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Patients with a fever
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Box 10.5
Familial Mediterranean fever (FMF)
TNF receptor- associated periodic syndrome (TRAPS)
Hyperimmunoglobulinemia D with periodic fever
syndrome (HIDS)
Figure 10.6 Livedo reticularis in a 39- year- old woman with
polyarteritis nodosa.
The classic periodic fever syndromes (monogenic
autoinflammatory diseases)
Table 10.3 Mechanisms of drug fever
Mechanism Examples
Hypersensitivity Anticonvulsants, penicillin,
minocycline, sulfonamide,
allopurinol
Altered thermoregulatory
mechanisms
Directly related to
administration of the drug
Direct extension of the
pharmacologic action of
the drug
Idiosyncrasy Succinylcholine, haloperidol,
Thyroxine, drugs with
anticholinergic activity,
amphetamine, cocaine
Paraldehyde, pentazocine,
amphotericin B, bleomycin
Chemotherapy
serotonin syndrome
Investigations for infectious causes of
fever
Testing for infectious disease should include both
laboratory and radiological investigations.
Laboratory
Figure 10.7 Ischaemic changes in the right second digit in a
39- year- old woman with polyarteritis nodosa.
with lupus presents with high fever, respiratory
symptoms and radiographic changes. The difficulty
is whether the radiographic changes are caused by
complicating infection or organizing pneumonia.
Fever is not a feature in patients with uncomplicated
scleroderma.
Drug fever
Drugs can cause fever via several mechanisms (Table
10.3). This is a diagnosis by exclusion. A rash is not
always present nor is eosinophilia. By definition, the
fever coincides with administration of the drug and
disappears when the drug is discontinued. The risk
of developing drug fever increases with the number
of drugs prescribed, especially in elderly patients,
patients with active HIV infection and patients with
cystic fibrosis.
Both routine and specialist tests should be performed
in the haematology, chemistry, microbiology and
virology laboratory where appropriate.
Full blood count with differential and film
White blood cell count is often raised in infection,
although a low count may indicate specific pathogens
or overwhelming infection. In patients on immune
suppression or chemotherapy the white cell count
should not be used as a marker of infection because
it may be falsely raised or suppressed.
Neutrophilia with band forms and toxic
granulation suggest bacterial infection.
Neutropenia may be seen post chemotherapy or
with typhoid fever, brucellosis, severe sepsis or
viral infection.
A reactive lymphocytosis may be seen in acute viral
illnesses, particularly infectious mononucleosis
when atypical lymphocytes may be present. It
may also occur in tuberculosis, brucellosis or in
leukaemias and lymphomas.
Lymphopaenia is common in viral infection
(influenza, dengue, HIV) and typhoid fever.
Eosinophilia is seen in hypersensitivity reactions,
as well as in invasive parasitic infections.
Platelets
Thrombocytopaenia may be seen in malaria,
haemorrhagic fevers, meningococcal sepsis or
disseminated intravascular coagulation (DIC)
associated with overwhelming infection.
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Patients with a fever
Thrombocytosis may occur as an acute response
to inflammation or can occur in chronic infections
such as TB.
A blood film or smear is used to look for parasites
that may be present in the blood. The most
common of this is malaria, but can also be used to
detect babesia, trypanosomiasis or microfilaria. It
may suggest Epstein- Barr virus (EBV) if atypical
lymphocytes are seen.
Inflammatory markers
Acute- phase reactants (APRs) are a heterogeneous
group of plasma proteins that increase or decrease
in response to inflammatory stimuli such as
infections, trauma, arthritis, autoimmune disorders
and malignancies. The levels of APRs rise and fall
in response to the rise and fall of the inflammatory
process. Common tests used for this purpose
include C- reactive protein (CRP) and erythrocyte
sedimentation rate (ESR) and, more recently,
procalcitonin (PCT). ESR is an indirect APR because
it measures the rate of movement of red blood cells,
which is increased by binding of an APR. Most APRs
are produced in the liver.
