Art & science long-term health conditions

Diagnosis and management of

patients with Raynauds phenomenon
Brown S (2012) Diagnosis and management of patients with Raynauds phenomenon.
Nursing Standard. 26, 46, 41-46. Date of acceptance: May 15 2012.

Abstract
This article describes the characteristics of Raynauds phenomenon,
focusing on the role of the specialist nurse in diagnosis and management
of the condition. Pharmacological and non-pharmacological treatment
options are discussed, along with the importance of self-management.
Advice is provided to help nurses enable patients to minimise episodes and
improve symptoms. In the majority of cases, Raynauds phenomenon is a
treatable condition, and patients can learn to self-manage the disease.

Author
Susan Brown
Lead specialist nurse in rheumatology, Royal National Hospital for
Rheumatic Diseases NHS Foundation Trust, Bath.
Correspondence to: sue.brown@rnhrd.nhs.uk

Keywords
Raynauds phenomenon, rheumatology, self-management

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Raynauds phenomenon is an episodic,

triphasic response to stimuli such as temperature
change or stress. This spasmodic reaction usually
occurs in the fingers and toes, but can also affect
the nose, nipples, ears, lips and penis (Mawdsley
and Brown 2005). Symptoms associated with
Raynauds phenomenon include numbness, pain and
paraesthesia, particularly during the recovery period
following a prolonged episode. The term Raynauds
phenomenon replaced the terms Raynauds disease
and Raynauds syndrome (LeRoy and Medsger
1992) because the terminology was confusing.
Raynauds disease is now known as primary
Raynauds phenomenon and Raynauds syndrome
is now known as secondary Raynauds phenomenon.

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Primary Raynauds phenomenon is idiopathic

and related to functional alterations in the
endothelium of the blood vessel walls, whereas
secondary Raynauds phenomenon occurs as a
result of structural microvascular abnormalities.
Secondary Raynauds phenomenon is associated
with various diseases, most commonly
rheumatological disease, but also haematological
disease such as occlusive arterial disease (Gayraud
2007). Raynauds phenomenon is a common
presenting feature of systemic sclerosis (scleroderma)
and is also seen in other connective tissue diseases
such as systemic lupus erythematosus (SLE),
mixed connective tissue disease and polymyositis
or dermatomyositis. Systemic sclerosis is an
autoimmune connective tissue disease of unknown
aetiology, characterised by inflammation, fibrosis,
and vasculopathy (LeRoy et al 1988). Raynauds
phenomenon is the presenting feature in 10-20%
of people who go on to develop a connective tissue
disease (Goundry et al 2012).

Triphasic response
The classic triphasic response that characterises
Raynauds phenomenon is an intermittent reaction
affecting the bodys extremities that is visible
to the naked eye. This sudden, reversible colour
change was described by Herrick (2005) as an
exaggerated vasospastic response. The first sign
is a whitening of the digits (pallor) as a result of
vasoconstriction, followed by a blue or black
cyanosis resulting in a feeling of severe coldness
and discomfort. This is followed by red flushing
(erythema) as the affected tissue is reperfused,
often resulting in a burning sensation.
These changes are usually symmetrical and
reversible, and there is often a clear line of
demarcation between the ischaemic and unaffected
digits. Symptoms usually resolve within one hour
and the thumb is often spared (Block and Sequeira
2001). If the thumb is involved, this can be an
indicator of secondary Raynauds phenomenon
thought to be due to different pathophysiological
processes that occur only in secondary Raynauds
phenomenon (Chikura et al 2010). Unilateral
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Art & science long-term health conditions

Raynauds phenomenon suggests either an arterial
lesion, thoracic outlet syndrome or an occupational
injury such as vibration white finger (Wigley 2002).
This occurs in people who use vibratory tools as
part of their profession, and can result in damage
to the small blood vessels in the hands. Thoracic
outlet syndrome results in neck and shoulder pain,
paraesthesia and weak grip in the fingers, which
can sometimes be related to the presence of an extra
cervical rib. Anyone presenting with unilateral
symptoms of Raynauds phenomenon should be
given a chest X-ray to identify whether an additional
cervical rib is causing thoracic outlet syndrome.
A diagnosis can be confirmed by computed
tomography, magnetic resonance imaging or
electromyography, and the problem can be resolved
with surgery (Povlsen et al 2010).

