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270 Chak Sing LAU
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Soft tissue syndrome Presenting feature(s) Physical findings Injection site and steroid dose (in
mg methylprednisolone or equiv.)
Stenosing
digital
tenosynovitis
(Trigger finger)
Triggering of the
affected finger
Pain during resisted finger
flexion and on stretching
the tendon passively
in extension. A tender
nodule may also be felt
Over the involved tendon sheath.
AVOID DIRECT INJECTION
(12–20 mg)
Foot and ankle region
Achilles’
tendonitis
Painful Achilles
tendon during
walking
Localised tenderness
+/- nodular or diffuse
swelling
INJECTION BEST AVOIDED
Plantar
fasciitis
Pain on the under-
surface of the
heel on weight
bearing. Worse after
immobility
Localised tenderness,
without swelling, over
the anteromedial portion
of the plantar surface of
the calcaneum. Passive
dorsiflexion of the toes
worsens pain
From the side of the plantar fascia
around the point of maximum
tenderness. AVOID DIRECT
INJECTION
(20–40 mg)
https://t.me/medicina_free
Painful Arthritis and Rheumatic Conditions 271
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Introduction
Pain is traditionally regarded as a sign of disease and the
function of the pain sensory system is to detect, localise and
identify tissue-damaging processes in order to protect and
maintain the body’s homeostasis. Hence, pain is the most
common symptom that leads a patient to seek medical advice
[26]. In most situations, the appropriate treatment is to limit
the disease process and the pain will be alleviated. However, in
some situations in which definitive treatment is lacking, such
as human immunodeficiency virus (HIV) disease, patients
continue to suffer severe chronic pain despite the correct
diagnosis having been made. Pain management thus becomes
an integral part of the overall patient care in order to improve the
quality of life. Different aetiologies and pathological processes
mean that different diseases produce different pain syndromes,
and an understanding of the underlying pathophysiology of
each disease as well as its related pain syndrome is important
in managing these patients.
Pain and Endocrine Disease
Diabetes mellitus
Background
Diabetes mellitus (DM) is a common disease which affects
multiple organ systems, such as the cardiovascular, renal,
peripheral nervous system and the eye. In the setting of the
pain clinic, pain physicians are likely to be involved in the
care of diabetic patients with diabetic peripheral neuropathic
pain (DPNP) or peripheral vascular disease and its related
complications. Diabetic peripheral neuropathy (DPN)
is a disorder that is characterised by signs and symptoms
of peripheral nerve dysfunction in patients with DM in
INTRODUCTION
PAIN AND ENDOCRINE DISEASE
Diabetes mellitus
PAIN AND CARDIOVASCULAR
DISEASES
Peripheral arterial disease
Coronary artery disease
Non-cardiac c
hest pain
P
AIN AND INFECTIOUS DISEASES
Human immunodeficiency virus
disease
Sev
ere Acute
Respiratory
Syndrome
PAIN AND HAEMATOLOGICAL
DISORDERS
Haemophilia
Sic
kle cell disease
PAIN AND
PANCREATIC
DISORDERS
Acute pancreatitis
Chronic pancreatitis
Pancreatic cancer
VISCERAL P
AIN
Functional gastrointestinal
disorders
Chronic pelvic pain
Pain Associated with Medical Diseases
17
Simon K.C. CHAN, Alice K.Y. MAN
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276 Simon K.C. CHAN, Alice K.Y. MAN
whom other causes of peripheral neuropathy are
excluded. Although most patients with DPN do
not experience pain, pain associated with DPN
significantly impairs the quality of life in diabetic
patients [7].
Epidemiology
In 2000, it was estimated that 150 million people
worldwide were suffering from DM and that the
number would double by the year 2025 [97].
e incidence of DM is higher in the developed
world; 20.8 million people (or 7% of the overall
population) in the United States have DM [7].
e prevalence of DM is related to the ageing
population and excess weight gain. In Hong Kong,
the prevalence of DM in the elderly (over 50 years
of age) was found to be 15–20% [94].
Depending on the sampled population, the
prevalence of DPN in diabetic patients ranged from
20–60% in a recent review [69]. Among those with
type I and type II DM, 54% and 45% respectively
had DPN [7]. However, not all patients with
DPN have symptoms. Up to 50% of patients with
DPN experience some degree of pain and of these,
10–20% have symptoms severe enough to seek
treatment [7]. Because of the different definition of
DPNP, its prevalence varies from 11–20% and the
number of people suffering pain from DPN ranges
from 600,000 to 3.6 million in the United States
[7].