The ESR rises fairly rapidly (within 24–48 hours)
from the onset of inflammation and is slow to fall
once the cause of inflammation resolves. It has a
low sensitivity for infection and is affected by many
factors, including age, gender, weight and renal
function. Despite this, an ESR over 100 mm/hour
warrants further investigation.
CRP is a more sensitive marker of inflammation
than ESR and is less affected by external factors such
as age and gender. It rises more rapidly (within 6–24
hours) and is quicker to fall than ESR. Very high
levels of CRP are more likely to be associated with
bacterial infection than other causes of inflammation.
Procalcitonin has several advantages over both
ESR and CRP. It rises within 3–4 hours, quicker
than either ESR or CRP, and a result can be obtained
in 30 minutes or less using a semiquantitative
point- of- care test. It is a more sensitive marker
of bacterial infection because raised PCT levels
are not seen in other non- infectious inflammatory
conditions, and viral infections tend to inhibit PCT
rather than raise it. It can, however, be raised in
invasive fungal infection, malaria, by massive
trauma such as severe burns or major surgery, any
therapy that stimulates cytokines such as T- cell
antibody therapy, granulocyte transfusion or graftversus- host disease.
The usefulness of the above tests may differ,
depending on the situation and site of infection.
Basic biochemistry tests
Renal and liver function tests are useful in
determining the presence of any renal or hepatic
impairment, which may assist in determining severity
of disease and affect antimicrobial dosing. Abnormal
liver function tests may also assist in diagnosis
of gastrointestinal infections such as hepatitis or
cholecystitis. Serum ferritin is hugely raised in adult
onset Still’s disease.
Microbiology and virology tests
The type of samples sent will depend on the site
of infection identified. A few examples are listed
below.
Blood cultures should be taken if you suspect the
patient may have bacteraemia from any source. The
signs of sepsis, severe sepsis or septic shock should
be used to indicate the need to take these cultures.
If possible, two sets should be taken aseptically
prior to any antibiotic therapy. There should be
a low threshold for taking blood cultures, before
antibiotics are given, so as not later to regret the
missed opportunity to take antibiotic- free cultures.
Bone marrow cultures may be more useful than
blood cultures for some intracellular pathogens.
Sample any fluid that represents the possible site
of infection as follows:
1. Urine
Dip, culture and microscopy for lower or upper
urinary tract infection and urogenital infections
Molecular tests for urogenital infections
Urine antigen testing for Legionella and
Streptococcus pneumoniae in cases of
community- acquired pneumonia
2. Urethral, vaginal and cervical swabs for
urogenital infections
Culture and microscopy for lower or upper
urinary tract infection and urogenital infections
Molecular tests for urogenital infections
3. Cerebrospinal, peritoneal, joint and pleural fluid,
biopsy tissue, sputum and bronchoalveolar lavage
Microscopy, culture and sensitivity for bacterial
and fungal infection
Ziehl- Neelsen (ZN) staining and culture for
acid- fast bacilli for diagnosis of TB
Molecular tests for viral pathogens
4. Stool
Culture and sensitivity for bacterial infection
Microscopy for parasites
Molecular tests for viral pathogens
5. Pus and tissue samples from abscesses, surgical
debridement, biopsies and wound infections
Microscopy, culture and sensitivity for bacterial
and fungal infection
ZN staining and culture for acid- fast bacilli for
diagnosis of TB
Serology
Serology is used mainly in the diagnosis of viral
infections. A positive IgM usually indicates current
or recent infection and a positive IgG indicates a
previous infection or vaccination. The following
are common serology tests used in the diagnosis of
infectious diseases:
Rash diseases: Measles, rubella, parvovirus, varicella,
rickettsia, typhus, syphilis
Gastrointestinal infection: Viral hepatitis, cytomega-
lovirus (CMV), amoebic liver abscess
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Systemic infections: HIV, Lyme disease, dengue,
brucellosis, leptospirosis
Molecular diagnostics
This diagnostic platform is used mainly in the
diagnosis of viral infections, but is increasingly
used for bacterial, fungal and parasitic infections.
