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290 Simon K.C. CHAN, Alice K.Y. MAN
As acute pancreatitis is accompanied by persistent
severe pain which may have potential adverse effect,
analgesia is considered to be crucial in managing
patients with acute pancreatitis and buprenorphine
is recommended [80]. However, when potent
opioid is required, there is always concern for the
effect of opioid on the pressure of the sphincter
of Oddi. In a recent review by ompson [82],
it was noted that all opioids including pethidine
increase the pressure of the sphincter of Oddi, but
there is no evidence to indicate that morphine
is contraindicated in acute pancreatitis. Hence,
morphine is considered to be more appropriate
than pethidine as it provides a longer duration of
analgesia without the risk of norpethidine-induced
seizure [82].
Although various invasive pain relief procedures
have been described, they are rarely used in the
clinical setting because of potential cardiovascular
instability and sepsis.
Chronic pancreatitis
Background
Chronic pancreatitis (CP) is a progressive
inflammatory process of the pancreas leading
eventually over years to fibrotic destruction of
the pancreas resulting in exocrine and endocrine
insufficiency. Although other symptoms may
also occur, pain is a prominent symptom and at
least 85% of patients with CP will develop pain
at some time during the course of the disease; as
there is no definitive treatment to counteract the
inflammatory process[4], pain control becomes an
important element in the management of CP.
Aetiology and pathophysiology
e incidence of CP was estimated to be between
7.7 and 8.2 per 100,000 per year with an overall
prevalence of 27.4 cases per 100,000 in a population
[49, 73]. e commonest cause of CP is alcoholism
(70–80%), followed by idiopathic CP (20%).
Some other rare causes include genetic mutation,
hyperparathyroidism, trauma or autoimmunity.
It was previously thought that acute pancreatitis and
CP were two separate disease entities with different
pathophysiological mechanisms, but there is now
increasing evidence that alcoholic acute pancreatitis
and CP are different stages of the same disease
entity (sentinel acute pancreatitis event hypothesis)
[73]. Alcoholic CP is a slow process evolving in two
stages: early-stage CP with recurrent episodes of
acute pancreatitis; and late-stage CP with exocrine
and endocrine insufficiency and calcification of
pancreas. e progression rate to late-stage CP
due to alcoholism is variable with an average of 5
years. Whereas hereditary and idiopathic CP have
a significantly prolonged early-stage and a marked
delay in onset of late-stage [3]. Although acute
and late-stage CP are easily diagnosed, it is always
difficult to diagnose the onset, i.e. early-stage CP.
e pathogenesis of CP is still unknown and
several hypothetical concepts have been proposed
to explain the early and late pathophysiological
changes in CP including [73]:
1. Intraductal obstruction hypothesis — chronic
alcohol ingestion, by unknown mechanism,
causes reduced bicarbonate concentration
and volume of pancreatic secretion leading
to precipitation of protein and calcium salts;
and the resultant ductal obstruction. Ductal
hypertension plays an important role in
pancreatic inflammation and finally fibrosis.
2. Necrosis-fibrosis hypothesis — repeated
episodes of acute pancreatitis lead to areas of
focal necrosis and healing which eventually
end up with pancreatic fibrosis. CP represents
a late stage of relapsing acute pancreatitis.
3. Toxic-metabolic hypothesis — alcohol or
other toxins change the intracellular lipid
metabolism leading to fatty degeneration of
pancreatic acinar cells.
4. Oxidative stress hypothesis — oxygen free
radical formation from alcohol/toxin exposure
damages the pancreatic acinar cells with
resultant CP.
5. Sentinel acute pancreatitis event hypothesis
— chronic alcohol exposure leads to
elevation of stress cytokines, oxidative stress
and mitochondrial damage. Pancreatic
autodigestion during an episode of acute
pancreatitis leads to the release of cytokines,
recruitment of neutrophils, monocytes and
lymphocytes into the pancreas and activation
of pancreatic stellate cells. With recurrent
injury to the pancreas, there is continued
release of cytokines leading to the eventual
pancreatic fibrosis.