Pathophysiology
e pathophysiology of diabetic neuropathy
remains unclear, but the incidence of DPN is more
frequent with increasing age and duration of DM,
as well as the duration and severity of exposure
to hyperglycaemia. e pathogenesis of diabetic
neuropathy is multifactorial and a number of
mechanisms have been proposed [75]:
1. Metabolic — activation of the polyol pathway
and the resultant reduction in Na
+
/K
+
-ATPase
activity
2. Non-enzymatic glycation leading to
glycosylation and changes in proteins in nerve
fibres
3. Vascular — hyperglycaemia, thought by way
of activation of protein kinase C to result in
a poor blood supply to and even infarction of
the nerves
4. Oxidative stress — reduced blood supply to
nerve fibres leads to free radical formation
5. Auto-immune mechanism
6. Nerve growth hormone (neurotrophins)
deficiency leading to axonal atrophy.
Irrespective of the mechanism, neuronal, axonal
and Schwann cell metabolism are deranged
leading to impaired axonal transport and neuronal
dysfunction.
Clinical Features
Diabetes-associated neuropathies can manifest
as generalised symmetrical polyneuropathies and
focal or multifocal neuropathies. A classification of
diabetic neuropathy based on the clinical features,
which are either symmetrical or asymmetrical,
has been summarised by Bansal et al. [11]. e
symmetrical neuropathies include: diabetic
polyneuropathy, painful autonomic neuropathy
and painful distal neuropathy; asymmetrical
neuropathies include: radiculoplexoneuropathies
such as lumbosacral, thoracic, cervical and
cranial neuropathy, and asymmetric proximal
diabetic neuropathy, previously known as diabetic
amyotrophy.
Although various neuropathies have been described,
DPN (also known as chronic sensorimotor distal
symmetrical polyneuropathy) accounts for 75%
of diabetes-associated neuropathies. Both small
and large nerve fibres can be affected in DPN,
which impairs both sensory and motor function.
However, impairment of motor function is usually
mild; pronounced motor signs or asymmetrical
distribution would suggest a non-diabetic cause
of neuropathy. e small fibre disease may be
associated with diabetic autonomic neuropathy as
well. Diabetic peripheral neuropathy is insidious in
onset and usually affects the feet and lower limbs
first, with the hands affected later, in a “stocking
and glove” distribution.
e symptoms of DPN may be spontaneous or
evoked and are usually worse at night. e pain
(“positive symptoms”) which occurs in 11–20% of
DPN can be of type C fibre (lancinating, burning
and dysaesthetic) or A-delta type (deep seated,
dull and gnawing). Patients may also experience
“negative symptoms” such as numbness or a
“dead” feeling in their feet. Unsteadiness, which
may be secondary to abnormal proprioception or
muscle sensory function, is also seen. e presence
of clinical features such as tachycardia, painless
myocardial infarction, orthostatic hypotension,
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Pain Associated with Medical Diseases 277
oesophageal dysfunction, gastroparesis, diarrhoea,
constipation, incontinence, erectile dysfunction,
neurogenic bladder, and dry and warm feet would
indicate autonomic neuropathy.
Acute sensory neuropathy is rare; it tends to
occur after a period of metabolic instability, such
as ketoacidosis or poor glycaemic control, and
is characterised by pain with few clinical signs.
e blood glucose level correlates with pain
symptoms and a return to euglycaemia often
results in resolution of pain. Sometimes acute
diabetic neuropathic pain associated with weight
loss and depression is called diabetic neuropathic
cachexia.
During the progression of disease, patients
develop tolerance to medical therapy and chronic
diabetic neuropathy results. Patients with
chronic diabetic neuropathy are susceptible to
foot injury and ulcer, which can cause significant
morbidity.
e natural history of DPN and DPNP is largely
unknown with conflicting reports [7]. It has been
reported that symptoms of DPNP decreased after
3.6 years, but there was no change in pain severity
after 5 years in another study. Moreover, pain
symptoms and nerve conduction velocity were
reported to decline at 1 year follow-up.
Diagnosis
e diagnosis of DPN is made clinically and is based
on history, physical examination and investigations.
Physical examination including muscle power and
sensation (pin prick, vibration with 128Hz tuning
fork and temperature) is essential. e common
finding is symmetrical loss of sensation in a stocking
distribution. e presence of asymmetrical motor
deficit highly suggests a non-diabetic cause of
neuropathy [13]. Signs of autonomic neuropathy
like warm and dry skin may be present. Regular
examination of the feet in diabetic patients is
essential. Plantar callosities, foot ulcer, pes cavus
and clawed toes represent a picture of the diabetic
foot. e presence of unilateral heat and swelling in
a neuropathic diabetic foot suggests acute Charcot
neuropathy [69].