It is a rapid and sensitive technique and is not
affected by previous antibiotic treatment or the
inability to culture the pathogen. Most sample
types can be used for molecular diagnostics. It is
used routinely to diagnose viral infections, such as
gastroenteritis, respiratory tract infections, central
nervous system infections and viral haemorrhagic
fevers. Bacterial infections commonly diagnosed in
this way include pertussis, meningococcal disease
and tuberculosis.
Immunological tests
Systemic lupus erythematosus is defined by the
presence of autoantibodies. Antinuclear and
double- stranded antibodies, antibodies to the
extractable nuclear antigens and complement 3
and 4 need to be tested. The predictive value of
of the patient and the laboratory performing the
test. It is best that all reasonable attempts to
confirm clinical suspicions of systemic vasculitis
with histopathological proof should be undertaken
before treating the patient with potentially toxic
medications.
Histopathology
Biopsy and staining of lymph nodes, tissue, fluid or
bone marrow may reveal infectious structures such
as caseating granulomas, acid- fast bacilli, protozoal
cysts, fungal hyphae or spores.
Radiology
Imaging studies may help to elucidate the source
and extent of infection in those with a fever and
localized site. All modalities of imaging have a
role in diagnosis with the indications for X- rays,
including ultrasound, computed tomography (CT)
and magnetic resonance imaging (MRI) scanning,
depending on the site of infection being investigated.
Radionucleotide or PET scan may be more sensitive
at defining foci of infection.
Pyrexia of unknown origin (PUO)
Box 10.6
Bacterial
Common disease presenting atypically
Abscesses (dental, subphrenic, liver, ovarian, prostate)
Vascular infections
Extrapulmonary TB, atypical mycobacteria
Protected sites
− Sinuses/Ears
− Heart
− Prostate/Ovaries
− Bone, joint, intervertebral disc
− Thyroid
Partially treated infections
Viral
Immune compromised host
Partial immunity
Fungal
Immune compromised host
Protozoal and rickettsial
Travel history
Box 10.7
Bacterial
Brucella
Bartonella
Atypical mycobacteria
Borrelia
Viral
HIV
Hepatitis D & E
Fungal
Uncommon disease presenting typically
HACEK organisms
Leptospirosis
Nocardia
Actinomycosis
EBV, CMV
Viral haemorrhagic fever
*
Cryptococcus Histoplasmosis
Protozoal
Malaria
Amoebiasis
Trypanosomiasis
Rickettsial
Leishmaniasis
Schistosomiasis
Toxoplasmosis
Q fever
Mycoplasmas
*
HACEK includes Haemophilus parainfluenzae, Haemophilus aphrophi-
lus, Actinobacillus, actinomycetemcomitans, Cardiobacterium hominis,
Eikenella corrodens, and Kingella kingae.
Despite an adequate history, examination and set
of investigations, the cause of some fevers remains
unknown. This is termed a PUO or pyrexia of
unknown origin. The classic definition of a PUO is
a fever of more than 38.3°C for more than 2 weeks
during which time there has been at least:
Three separate outpatient appointments, OR
3 days in hospital, OR
1 weeks’ worth of appropriate and thorough
investigation
Infections account for 40% of cases of PUO. Causes
of a PUO often fall into one of two categories:
1. A common disease presenting in an atypical way
2. An uncommon disease presenting typically
A common disease presenting in an atypical way
requires more thought about the less- common sites
of infection, acquiring samples from more protected
sites, consideration of testing in the immune
compromised and the possibility of partially treated
infections (see Boxes 10.6 and 10.7 for examples.)
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Patients with a fever
An uncommon disease presenting in a typical
manner requires thought about travel, occupation,
pets, hobbies, habits and any other unusual activity
that may present an infection risk.