Although different aetiologies lead to different
courses of the disease and different pain profiles
(see below), continuous damage to pancreatic
acini and lobular destruction result in progressive
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Pain Associated with Medical Diseases 291
loss of pancreatic exocrine tissue irrespective of the
aetiology. e islets of Langerhans are not initially
involved in the inflammatory process; however,
gradual loss of endocrine tissue occurs eventually.
e neuroanatomy for the pain transmission in
CP has been reviewed by Bradley et al. [14] and
splanchnic nerves are thought to carry most of
the afferent fibres from the pancreas. In addition,
afferent pain fibres from the pancreas are also
found in some of the somatic nerve pathways and
other mixed nerves, such as the vagus. Different
mechanisms of pain have been proposed: ductal
hypertension leads to increased pancreatic
parenchymal pressure and produces pain by direct
pressure on sensory nerves; increased pancreatic
pressure results in a “compartment syndrome”,
producing chronic ischaemia and parenchymal
acidosis; and direct contact of the sensory nerves
with parenchymal neural irritants.
Clinical features and pain prole
e early-stage CP is characterised by recurrent
painful attacks of acute pancreatitis. e early-
stage may last for several years and is followed by
the late-stage CP with development of chronic
pain, pancreatic calcifications and pancreatic
insufficiency. Abdominal pain is typically worsened
after a meal, which limits the food intake and
contributes to weight loss and malnutrition. Two
types of pain in CP have been described: A-type
pain — short relapsing pain episodes which last
for 2 to 10 days and separated by long pain-free
periods of months (or years); and B-type pain —
prolonged periods of either persistent (daily) pain
or clusters of recurrent severe pain exacerbations
for at least 2 months which require repeated
hospitalisation [3]. Type-A pain links recurrent
attacks of acute pancreatitis with the initiation of
alcoholic CP, whereas persistent severe B-type pain
is usually associated with local complications, such
as pseudocysts or obstructive cholestasis.
e course of pain in CP remains unpredictable
and highly variable, but spontaneous partial or
complete pain relief in late-stage CP is common
and noted in 50–80% of patients and is closely
related to the development of marked exocrine
insufficiency. e interval between the onset and
occurrence of persistent exocrine insufficiency
and pancreatic calcification is about 5 years in
alcoholic CP, but is less well defined in non-
alcoholic CP.
Management
ere are three aspects to the management of CP:
abstinence from alcohol and smoking; supportive
therapy for exocrine and endocrine insufficiency;
and pain control. Alcohol and smoking are noted
to be independent risk factors for the developments
of CP, and avoidance of the precipitating factors
have been shown to reduce the pain as well as to
slow the progression of the disease [66]. Details
of supportive therapy for exocrine and endocrine
insufficiency are beyond the scope of this book and
the reader is referred to other medical textbooks.
A number of measures have been proposed to
reduce pancreatic enzyme secretion and thereby
reduce pain. ese measures include pancreatic
enzyme supplementation, elevation of duodenal
pH with cimetidine or proton pump inhibitors;
and somatostatin analog octreotide. Although
conflicting results have been found with these
measures, they are still widely used in the clinical
setting [66].
When avoidance of precipitating factors and
other general measures fail to provide pain relief,
a pharmacological approach using the WHO
analgesic ladder is recommended [58]. It should
be noted that although all opioids will increase
the sphincter of Oddi pressure, it is thought that
the benefits of morphine may outweigh its risk in
treating pancreatitis [82]. Nevertheless, caution is
advised when using potent opioids in CP patients,
and a partial agonist or agonist/antagonist may be
considered [66].
When the pain becomes intractable or in the setting
of increasing pain (type-B pain), radiological
examination of the pancreatic morphology is
recommended and endoscopic intervention,
denervation procedures or surgical therapy should
be considered. Endoscopic interventions such
as stent placement, stone extraction, stricture
dilatation and pancreatic sphincterotomy were
found to be beneficial in patients with large duct
and ductal hypertension [66]. Variable results of
neurolytic coeliac plexus block either by endoscopic
ultrasound or transcutaneous approaches have been
observed in CP patients; the mean pain-free period
was only 2 months, even for successful blocks,
and the procedure is therefore not recommended
for routine practice [66]. Various open surgical
denervation procedures have been described. ese
include bilateral thoracoscopic splanchnicectomy
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292 Simon K.C. CHAN, Alice K.Y. MAN
after patient selection with differential epidural
analgesia, which appears to be promising [14].
Operative treatments, such as surgical resection or
drainage and longitudinal pancreatico-jejunostomy,
have been advocated for the management of CP
and have been found to be superior to endoscopic
intervention [66].
It should be reminded that operative therapy in CP
is effective in reducing pain, but does not retard the
disease process and hence should not be undertaken
for the purpose of improving endocrine or exocrine
function.