Nerve conduction study changes in diabetic
neuropathy are non-specific and aim at excluding
other important differential diagnoses like
entrapment and nerve demyelination. e nerve
conduction velocity diminishes gradually in
diabetic neuropathy by 0.5 m/s/year. Autonomic
function tests are based on specific manoeuvres for
variation in blood pressure and heart rate.
e American Academy of Neurology has
recommended that diabetic neuropathy be
diagnosed in the presence of somatic or autonomic
neuropathy when other diagnoses have been
excluded (Table 17.01) [1].
Management
Once a diagnosis of DPN has been made,
the patient should have the disease explained,
including its prognosis and treatment goals,
so that a a good rapport and an effective
management plan can be established. ere are
three aspects to the management of DPN: disease
modification, symptomatic relief and prevention of
complications.
1. Disease modification
Secondary preventive measures, including treatment
of hypertension and hyperlipidaemia, and good
glycaemic control can substantially reduce the
risk of developing complications and slow their
progression in all types of DM.
Glycaemic control aims at maintaining glycated
haemoglobin (HbA1c) at less than 6%;
appropriate measures include: diet; exercise; oral
hypoglyacaemic agents; and insulin administration.
Intensive insulin therapy can reduce the prevalence
of diabetic neuropathy by 50% [2]. In addition,
carnitine has been shown to improve sural nerve
fibre number and vibration perception, as well as
pain control [74].
Table 17.01 Non-diabetic causes of peripheral
neuropathy
Causes Example
Malignancy Carcinoma of lung
Nutritional
deficiency
Vitamin B12 deficiency
Toxins Alcohol
Infection Human immunodeficiency
virus
Drugs Vinca alkaloids, isoniazid,
chemotherapy
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278 Simon K.C. CHAN, Alice K.Y. MAN
2. Symptomatic Relief
A number of pharmacological agents with different
mechanisms of action have been shown to be
effective for neuropathic pain with variable efficacy.
Recently, consensus guidelines specifically for the
treatment of DPNP based on evidence from clinical
trials have been developed [6]. Drug treatment of
DPNP has been ranked in three categories: first-
tier, second-tier and “honorable mention”.
(a) First-tier agents
Four agents or class of agents have been ranked
in this category.
• Duloxetine — a serotonin-noradrenaline
reuptake inhibitor (SNRI) is one of the only
two agents approved by the Food and Drug
Administration (FDA) for the treatment of
DPNP. e recommended dosage is 60–120
mg/day; adverse effects, such as somnolence
and constipation are manageable.
• Pregabalin — an anticonvulsant and the
second drug approved by the FDA for
treatment of DPNP. e recommended dose
for DPNP is 300–600 mg/day; side effects,
which include somnolence and dizziness, can
be troublesome at that dosage.
• Oxycodone CR — a long-acting opioid
that has been shown to be effective in swell-
designed clinical trials. Adverse effects are
similar to other opioids; the starting dose of
20mg/day can be increased to 60 mg.
• Tricyclic antidepressants — the number
needed to treat (NNT) of amitriptyline for
the treatment of DPNP has been shown to be
1.3 in the Cochrane collaborative analysis, but
wide clinical use of tricyclic antidepressants is
limited by their adverse effects.
(b) Second-tier agents
is tier of agents was recommended based
on the positive results of both a randomised
controlled trial (RCT) for DPNP and RCTs
for treatment of other neuropathies. Five
agents have been ranked in this category:
carbamazepine, gabapentine, lamotrigine
(an anticonvulsant with antidepressant
properties), tramadol and venlafaxine ER (an
SNRI). Please refer to Chapters 21 and 23 for
their pharmacology.
(c) Others (“honourable mention” category)
Recommendations in this category were based
on positive results of RCTs for treatment
of other neuropathies and include: topical
agents (capsaicin and lignocaine), bupropion,
citalopram, paroxetine, phenytoin, topiramate
and methadone.
e choice of medication should not be based on the
mechanism of action but rather on consideration
of other factors, including: patient comorbidities,
drug side-effect profile and contraindications, drug
interaction, costs and availability. If patients do not
respond to or do not tolerate the drug because of
side effects, another agent within the first-tier or
from the second-tier with a different mechanism
of action should be chosen. It may be also useful
to add another first- or second-tier agent, but it is
necessary to watch carefully for additive adverse
effects.
Some complementary pain management techniques
may have value as adjuvant therapy; acupuncture
has been shown to be effective in DPNP and to
reduce analgesic requirement. ere is no good
evidence to support the use of transcutaneous
electrical nerve stimulation or magnetic insoles
in DPNP. ere is limited evidence for the use of
spinal cord stimulation, but due to the cost and
the risk inherent with the procedure, its use in the
clinical setting is yet to be established [6].