Non- infectious causes of a PUO need to be
considered; they include neoplasms, autoimmune
syndromes, granulomatous diseases, drug fevers and
other miscellaneous causes, such as haematomas,
brain lesions, hyperthyroidism, tissue ischaemia or
infarction.
A thorough history, examination and investigations,
as described above, should be performed on all
patients with pyrexia of unknown origin, and the
examination repeated from time to time.
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ASSESSMENT IN PARTICULAR GROUPS
Patients in pain
Shankar Ramaswamy
11
Introduction
Pain is a familiar phenomenon that is part of our everyday life and is a feature of various diseases. It most
commonly accompanies an injury, where it serves its
most important purpose, namely, to protect us, alert
us and make us remove ourselves from danger. It can
possibly trigger a spinal withdrawal reflex (Fig. 11.1).
Both congenital insensitivity to pain and extreme sensitivity to pain (paroxysmal extreme pain disorder and
erythromelalgia) are rare genetic conditions, which are
disabling and shorten life span, highlighting the importance of pain to our welfare and survival. Pain severity
and its impact on an individual ranges from a trivial
occurrence, such as a needle- prick injury, to a sensation
of such intensity that it induces thoughts of suicide.
Definition
The International Association for the Study of Pain
(IASP) proposed the following definition (1979):
‘Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of damage’. This definition
has important implications. Pain is not necessarily or
always associated with ongoing tissue damage; rather,
it is a subjective experience and has an emotional as
well as a sensory component and is always unpleasant.
Pain is notoriously difficult to describe and even
harder to assess and quantify. Nevertheless, pain assessment is crucial in order to evaluate its impact on the
sufferer and also to plan a treatment strategy. It has
been termed ‘the 5th vital sign’ and is mandated as part
of routine assessment of patients in hospital. In 2004
the IASP declared that the relief of pain should be a
human right.
Although pain is a major source of suffering and
economic burden for patients, until recently, it was
not considered as a separate condition and systematically classified. Recognizing this, the World Health
Organisation (WHO), in their recent adoption of the
International Classification of Diseases (ICD- 11) in
May 2019, for the first time included chronic or longstanding pain as an independent disease and paved the
way for a systematic classification of the condition.
Classification of pain
There are many ways in which pain can be classified
in order to formulate an optimal treatment strategy.
Despite this, classifying a particular pain state can be
challenging because the pain syndrome may be of
mixed aetiology rather than fit into a single category.
Pain is commonly classified according to the fol-
lowing:
Aetiology and underlying condition
Mechanism
Duration
Aetiology/underlying condition
Trauma: an acute response to an injury
Surgery
Medical illness, such as myocardial infarction or
appendicitis
Physiological conditions, such as menstruation
and labour
Cancer
Mechanism
Inflammatory/Nociceptive: Pain generated and
maintained by inflammatory mediators (such as
prostaglandin E2), secondary to an ongoing disease
process. Examples include inflammatory arthritis.
Neuropathic: Neuropathic pain, which is gen-
erated in malfunctioning nerves, is defined as
‘pain arising as a direct consequence of a lesion
or disease affecting the somatosensory system’.
This type of pain has special clinical features as
described below and may arise from injury or
dysfunction of the central or peripheral nervous
system. Examples include painful diabetic neuropathy and post- stroke pain.
Nociplastic: Nociplastic pain is a new terminol-
ogy described in 2017. It is defined as pain that
arises from altered nociception despite no clear
evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the
somatosensory system causing the pain. Examples include fibromyalgia, complex regional pain
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‘Spinal withdrawal reflexes’
‘Perceive unpleasant sensation’
Pain ‘warning system’ essential for survival
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Patients in pain
Figure 11.1 Spinal withdrawal reflex with
pain.
Rapid behavioural response
syndrome (CRPS) type 1, some ‘musculoskeletal’
pain conditions, such as ‘nonspecific’ chronic low
back pain, and ‘functional’ visceral pain disorders,
such as irritable bowel syndrome, bladder pain
syndrome.
