Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Complex regional pain syndrome
Musculoskeletal medicine and orthopaedics · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
!
Exclude limb-threatening alternatives first
Disproportionate limb pain can also signal compartment syndrome, infection, arterial compromise, DVT, unstable fixation or acute nerve injury, each of which requires a different urgent pathway.
Action: Repeat skin, wound, vascular, neurological and compartment assessment, remove constricting casts or dressings when indicated and obtain urgent surgical or vascular review before attributing acute deterioration to CRPS.
Overview
Diagnose complex regional pain syndrome clinically without missing dangerous mimics, then restore function through early coordinated rehabilitation, pain treatment and psychologically informed support.
Ask about the original injury, surgery, cast or immobilisation and the timing and spread of pain. Map pain without forcing it into one nerve, and characterise allodynia, hyperalgesia, swelling, colour, temperature, sweating, stiffness, weakness, tremor, dystonia and hair, nail or skin change. Establish sleep, mood, work, self-care and avoidance. Examine wounds, joints, fixation, pulses, capillary refill, compartments and named nerves first because infection, ischaemia, compartment syndrome and mechanical failure cannot be missed.
Apply Budapest criteria at the bedside. The patient must have continuing disproportionate pain and report at least one symptom in three of sensory, vasomotor, sudomotor or oedema, and motor or trophic categories. Examination must demonstrate at least one sign in two or more categories, and no other diagnosis may explain the findings better. Temperature asymmetry over one degree supports a vasomotor sign. Signs can fade over time, so reliable documentation of earlier features can support CRPS not otherwise specified in selected specialist assessment.
Aetiology
01
Trauma and fracture
CRPS commonly follows limb fracture, sprain or soft-tissue injury, with symptom severity disproportionate to the original tissue damage and no relationship to injury magnitude.
02
Surgery and immobilisation
Operative tissue injury, nerve irritation, swelling, tight dressings and prolonged disuse can provide a trigger, although CRPS is not proof of negligent care.
03
Nerve lesion subtype
CRPS type I has no confirmed major nerve lesion, while type II follows demonstrable nerve injury; both share regional sensory, autonomic and motor abnormalities.
04
No obvious inciting event
A minority develop a compatible syndrome without recognised trauma, so absence of a remembered injury does not exclude diagnosis once alternative disease is assessed.
Pathophysiology
1
Peripheral sensitisation
Inflammatory mediators and injured nociceptors lower peripheral thresholds, producing hyperalgesia and pain from normally innocuous touch, temperature or movement.
2
Central amplification
Spinal and cortical processing becomes sensitised, altering body representation, movement planning and pain modulation beyond the anatomical territory of one nerve.
3
Autonomic dysregulation
Abnormal sympathetic and microvascular control contributes to temperature, colour, sweating and oedema asymmetry, which may change from warm to cool phenotypes over time.
4
Motor disuse cycle
Pain, fear and altered motor control reduce movement; stiffness, weakness and cortical reorganisation then magnify disability and make ordinary loading more threatening.
5
Trophic tissue change
Persistent autonomic, inflammatory and disuse effects can alter skin, hair, nails, fascia and bone, sometimes producing contracture and regional osteopenia.
Clinical features and red flags
Disproportionate regional pain
Pain exceeds the expected tissue course and is regional rather than confined to one dermatome or peripheral nerve.
Sensory abnormality
Allodynia to light touch or temperature and hyperalgesia to pinprick fulfil the sensory category when demonstrated clinically.
Vasomotor asymmetry
Side-to-side temperature greater than one degree or colour asymmetry provides an objective Budapest vasomotor sign.
Oedema or sweating change
Regional swelling, hyperhidrosis or hypohidrosis that differs from the other limb contributes the sudomotor category.
Motor and trophic change
Reduced range, weakness, tremor, dystonia or altered hair, nail and skin growth can complete the multisystem pattern.
Changing warm and cool features
Temperature and colour signs often lessen or change over time even while pain and motor disability remain active.
Red flags requiring action
Pain on passive stretch, tense compartments or rapidly escalating analgesic need after injury or casting requires emergency compartment-syndrome assessment.
Fever, wound discharge, spreading erythema, joint effusion or systemic illness raises concern for infection and needs prompt source investigation.
A cool pale pulseless limb, acute motor loss or worsening perfusion needs immediate vascular and orthopaedic assessment.