Pancreatic cancer
Background
Pancreatic cancer is the fifth commonest cause
of cancer-related deaths in Australia [83]. e
majority of patients have metastasis or advanced
local disease at the time of presentation and are
unresectable. erefore, palliative management of
symptoms becomes the prime concern. e three
main symptoms in pancreatic cancer are pain,
weight loss and jaundice; but pain is often the most
feared by patients. Moreover, the presence of pain
has been shown to have an inverse correlation with
survival [5].
Management
e general principle in cancer pain management has
been discussed in Chapter 9, and pain management
relevant to pancreatic cancer is highlighted in this
section. A recent systematic review on neurolytic
coeliac plexus block for pain control in pancreatic
cancer has found that the intervention improves
the quality of analgesia and reduces the opioid
requirement, but has no effect on survival [98]. In
addition, bilateral thoracoscopic splanchnicectomy
has been shown to significantly reduce the mean
pain score from 7.4 to 0.6, and the effect persisted
for 3 months at the time of follow-up in unresectable
pancreatic cancer [67]. erefore, depending on the
availability of expertise and facility, it is appropriate
to consider neuroablation procedures for those
patients who continue to suffer from severe pain
despite pharmacological analgesia.
Visceral Pain
Visceral pain may arise from any internal organs
within the thorax, abdomen or pelvis. Viscera are
innervated by both extrinsic and intrinsic nervous
systems but they interact in a poorly understood
manner. Visceral sensory neurons are responsible
for detecting chemical, thermal and mechanical
stimuli, and can be sensitised by local ischaemia,
hypoxia and the consequent release of inflammatory
mediators after local inflammation or tissue
injury [17]. Viscero-visceral convergence occurs
when visceral afferents from the different internal
organs, such as the urinary bladder, uterus and
vagina, converge on the same dorsal horn neurons,
resulting in augmentation of pain symptoms. In
addition, most visceral afferents also converge on
dorsal horn neurons innervated by somatic afferent
neurons, causing viscero-somatic convergence. is
convergence of inputs is thought to be responsible
for the vague, poorly defined pain pattern and
referred pain in visceral pain.
Pain arising from viscera can be due to an
underlying pathological process, such as myocardial
ischaemia; or is deemed “functional” when no
identifiable cause is found, for example irritable
bowel syndrome. Treatment of organic visceral pain
should be directed to the underlying cause, whereas
a multidisciplinary approach is needed to manage
visceral pain that is functional in origin. A detailed
description of all visceral pain is beyond the scope
of this book and only functional pain arising from
the gastrointestinal tract and pelvic organs will be
discussed.
Functional gastrointestinal
disorders
Background
A variety of functional gastrointestinal disorders
(FGIDs) with variable symptoms including pain,
diarrhoea, constipation, bloating, nausea and
vomiting have been described, but the recent
Rome III Classification System of FGID, which
is based on symptomatology and age group, is
gaining popularity [24]. For example, irritable
bowel syndrome has been defined as recurrent
abdominal pain or discomfort occurring at least
3 days a month in the previous 3 months with
an associated change in bowel habit [24]. e
incidence of irritable bowel syndrome is around
10–15% of the general population in the developed
world [72, 93]. Although no aetiology has been
identified, a number of contributory factors have
been implicated in relation to the pathophysiology
of FGIDs [24]: genetic predisposition; early family
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Pain Associated with Medical Diseases 293
environment; psychosocial factors; abnormal gut
motility; activated mucosal inflammatory cells;
altered bacterial flora; and interactions of brain-gut
via the central nervous system and enteric nervous
system.
Management
Once serious pathological processes, such as
neoplastic, inflammatory and infectious disorders,
have been excluded and a diagnosis of FGID is
made, a number of therapeutic options, which
depend on severity of symptoms, are available
[24].
1. Education — emphasising that both
physiological and psychological factors
interact to produce symptoms.
2. Reassurance.
3. Dietary and/or medication modification.
4. Symptom monitoring — to identify
precipitating factor, if any.
5. Pharmacotherapy for symptomatic relief, such
as laxativess or antispasmodics.
6. Psychological treatment.
7. Antidepressants — there is moderate evidence
(NNT 4.2) to support the use of tricyclic
antidepressant in irritable bowel syndrome
probably due to their anticholinergic effect
and mechanism relating to pain modulation
in the central nervous system. Furthermore,
serotonin-noradrenergic reuptake inhibitors,
such as duloxetine, were recently found to have
a role in controlling pain in FGIDs, probably
via a central analgesic action as well as relief of
associated symptoms of depression.