Mixed pain: This includes features of both noci-
ceptive and neuropathic pain, such as back pain
with radiculopathy (radiating leg pain caused by
nerve irritation or compression).
Psychosomatic: Pure psychosomatic pain is rare.
However, pain, especially chronic pain, almost invariably has an emotional and behavioural component.
Dominates attention
Modify behaviour
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Duration
Acute: Most commonly a physiological response
Chronic: It can either be associated with
Mechanisms of pain
stimulus that excites the central nervous system.
This mechanism was first proposed by Descartes in
the 16th century and conceptually still holds true.
However, it is crucial to appreciate that the final
subjective experience of pain is shaped by various
modulatory factors (Fig. 11.2).
to an injury. It resolves with the disappearance of
a noxious stimulus or within the time frame of a
normal healing process.
an ongoing pathological process, such as
rheumatoid arthritis or degenerative disc disease,
or be present for longer than is consistent with a
normal healing time. Pain is arbitrarily described
as chronic if it persists for longer than 3 months.
Chronic pain is often associated with disability,
mood and sleep disturbance and a significant
behavioural response.
At its simplest, pain is generated by a noxious
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A stimulus (which can be thermal, pressure or
chemical) excites nociceptors and the resulting
impulse is then transmitted to the spinal cord by
two different classes of nerve fibres, via the firstorder neurons located in the dorsal root ganglion
(Fig. 11.3): (i) faster, myelinated Aδ fibres and (ii)
smaller, slower unmyelinated C fibres. They transmit
the sensation to the dorsal horn of the spinal cord,
where these primary afferents synapse in lamina
I, lamina II (substantia gelatinosa), lamina IV and
some in lamina V. All these afferent sensory fibres
are excitatory. Second- order fibres are then carried
in the spinothalamic and spinoreticular tracts to the
thalamus, where they synapse. From the thalamus,
third- order neurons project to the somatosensory
cortex, anterior cingulate gyrus and the insular cortex, where they terminate. It is at this cortical level
that a stimulus is perceived as pain (see Fig. 11.3).
SECTION TWO
Cingulate cortex
Somatosensory cortex
Nociceptor
Spinal cord
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Patients in pain
163
Thalamus
Periaqueductal grey
Rostral ventral medulla
Figure 11.3 Pain pathway.
However, it is now known that the noxious sensory
input may be modulated at several levels in the spinal
cord and brain, thus altering the final pain experience.
The gate control theory proposed by Melzack and
Wall in 1965 states that non- noxious stimulation of
the large Aβ fibres inhibits the response to painful
stimuli of neurons with wide dynamic range (WDR
neurons, located primarily in lamina V of spinal
cord), reducing the input of small fibres mediating
the sensation of pain. A good example of this
modulation at the spinal level is ‘rubbing it better’
i.e. rubbing a painful area can decrease the intensity
or perception of pain. In addition, descending input
from higher centres (periaqueductal grey matter
and rostral ventral medulla) also modulates neural
activity in the spinal cord, reducing or enhancing
the pain sensation. Such descending input is one of
the mechanisms by which emotional and cognitive
factors modulate pain perception. Much remains to
be understood about the central pathophysiology of
pain.
In recent years, pain management has increasingly
adopted a biopsychosocial model. This has
highlighted the need to take into account the
interactions between biological, psychological and
Insular cortex
Amygdala
Parabrachial nucleus
Brain stem
social factors leading to an individual’s emergent
pain experience.
The patient in pain
As with any other branches of medicine, careful and
meticulous assessment of a patient’s symptoms and
signs is fundamental. Two key questions should be
considered when dealing with a patient in pain:
Is the pain a symptom of ongoing tissue damage
or of another condition that needs to be dealt
with by another medical professional?
What is the optimal treatment strategy: either to
abolish the pain altogether or reduce it to a more
bearable level?