Prevalence and epidemiology

Raynauds phenomenon is more common in
women than men (Fraenkel 2002). Onset is often
during the teenage years, with the median age of
onset at 14 years; only 27% of people presenting
with the condition for the first time are 40 years
or older (Planchon et al 1994). The majority
of women with Raynauds phenomenon (85%)
have primary disease while 15% have secondary
disease, whereas in men the incidence of the
two types is equal (Gayraud 2007). It has been
suggested that Raynauds phenomenon is more
prevalent in colder climates (Fraenkel 2002). The
Raynauds and Scleroderma Association (2011)
has reported that oversensitivity of the peripheral
circulation to stressors such as temperature change
and stress affects 3-20% of adults worldwide and
as many as 10 million people in the UK. Riera et
al (1993) reported that 89% of cases of Raynauds
phenomenon is primary; approximately 12.5%
of people with Raynauds phenomenon develop
scleroderma and 13.6% develop other connective
tissue diseases (Koening et al 2008).

Pathophysiology
Risk factors for developing Raynauds phenomenon
include a family history of the disease, female
gender and secondary risks such as occupational
use of vibrating tools, medication such as betaadrenoceptor blocking drugs or amphetamines
and underlying conditions such as atherosclerosis,
hypothyroidism, polycythaemia and other
hyperviscosity states. A comprehensive patient
history is essential to exclude differential diagnoses
such as thoracic outlet syndrome, complex regional
pain syndrome, embolic disease and neuropathy
(Goundry et al 2012).
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Primary and secondary Raynauds phenomenon

differ in pathophysiology, with some authors
suggesting a functional cause in primary disease
and a structural cause in secondary disease
(Herrick 2005). If autoantibodies usually found in
connective tissue diseases, such as anti-centromere
or antiScl-70 (topoisomerase I), are present
but there is no clinical evidence of established
autoimmune disease, a diagnosis of autoimmune
Raynauds phenomenon can be made. Patients with
autoimmune Raynauds phenomenon should be
monitored closely as they may develop a connective
tissue disease such as scleroderma. Secondary
Raynauds phenomenon is diagnosed in the
presence of autoantibodies, such as anti-centromere
or antiScl-70 (topoisomerase I), in the presence of
signs and symptoms consistent with a diagnosis of
a connective tissue disease such as scleroderma.
Raynauds phenomenon results from an
imbalance between the effects of vasoconstriction
and vasodilation. In secondary Raynauds
phenomenon, there is also evidence of endothelial
abnormalities, changes in vascular tone and in
circulating mediators responsible for platelet
activation, and oxidative stress that predispose
to vasoconstriction (Herrick 2005).
In primary Raynauds phenomenon, the capillary
loops along the nail bed are normal. However in
secondary Raynauds phenomenon, capillaries
in the nail bed can be enlarged and disorganised,
show drop-out (loss of capillaries from cuticle bed)
or may haemorrhage, and avascular areas are often
visible. Video capillaroscopy is a safe and easy
method of assessing capillary beds and is helpful
in differentiating between primary and secondary
disease (Herrick and Cutolo 2010).

Diagnosis
A clinical diagnosis of Raynauds phenomenon
is made following assessment, examination and
investigation. The diagnosing clinician can ask
three simple questions, including (Wigley 2010):
Are
 you more sensitive to the cold than others
you know?
Do
 you notice colour changes on the skin of
your fingers when you are exposed to the cold?
Are
 the skin colours white and/or blue?
Obtaining a comprehensive history is essential in
distinguishing primary from secondary disease,
and includes:
Observed

triphasic response to stress or cold;
this should include details of the frequency and
pattern of changes and associated symptoms.
Symmetry

(or asymmetry) of symptoms.
History

of digital ischaemia and pattern of
presentation.