3. Prevention of Complications
As leg ulceration can lead to significant morbidity
in diabetic patients, it is important to prevent foot
ulcers in patients with DPN. Strategies to prevent
leg ulcers are readily available and include [97]:
education of patients to examine their feet daily;
a check of the insides of shoes (to guard against
chafing); the avoidance of walking barefoot; and the
routine hand-testing of water temperature before
bathing. Practical measures should be stressed, such
as the use of a bed cradle to lift bed clothes clear of
hyperaesthetic skin.
Impact of comorbid chronic pain
Diabetic patients with chronic pain tend to report
their health as fair or poor, and depressive symptoms
are associated with significant impairment in
quality of life [45]. Moreover, chronic pain is
very strongly associated with a greater difficulty in
exercising and the ability to follow a recommended
eating plan. Comorbid chronic pain may also
make self-care hard. As patients with DPNP may
potentially progress to a chronic pain state, it is
important to establish a good rapport with them
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Pain Associated with Medical Diseases 279
in order to emphasise the positive aspects of pain
management rather than to allow them to focus on
the pain-related limitations. It is helpful to explain
to patients the concept of pain as a warning sign
versus pain as a disease, as in low back pain [6].
Pain and Cardiovascular
Diseases
Peripheral arterial disease
Background
Peripheral arterial disease (PAD), also known as
arteriosclerosis obliterans, is the chronic obstruction
of the arteries supplying the lower extremities, and is
the peripheral arterial manifestation of generalised
atherosclerosis. e most widely accepted
definition of PAD is a resting ankle brachial pulse
index (ABPI) of 0.9 in which the ABPI is the ratio
of ankle systolic pressure as measured by Doppler
ultrasound and the higher of the 2 brachial systolic
pressures [23]. In comparison, thromboangiitis
obliterans (TAO), also called Buerger’s disease, is
a segmental occlusive inflammatory condition of
arteries and veins of non-atherosclerotic origin.
Although it has similar clinical manifestation to
PAD, TAO can also affect the upper limbs and is
predominantly seen in a younger age group.
Epidemiology
e prevalence of PAD is approximately 20% in
adults older than 55 years of age, or 27 million
people in North America and Europe; the incidence
increases with age. However, only half of the people
experience symptoms from PAD and about one-
fifth of those with PAD have typical symptoms of
intermittent claudication, rest pain, ulceration and
gangrene [34]. Approximately 5–10% of individuals
with asymptomatic PAD develop symptoms over
5 years. A similar finding in Hong Kong showed
patients with PAD had a mean age of 72 years when
first presenting with symptoms, with a male to female
ratio of 1:1.6 [18]. Furthermore, a high proportion
of patients were found with DM as a comorbidity.
Femoro-popliteal artery occlusive disease contributed
to the majority of PAD cases (47%).
Peripheral artery disease is one of the major causes
of loss of work, disability and life changes in the
United States [28]. e quality of life as measured
by the Medical Outcome Short Form-36 (physical
functioning, bodily pain, vitality, social functioning,
emotional role and mental health) was shown to
deteriorate significantly with increasing severity of
peripheral ischaemia in Chinese patients [46]. In
addition, severity of PAD and ankle-brachial index
are both independent predictors of mortality [31].
e prevalence of TAO is reportedly highest in the
Middle and Far East. Among patients investigated
for PAD, it was found that a proportion in fact had
TAO; numbers ranged from 0.5–5.6% in Western
Europe, 16–66% in Korea and Japan, and up to
80% among Jews of Ashkenazi ancestry in Israel
[8].
Pathophysiology
e pathophysiology of PAD has been reviewed
and there is evidence to suggest that Virchow’s
triad: abnormal blood flow, hypercoagulability of
the blood and abnormal vessel wall, is applicable
in PAD [51].
Atherosclerosis is thought to be the most
common culprit in PAD and is a systemic
inflammatory response where cholesterol-laden
plaque builds up in the artery and eventually
blocks the lumen, contributing to symptomatic
obstruction in the peripheral artery [28]. Risk
factors that are contributory to PAD include:
diabetes (or glucose intolerance), smoking,
hyperlipidaemia, raised fibrinogen concentration
and hyperhomocysteinaemia. e underlying
mechanism for TAO remains unknown, but it
is strongly associated with tobacco smoking; an
immune-mediated endarteritis mechanism has also
been implicated [8].
e pain mechanism due to ischaemia in PAD
remains undetermined and suggested mechanisms
have included [65]: putative nociceptive fibres
mediate ischaemic pain; accumulation of
metabolites causes sensitization of peripheral
nociceptors; involvement of “mechanical
determinants” of the nociceptors during
ischaemia; and a central mechanism leading to a
chronic pain state. Regardless of the mechanism,
the pain in PAD varies depending on the speed
of onset of symptoms, the extent and anatomical
location of the occlusion, and the extent of
collateral formation. In addition, a neuropathic
pain mechanism may also play a role, especially
in patients with diabetes, which is commonly
associated with PAD.
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