History
Taking a history from a patient in pain is more com-
plex than recording symptoms and making a diagnosis. Even in acute pain states, where pain represents
a protective function and is a symptom of an injury,
approaching the patient as a whole and bearing in
mind the overall context, emotional, cognitive and
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Patients in pain
behavioural aspects is crucial for optimizing the
treatment strategy.
The first step is to evaluate the pain and thereby
try to understand its underlying mechanisms. This
process is described in Boxes 11.1 and 11.2 and
Tables 11.1 and 11.2.
Examination
The purpose of examination as part of pain evaluation
is described in Box 11.3.
Detailed examination will focus on different
systems according to a particular pain condition. It
may involve basic orthopaedic, neurological or surgical examination. Regardless of the approach, it
should follow conventional basic methods: inspection, palpation and range of movement, where
appropriate. For example, a patient who presents
with back pain will require at least inspection to
check for muscle spasm, posture, deformity, gait
and use of aids, such as crutches, and evidence of
previous surgery; palpation of paravertebral and
bony areas; and range of movement to evaluate
any restriction. The examination will also need
to include a neurological examination looking
at dermatomal sensory dysfunction (suggesting
radiculopathy) and particular tests (depending on
the region of the spine) to detect signs of nerve
root irritation using stretch tests such as Lasègue’s
test (or straight leg raising test) for low back pain;
and for the neck, the Spurling test (turning the
patient’s head to the affected side while extending and applying downward pressure to the top of
the patient’s head; a positive test is indicated by
pain arising in the neck radiating in the direction
of the ipsilateral corresponding dermatome). The
examination should also assess glove and stocking
sensory loss (characteristic of peripheral neuropathy), reflexes and plantar response, muscle power,
sensation and reflexes.
As part of the clinical examination it is important to
elicit features of neuropathic pain, such as allodynia
(pain caused by a stimulus that does not usually
provoke pain, for example a light touch using cotton
wool eliciting pain), and hyperalgesia or hypoalgesia
(increased or decreased pain, respectively, from a
stimulus such as pressure or pinprick that usually
provokes pain).
Investigation
Investigation of a patient in pain is tailored to the
individual’s presentation. It serves three important goals:
To exclude more sinister pathology
To provide diagnostic clues
To arrive at an optimal management strategy
The most common investigation employed by
pain specialists is imaging, for example using simple X- rays to exclude a pathological fracture, MRI
Box 11.1
The site of pain: This may give a clue to the underlying
pathology.
Distribution: Pain may follow a dermatomal or peripheral
nerve distribution or have no relation to anatomical
patterns.
Character of pain: Nociceptive (somatic or visceral)
versus neuropathic (see Table 11.1).
Duration of pain: This may have a bearing on the level of
disability and psychosocial cost of the pain.
Rapidity of onset and any precipitating factors: A
rapid or relatively recent- onset pain syndrome is
more likely to follow a conventional medical model,
whereby it is appropriate to search for an underlying
cause. Chronic pain requires a more biopsychosocial
approach.
Severity of pain and its change over time: This requires a
consistent method for measuring pain (see below).
Alleviating and exacerbating/aggravating factors: These
may support a better understanding of mechanisms that
sustain the pain.
Exclusion of more sinister pathology: ‘Red flags’.
Important conditions not to be missed include pain
related to underlying (or undiagnosed) cancer, pain
related to inflammation (such as rheumatoid arthritis)
and pain related to other serious medical/surgical
conditions requiring emergency treatment such
as cauda equina syndrome caused by spinal cord
compression.
Evaluation of psychosocial elements also known
as ‘yellow flags’ (see Box 11.2): These are not lifethreatening symptoms, but their presence means that
the psychosocial history has special relevance. Major
psychological illness should be addressed, along with
symptomatic relief of the pain, in the interim.