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Exposure

to any precipitating factors such
as drugs known to aggravate the condition,
occupational exposure (to exclude vibration
white finger) or smoking.
Full
 clinical history to exclude any secondary
causes such as arthralgias or mylagias,
digital ulceration, dry eyes or mouth, rashes,
photosensitivity or migraines.
A thorough clinical examination is essential and
should include:
Observation

for any colour changes of the
hands, noting any visible nail bed changes and
evidence of digital ischaemia or digital ulcers
(Figure 1). Digital ulceration is rarely seen in
primary Raynauds phenomenon; an underlying
connective tissue disease should be suspected
if either a history of ulceration is described
or evidence of previous ulceration is seen on
examination (Goundry et al 2012).
Examination

of the integrity of the skin for
evidence of chronic paronychia (a bacterial
or fungal infection of the skin around the
nail), finger tip scarring or loss of finger pulp
suggesting previous ulceration.
Identification

of other cutaneous features
and rashes as they may help to diagnose an
associated connective tissue disease such as
dermatomyositis, SLE or scleroderma.
Evidence

of other associated conditions such
as carpal tunnel syndrome, neuropathic
conditions, thoracic outlet syndrome or any
signs of underlying autoimmune aetiology.

Investigations
To differentiate primary from secondary
Raynauds phenomenon, the assessing clinician
needs to conduct several important investigations.
These include:
Blood

tests, comprising a full haematological
and biochemical screen including
inflammatory markers of C-reactive
protein and plasma viscosity.
If
 there is clinical suspicion of an underlying
autoimmune disease, then bloods should
include a full autoimmune screen. This should
include antinuclear antibody, extractable
nuclear antibodies, including those associated
with scleroderma (such as anti-centromere or
antiScl-70 (topoisomerase I)) and antibodies
associated with other conditions, such as
Sjogrens syndrome (anti-Ro (SS-A) or
anti-La (SS-B)), SLE (anti-Sm, crithidia and
double-stranded DNA) or rheumatoid arthritis
(anti-cyclic citrullinated peptide antibodies).
Anti-Pm/Scl-70 is found in 50% of patients
with overlapping polymyositis and scleroderma

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in which Raynauds phenomenon can also

be a feature (Oddis et al 1992).
For
 those with unilateral symptoms,
investigations for thoracic outlet syndrome
should be conducted. A chest X-ray, including
spinal views, will determine the presence of
a cervical rib that may be compressing the
bronchial and cephalic vascular branches.
Nailfold

capillaroscopy is an important test,
which helps differentiate between normal
shaped capillaries found in primary Raynauds
phenomenon from abnormal capillaries found
in secondary disease. Video capillaroscopy is the
gold standard if available.
The
 cold stress test is useful for cases in
which diagnosis is uncertain. An abnormal
exaggerated response to cold is seen in
Raynauds phenomenon. Rewarming usually
occurs in less than 15 minutes, but in patients
with Raynauds phenomenon this can take
more than 20 minutes (Goundry et al 2012).
Laser

Doppler flowmetry can be used
to measure the microcirculation blood
flow (Goundry et al 2012) and infrared
thermography is an indirect method of blood
flow assessment that can also measure skin
temperature (Herrick and Clarke 1998).
Arterial

Doppler studies should be conducted in
any patient with clinical evidence of large vessel
occlusive disease.

Treatment options
Non-pharmacological approaches
Treatment for patients with Raynauds phenomenon
depends on the severity of symptoms and any
other presenting features or evidence of underlying
disease. There are some lifestyle approaches that

FIGURE 1
Ulceration in a patient with secondary Raynauds phenomenon

Reproduced with kind permission from the patient

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Art & science long-term health conditions

can be adopted to improve symptoms. Advice
should include reducing exposure to known triggers
such as temperature change and stress. Sensible
measures can be taken in the home, at work and
when outside to minimise temperature variation.
Stress is inevitable in life, but steps can be taken to
decrease stressful experiences wherever possible
(Wigley 2002). Smoking cessation is important
as not only does smoking constrict blood vessels
but also reduces blood flow and oxygen levels in
the peripheries (Herrick 2005). Development of
complications, including worsening of frequency
and severity of exacerbations and ulceration,
should be investigated immediately (Brown 2010).

