood flow
 Changes in peripheral nociceptors leading to increased
perception of pain
 Changes in the perception of pain secondary to
dysfunction of the central nervous system. Abnormal
function of the hypothalamic-pituitary-adrenal (HPA) axis
may result in abnormal pain perception via
neurohormonal dysfunction
 Page 29 of 32

 Immunologic abnormalities (fibromyalgia has been noted

after infections with coxsackievirus, parvovirus, HIV, and
Lyme disease in up to 55% of fibromyalgia patients)

Anesthesiology 250
Physical injury or tissue trauma such as surgery (between
14% and 23% of fibromyalgia patients become
symptomatic after trauma or surgery)
 Psychological distress and a somatic manifestation of
depression

Treatment
Treatment of fibromyalgia is symptomatic. No one medication can treat
the disease. Treatment, as with that of other chronic diseases, in an
ongoing process rather than management of a single episode.

1. Pharmacologic therapy:
a. Antidepressants and anticonvulsants for the neuropathic
component
b. Muscle Relaxants
c. Paracetamol/ Acetaminophen
d. NSAIDs – not first-line therapy
2. Nonpharmacologic therapy
a. Adequate sleep
b. Exercise – increase TePs threshold
c. Massage – increase TePs threshold
 Page 30 of 32

Anesthesiology 250 MYOFASCIAL PAIN SYNDROME

Definition
Myofascial pain syndrome (MPS) or muscular rheumatism, myelogelosis,
interstitial myofibrositis or fibrositis is muscle pain and/or autonomic
phenomena associated with stimulation of active myofascial trigger points.
A trigger point is a hyperirritable focus within a tight band of skeletal
muscle which is painful on compression and can evoke referred pain and
or autonomic responses. The referred pain may present in a distant area of
the body and does not necessarily follow any segmental or neurological
pattern of distribution, but often is found at the same dermatome.
Autonomic phenomena may include pallor, hyperemia, lacrimation and
coryza, (pilomotor activity) gooseflesh or increased sudomotor activity.

Most patients are between 31-50 years old. Women who are sedentary
are of greatest risk. Pain is not life threatening but MPS is a debilitating
and costly disease because of decrease in productivity as well as the
expense of treatments.

Characteristics
Trigger points are sharply circumscribed spots of exquisite tenderness
within a taut band. The pain is typically out of proportion to the pressure
applied and finger pressure elicits a “jump” and cry out called a “jump
sign.” They are directly activated by excessive movement, muscle fatigue
from excessive repetitive motions, direct trauma, chilling, visceral disease,
arthritic joints, emotional distress or by another trigger point. It can be
aggravated by postural stresses such as misfitting furnitures, poor posture
and abuse of muscles by poor body mechanics such as leaving a muscle in
a shortened position for a period of time (eg. sleeping). The pain might
outlast the triggering event because even though tissue injury heals, the
muscles learn to “avoid” pain. It may also cause stiffness of the involved
muscle especially after a period of inactivity because of a central inhibition
to protect the muscle from painful contractions.

History may include the following:

 steady, deep, aching and occasionally lancinating and sharp pain
 augmentation of pain by strenuous use of muscles, passive stretch,
pressure on trigger points, cold weather, viral infections, marked
nervous tension
 reduction of pain by short period of rest, slow passive stretching,
warm moist heat applied on trigger point
 Page 31 of 32

 possible limitation of motion especially in the morning (after the

muscle has been left in a shortened position for a period of time)
 association with vasomotor symptoms (lacrimation, nasal
secretions, pilomotor activity, etc)
Anesthesiology 250
 awareness of weakness of certain movements (muscles learn to
limit the movement below the pain threshold of the trigger point)
 might be associated with depression and sleep disturbances

Physical Exam may reveal:

 observe for abnormal patient mobility and changes/poor posture
 observe for restriction in range of motion and weakness during
active and passive motion in all directions of movement
 cutaneous signs. demographia may be found in the skin overlying
muscles with active trigger points

Pathophysiology
Trigger points develop in a particular area in a braced, stressed muscle or
fascia which is more sensitive than the surrounding tissue either from
genetic susceptibility or previous injury. When this area is fatigued, it
begins to signal its distress to the central nervous system which results in
various responses. Muscles surrounding the area associated with the
trigger points becomes more tense. Sympathetic responses results in
vasoconstriction which might lead to ischemia or vasodilaton which might
lead to increased release of analgesic agents (bradykinin and
prostaglandins), osmotic and pH changes which might increase the activity
of the nociceptors around the area of the trigger point. This increased
nociceptor input results in further motor and sympathetic responses which
creates a vicious cycle of pain.

Treatment
Goals of treatment include resolution of the myofascial pain syndrome by
interruption of the pain cycle by eliminating the trigger point, restoring
tissue mobility and returning the functional capacity of the patient by
relieving the pain.

Treatment modalities include:

1. Pharmacologic therapy:
a. Paracetamol/ Acetaminophen
b. Muscle Relaxants
c. NSAIDs
 Page 32 of 32

d. Antidepressants and anticonvulsants for the neuropathic

component
e. Opiods for severe pain
2. Nonpharmacologic therapy
Anesthesiology 250
a. Dry needling (insertion of a needle in the trigger point area
followed by manipulation of needle till there is relief or
softening of the taut band. This is also called myofascial
release)
b. Injection technique (injection of local anesthetics, steroids,
saline or botulinum toxin into the trigger point)
3. Exercise (used to correct muscle imbalance and restore normal
strength and flexibility)
4. PT modalities
a. Heat therapy (hot pads or ultrasound)- increases blood
flow and tissue distensibility, relieves muscle spasm and
pain
b. Electrical therapy eg. TENS- improves vascular circulation
and eliminates inflammatory byproducts; relieves edema
and muscle spasm
c. Stretch and spray- spraying vapocoolant to inactivate
trigger point resulting in pain and spasm relief thereby
facilitating stretching
5. Alternative Medicine
a. Massage
b. Acupuncture