Previous and current treatments and their impact
Past medical history: Taking a full medical history must
not be overlooked. It may give invaluable clues as to
the aetiology and pathogenesis of pain. For instance,
history of recent herpes zoster (shingles) infection along
with a dermatomal distribution of neuropathic- type pain
(confirmed on examination with a residual, typical rash,
allodynia and hypoalgesia/hyperalgesia) will suggest a
diagnosis of postherpetic neuralgia. Certain common
illnesses associated with neuropathic pain are listed in
Table 11.2.
Impact of pain: Consider the effect of pain on the
patient’s activity, ability to work, mood, sleep,
relationships, etc.
Psychosocial history: The psychosocial assessment of
pain should be directed at finding the psychological
setting of the pain, particularly mood. It should
explore the patient’s beliefs and expectations.
Generally speaking, this is more relevant in chronic
pain states, because acute pain usually resolves
quickly.
Scheme for evaluating history associated with
pain
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165
to demonstrate changes within the central nervous system or an ultrasound examination of the
abdomen or soft tissues and joints. Neurophysiological (EMG) studies are helpful to determine
the presence and extent of any nerve damage, and
Box 11.2
Pain is described as having at least five dimensions, each of
which should be addressed:
The sensation of pain — the subjective experience
Suffering and distress — the emotional component
Expectations and beliefs — the cognitive component
Verbal (complaints) or non- verbal communication —
the behavioural component (illness behaviour) is the
way in which the patient responds to and expresses the
sensation of pain, which is influenced by various cultural
and social factors
Impact of social environment
Table 11.1 Nociceptive versus neuropathic pain
Description of pain Aching, localized, toothache- like,
Movement impact Associated with movement Independent
Physical examination Normal response Allodynia, hyperalgesia, vasomotor changes
Examples Injury, postoperative pain Peripheral neuropathies, shingles, cancer pain
Treatment strategies More classic approach, conventional
Psychosocial aspects of pain
Nociceptive Neuropathic
sharp, squeezing
analgesics
various blood tests may be used to determine,
for example, the activity of rheumatoid arthritis.
Any test used must be considered only as a part of
a more global approach, never in isolation. Some
tests such as Quantitative Sensory Testing and
functional imaging using PET- CT or fMRI are
used in the research setting to understand more
about the underlying pain mechanisms.
By the end of the assessment, any pathology
that needs to be dealt with by the relevant medical professional should be identified, either for
urgent management, if ‘red flags’ are elicited, or
electively.
Difficult cases
As the history is the key to pain assessment and treat-
ment, it is clear that communication is paramount.
Difficulty arises if there is a language barrier between
the physician and the patient, if the patient is a young
Shooting, radiating, stabbing, burning, electric shock- like
More biopsychological approach, conventional
analgesics ± non- conventional (antidepressants,
anticonvulsants, etc.)
Table 11.2 Common illnesses associated with chronic pain
Illness Nature of pain disorder
Diabetes Diabetic neuropathy: Commonly glove and stocking peripheral neuropathic pain
Connective tissue disorder Variable presentation of accompanying neuropathy
HIV Neuropathy owing to disease as well as to antiretroviral drugs
Trauma Multifactorial aetiology: Associated nerve injury causing neuropathy and or complex
Herpes zoster infection Post- herpetic neuralgia: Neuropathic pain with dermatomal distribution
Multiple sclerosis Central neuropathic pain, including trigeminal neuralgia
Cerebrovascular accident Post- stroke central neuropathic pain
Fibromyalgia Nociplastic musculoskeletal pain, usually primary but could be secondary to other
Complex regional pain syndrome Most likely owing to previous injury: Usually has features of allodynia, hyperalgesia and
Chronic post- surgical pain Variable incidence following variety of surgeries causing neuropathic pain
Degenerative bone and joint disease Variable sites: Mostly nociceptive, but with possible neuropathic component
Phantom limb pain Neuropathic pain following amputation, most commonly of extremities
Cancer Cancer and its treatment, such as radiotherapy and chemotherapy, cause chronic pain
regional pain syndrome
disorders, such as connective tissue disease
vasomotor changes of the extremities, recently classified as nociplastic pain
with neuropathic and/or nociceptive features
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11
Patients in pain
Box 11.3
To elucidate and evaluate any physical signs associated
To reassure the patient that pain does not imply any
To define baseline parameters and monitor their change
To understand the mechanisms that generate and
child or has learning difficulties, confusion or dementia. It is important as a physician to understand that
the pain a patient perceives could be influenced by
social and cultural factors as well as past experience.