Pharmacological approaches

The first approach should be to withdraw any

treatment that may be a precipitating factor. There is
some evidence to suggest that high doses of fish oils
improve microcirculation, evening primrose oil can
provide symptomatic relief from the cold, and gingko
biloba and ginseng can improve microcirculation
in the short term (Wright et al 2005). More
conventional approaches to managing and
improving symptoms include using vasoconstrictors
and vasodilators, such as calcium channel blockers,
angiotensin II-receptor antagonists, selective
serotonin-reuptake inhibitors, topical nitrates and
prostaglandins (Kowal-Bielecka et al 2009). Herrick
(2005) suggested that new approaches to treatment
need to include not only inhibiting vasoconstriction
and enhancing vasodilation, but also reducing
endothelial injury, and inhibiting platelet aggregation
and coagulation (Box 1).

BOX 1
Approaches to the management of patients with Raynauds
phenomenon
Inhibitors of vasoconstriction:
Angiotensin-II receptor antagonists, for example losartan.
Selective serotonin reuptake inhibitors, for example fluoxetine.
Endothelin-1 receptor antagonists, for example bosentan.
Enhancers of vasodilation:
Calcium channel blockers, for example nifedipine.
Phosphodiesterase type-5 inhibitors, for example sildenafil.
Prostaglandins, for example intravenous iloprost.
Topical nitrates (glyceryl trinitrate patches).
Reducing endothelial injury:
Antioxidants such as fish oils.
Endothelin-1 receptor antagonists.
Prostaglandins.
Smoking cessation.
Inhibition of platelet aggregation and coagulation:
Anti-platelet agents for example, aspirin.
Anti-fibrinolytics.
Smoking cessation.

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By adopting a stepwise approach to management

(Table 1), medications can be adjusted according
to severity of disease and side effects, and
complications such as digital fingertip ulceration
(as seen in secondary Raynauds phenomenon).
Calcium channel blockers are the most commonly
prescribed drugs for the treatment of Raynauds
phenomenon. A meta-analysis has shown that
nifedipine gives short-term relief of symptoms,
reducing severity by 33%, and may also reduce
the risk of ulcers developing (Thompson and Pope
2005). However, treatment with calcium channel
blockers is limited by their side effects. Angiotensin
converting enzyme inhibitors may show benefit,
although a randomised controlled trial found that
quinapril was not beneficial (Gliddon et al 2007).
Several treatment options are available for digital
ulceration in secondary Raynauds phenomenon
to prevent critical digital ischaemia. Intravenous
prostanoids, such as iloprost, are efficient in healing
ulcers in patients with scleroderma (Kowal-Bielecka
et al 2009). Sildenafil, a phosphodiesterase type-5
inhibitor, has been studied in case reports, case
series and open-label studies as a potential treatment
in digital ulceration (Impens et al 2011). Although
sildenafil is well tolerated and has been shown to
improve peripheral circulation, it remains an off
licence treatment for Raynauds phenomenon and
its use is limited because of lack of robust evidence
from clinical trials (Impens et al 2011). Bosentan is
a endothelin-1 receptor antagonist that reduces the
number of new ulcers in patients with sclerodermaassociated digital ulcer disease, but does not speed
healing of established ulcers (Korn et al 2004).
EUSTAR (the EULAR Scleroderma Trials and
Research group) made the following treatment
recommendations for scleroderma-related
vasculopathy, including Raynauds phenomenon
and digital ulceration, based on the best available
clinical evidence (Kowal-Bielecka et al 2009):
A
 combination of oral nifedipine and
intravenous iloprost to reduce the frequency
and severity of episodes.
Intravenous

iloprost is effective at healing
digital ulcers in those with secondary Raynauds
phenomenon and should be used in active digital
ulceration.
Bosentan

should be considered in those with
scleroderma with multiple digital ulcers if
calcium channel blockers and prostanoids have
been ineffective.