Regardless of treatment approaches, the key for
successful and satisfactory management is the
establishment of the physician-patient relationship.
Patients with severe symptoms who become
disabled or have severe function impairment should
be referred to a pain centre which can provide a
multidisciplinary approach for rehabilitation.
Chronic pelvic pain
Background
Chronic pelvic pain may have an apparent
gynaecological origin but no definite lesion or cause
on examination [56]. It is also defined as persistent
pain of at least 6 months’ duration felt in the lower
abdomen or pelvis and not associated exclusively
with menstruation, pregnancy or intercourse [57].
e prevalence of chronic pelvic pain is 25.4% in
women aged between 18 and 50 years, about half
of whom will have chronic pelvic pain of no known
aetiology [32].
Management
A multidisciplinary approach is recommended in
the management of patients with chronic pelvic
pain to reduce pain and improve daily activity [78].
Treatment modalities available specific to chronic
pelvic pain include:
1. Pharmacotherapy — simple analgesics
(e.g. paracetamol) and non-steroidal anti-
inflammatory drugs should be prescribed for
all patients with chronic pelvic pain. Adjunct
analgesics like the tricyclic antidepressants
are considered second-line treatment for
chronic pelvic pain. Hormonal treatments are
indicated if pelvic pain is strongly cyclical with
gonadotrophin-releasing hormone analogues,
which induce a reversible, menopause-like state
of hypogonadotropic hypogonadism [42].
2. Surgery — improvement in pain at 1 year
in 60% of patients following hysterectomy
was reported in a series of 300 patients with
chronic pelvic pain [36]. Adhesiolysis is not
associated with improved outcome unless
adhesions are very severe, but the use of
diagnostic ultrasound or laparoscopy to rule
out serious conditions and provide reassurance
in patients with persistent pelvic visceral pain
is recommended in a systematic review [78].
More recently, however, a blinded randomised
controlled study has found no difference
in chronic pelvic pain reduction between
laparoscopic adhesiolysis and diagnostic
laparoscopy alone [79].
3. Neurostimulation and neurolytic intervention
— the experience of neurostimulation and
neurolysis in managing chronic pelvic pain is
limited to anecdotal reports and case series.
ere is inadequate evidence supporting
the role of laparoscopic uterosacral nerve
ablation [78]. In a case series of patients with
deep pelvic, retropubic pain, vulvodynia,
dyspareunia and rectal pains, spinal cord
stimulation has been reported to provide
satisfactory pain relief [41].
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294 Simon K.C. CHAN, Alice K.Y. MAN
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Introduction
As the percentage of the population over the age of 65 years
increases in both the developed and developing world, so will the
number of people in this age group with pain. Unrecognised and
poorly managed pain results in an unnecessary and serious decline
in the quality of life. is chapter will review the epidemiology
of pain in the older person, look at some of the physiological
differences that age-related changes bring to pain processing and
perception, and the types and causes of pain in the older person,
together with its assessment and treatment options.
Epidemiology
Population growth varies from country to country with some
European countries reporting a negative growth while others
continue to increase. In most developed countries with stable
populations, the age distribution within the population is
changing dramatically. In these countries it is predicted that
the population over the age of 65 years will rise from 17.5%
to 36.3% by 2050. In addition the population over the age of
80 years is likely to more than triple [40]. is will occur with
a relatively stable birth rate.
With regard to persistent pain, studies in Australia suggest
approximately 17% of adult males and 20% of females report
chronic pain. Persistent pain in these studies was defined
as pain being present every day for at least 3 months in the
preceding 6 months. e prevalence of pain increases with
increasing age, such that 30% of females in the 80–84 year
age group reported persisting pain [13]. Comparing different
prevalence studies on long-term pain, their apparent wide
variance is complicated because different researchers have used
varying definitions for the terms “long term” or “chronic” [8,
21, 54]. Studies have used the following among others. “Have
INTRODUCTION
EPIDEMIOLOGY
PHYSIOLOGICAL,
PSYCHOLOGICAL
AND PSYCHOSOCIAL
CONSIDERATIONS
Threshold and tolerance
IDENTIFICATION
ASSESSMENT
PAIN MANAGEMENT OPTIONS
Physical Therapies
Cognitive or psycho educational
therapies
Pharmacological therapies
INTERVENTIONAL TECHNIQUES
POSTOPERATIVE PAIN
MANAGEMENT
SUMMARY
REFERENCES
Pain in the Older Person
18
C. Roger GOUCKE
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