The pain may prove refractory to treatment, with all
treatment options already exhausted, which again can
pose a challenging situation, necessitating a change in
goal setting.
The purpose of examination as part of pain
evaluation
with a particular painful condition
ongoing damage
over time
sustain the pain, in particular to identify neuropathic
elements
Measuring pain
Pain is a subjective experience and therefore
difficult to quantify. However, being able to quantify
pain will aid management by assessing severity
and allowing the measurement of treatment or
intervention effect and is crucial in research studies
looking at new treatment modalities. Measurement
tools may be unidimensional or multidimensional,
with the latter being more useful in chronic pain
conditions.
Unidimensional scales
Unidimensional scales are used very commonly,
particularly in cases of acute pain. They are simple,
sensitive, reproducible and quickly applied and give
a numerical value to the pain severity. They can be
either analogue or discrete. The latter may be numerical or verbal.
The most common of these scales is the Visual
Analogue Scale (VAS): The patient is given a horizontal line 10 cm long with ‘no pain’ on the lefthand side and ‘worst possible pain’ on the right and
is asked to mark the line according to the severity
of the pain.
The numerical rating scale: The patient is asked to
assign a number from 0 to 10 to his pain, 0 being no
pain at all and 10 being the worst imaginable pain. In
the verbal rating scale the patient rates his pain into
one of the following categories: none, mild, moderate or severe.
Multidimensional (complex) scales
The development of multidimensional scales acknowl-
edges the multidimensional impacts of pain on a
sufferer’s life. Common scales used include the
McGill Questionnaire and Brief Pain Inventory.
The original McGill Questionnaire assesses various
aspects of pain, including sensory qualities of pain,
affective qualities (e.g. tension, fear) and has evaluative words that describe the subjective intensity of
the total pain experienced. Various measurements
are derived from the data, but a short form of the
McGill Questionnaire is most often used (Fig. 11.4).
It is easy to apply and is reproducible.
To build up a complete assessment of a patient
with longstanding disabling pain, a battery of
measurement tools may be required, which may
include anxiety and depression measurement scales,
catastrophizing scales and disability index.
To assess for neuropathic pain, recently introduced
and validated tools such as the ‘painDETECT’ and
‘LANSS’ questionnaires are used to look for specific
features pertaining to neuropathic pain.
Treatment strategies
Acute pain
Acute pain management should be directed to the
treatment of the underlying cause as well as symptomatic pain relief itself. For example, fractures
should be reduced and immobilized and infections
treated with antibiotics. Pain in the acute setting as
well as that caused by cancer is then treated symptomatically with analgesic drugs in accordance
with the WHO pain ladder (Fig. 11.5). Pharma-
cological options include simple analgesics, such
as paracetamol, non-steroidal anti- inflammatory
drugs and opioids. There is also an option for
considering local anaesthetic nerve blocks, especially for pain following surgery and trauma. It is
increasingly recognized that poorly treated acute
pain can result in a chronic pain state, which can
become quite refractory to treatment.
Chronic pain
In chronic pain the emphasis shifts from management of the pain itself to addressing its psychosocial
sequelae and improving the patient’s function. This
often involves a multimodal treatment approach
under the umbrella of a biopsychosocial model. The
pharmacological options include the same as that
for acute pain, but medications can be less effective. In particular, there should be less emphasis on
the use of strong opioids in chronic pain, because
they become less effective and are associated with
significant short- term as well as long- term side
effects. The British Pain Society guidelines on the
use of opioids for persistent pain recommend a
maximum dose of 120 mg morphine- equivalent
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