Self-help and patient empowerment

Symptoms of Raynauds phenomenon may be
difficult for people to manage and affect their daily
activities. Pain can be difficult to control because of

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the spasmodic nature of Raynauds phenomenon,

which can affect the persons ability to manage
simple tasks such as opening jars, changing a nappy
or writing (Mawdsley 2011). A nurse specialist can
support patients in their activities of daily living
and in managing symptoms (Wilson and Vincent
2006). Nurses can give regular support via telephone
advice lines (Royal College of Nursing 2006), which
is especially important to people with Raynauds
phenomenon who may be concerned about critical
ischaemia. The effect of ulceration can be debilitating
and specialist nurses are best placed to support
patients by enabling them to develop effective
self-management strategies (Brown 2010).
An important aspect of management includes
prevention of exacerbations and minimisation of
risk of ulceration (Goundry et al 2012). Recognising
triggers and reducing stress are the most effective
approaches. Patients can be encouraged to use a
diary to document the frequency and intensity of
episodes, including the length of an episode and any
precipitating factors. This will help the individual to

pinpoint any triggers that need to be addressed.

Other conservative approaches include the use of
hand warmers as it is temperature change, rather
than the cold itself, that is likely to trigger a reaction
(Goundry et al 2012). Wearing layers of clothing
will keep the person warmer than wearing a thick
jumper and sensible approaches, such as avoiding
air conditioning may prevent exacerbations.
Informing patients about red flag symptoms
that may require urgent advice, such as severe
worsening of the condition, any permanent
discolouration of digits or severe pain, is
important as these warrant early access to
specialist services. The specialist nurse is able
to support and advise the patient about ways to
prevent critical digital ischaemic events. Dressings
are an important aspect of management; the
severity of the wound and any associated infection
should be assessed to prevent further tissue loss.
Simple dressing applications are often effective
in improving wound healing and providing
protection (Brown 2010).

TABLE 1
Stepwise approach to the management of symptoms
Drug

Dosing regimen

Side effects

5mg three times a day, up to 20mg three

times a day adjusted according to response.
5-20mg daily.
2.5-10mg daily.
30-120mg three times a day (or slow release
at 120-300mg daily).

Headaches, dizziness, facial flushing, tachycardia,

palpitations and ankle oedema. Start at low dose
to avoid problems with blood pressure.

Calcium channel blockers

Nifedipine
Amlopidine
Felodipine
Diltiazem

Angiotensin II-receptor antagonists

Losartan

25-100mg daily.

Headache, dizziness, fatigue and diarrhoea.

Selective serotonin-reuptake inhibitors

Fluoxetine

20-40mg daily.

Tremors, diarrhoea, insomnia and nausea.

Applied to the dorsum of the finger.

Headache, tachycardia, nausea, rash, angina,

impotence and rebound hypertension.

0.05mg diluted in 25ml sodium chloride

administered through a syringe driver up to
3ml/hour over a six-hour period.

Flushing, headache, nausea and vomiting,

abdominal cramps and hypotension.

Topical nitrates
Glyceryl trinitrate
Prostaglandins
Intravenous iloprost

Phosphodiesterase type-5 inhibitors

Sildenafil

Up to 75-150mg as split doses as tolerated.

Headache, facial flushing, indigestion, diarrhoea

and pain in the arms or legs.

Endothelin-1 receptor antagonists

Bosentan

62.5mg twice daily for 4 weeks, then 125mg

twice daily if full blood count and liver
function tests are normal.

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Anaemia, abnormal liver function tests, ankle

swelling, anaemia and reflux.

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Art & science long-term health conditions

In complex long-term health conditions such
as Raynauds phenomenon it is important to take
a multidisciplinary approach to management.
Referral to occupational therapy and physiotherapy
is essential to keep the patient as mobile and
independent as possible. This will depend on the
severity of the patients condition and whether or
not he or she has an associated diagnosis such as
scleroderma. Patient support groups such as the
Raynauds and Scleroderma Association, Arthritis
Research UK and the Scleroderma Society provide
essential support to patients. This can include patient
information leaflets and contact with other people
who have similar symptoms.

Conclusion
Raynauds phenomenon is a complex circulatory
disorder that either presents in isolation (primary)
or secondary to connective tissue diseases.
Although symptoms are problematic for some
patients and complications can be serious,
for the majority of patients Raynauds
phenomenon is manageable and treatable and
symptoms can be controlled by avoiding triggers.
Raynauds phenomenon is a complex condition
that is currently being investigated in several
specialist centres in the UK to gain a better
understanding of the disease processes and
improve symptoms for patients NS

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