Investigations
01First-line Budapest clinical assessmentFirst stepFirst line
Why
Establish the required pain, symptom and observed-sign pattern while testing whether another diagnosis is better.
Interpretation and limitations
All four logical requirements must be met; symptoms alone without signs do not satisfy current clinical criteria.
02Plain radiographs of the affected region
Why
Assess fracture union, alignment, hardware, arthritis and other structural causes of persistent regional pain.
Interpretation and limitations
Patchy osteopenia may occur but is neither required nor specific and must not be used as a solitary diagnostic test.
03Targeted vascular or infection testing
Why
Exclude DVT, arterial compromise, wound infection, septic arthritis or osteomyelitis when clinical features suggest them.
Interpretation and limitations
Select Doppler, blood tests, aspiration or imaging by the competing diagnosis; CRPS should not suppress investigation of red flags.
04MRI for a structural differential
Why
Evaluate occult fracture, marrow disease, infection, tendon injury or other local pathology when examination and radiographs remain discordant.
Interpretation and limitations
MRI can exclude alternatives but has no finding that independently confirms CRPS.
Differential diagnosis
01
Infection or inflammatory arthritis
Fever, raised inflammatory markers, a wound, true synovitis or effusion and progressive structural change requires microbiological or rheumatological assessment.
02
Vascular disease
Acute ischaemia, DVT, venous insufficiency and lymphoedema can create colour, temperature and swelling changes but follow different anatomical and imaging patterns.
03
Mechanical or fixation failure
Malunion, non-union, instability, tendon rupture or hardware prominence produces load-linked pain and structural findings that need orthopaedic correction.
04
Peripheral nerve lesion
Entrapment, neuroma, radiculopathy or plexopathy generally follows a defined neural distribution and may show focal weakness or electrodiagnostic abnormality.
05
Factitious or functional presentation
Functional symptoms or self-inflicted skin change may coexist with pain, but should be considered carefully only after positive assessment rather than inferred from distress.
Management
01RecognitionConfirm criteria and exclude dangerFirst stepRegional pain and autonomic or motor change persist beyond the expected injury course.+
1Repeat wound, joint, fixation, compartment, vascular and named-nerve examination before applying a pain label.
2Document Budapest symptoms and observed signs in each of the four categories.
3Order only targeted tests for infection, vascular, structural or nerve alternatives.
4ConfirmatoryExplain the working diagnosis and arrange early therapy and pain follow-up without waiting for a confirmatory scan.
02Early functional careRestore safe limb useCRPS is diagnosed or strongly suspected and structural loading limits are known.+
1Agree specific functional goals and give a non-threatening explanation that validates pain and supports recovery.
Complications
01
Persistent pain and disability
Ongoing allodynia, weakness and fatigue can restrict self-care, mobility, work and social participation long after the inciting tissue has healed.
02
Contracture and stiffness
Pain-avoidant positioning, dystonia and tissue shortening can cause fixed loss of joint range that becomes harder to reverse with time.
03
Psychological distress
Unpredictable pain and diagnostic delay increase anxiety, depression, sleep disturbance and threat beliefs, which deserve treatment without implying symptoms are imagined.
04
Medication-related harm
Sedation, falls, cognitive impairment, weight change, dependence and withdrawal can accumulate when medicines are escalated without functional review.
05
Recurrent perioperative flare
Further surgery or immobilisation of an affected limb may exacerbate symptoms, requiring planned analgesia and early rehabilitation rather than absolute avoidance of necessary treatment.
Monitoring and follow-up
Map Budapest signs and symptoms over time, recognising that autonomic signs may fade while pain and motor problems persist.
Track active range, oedema, limb use, gait or hand function and personally meaningful tasks rather than pain score alone.
Review medicine benefit after titration against sedation, cognition, falls, weight, oedema, renal function and dependence risk.
Screen and treat depression, anxiety, sleep disturbance, trauma responses and suicidal thinking without psychologising the diagnosis.
Re-examine new focal pain, fever, wound change, vascular symptoms or named-nerve deficit for a superimposed diagnosis.
After specialist intervention or programme, maintain a written self-management, flare and vocational plan across primary and secondary care.
Special situations
No confirmatory scan exists
Bone scan and MRI abnormalities can occur, but diagnosis rests on clinical criteria and exclusion of better explanations.
Signs can fade
Later coolness or absent swelling does not necessarily equal recovery when pain, dystonia and functional loss remain.
Movement is treatment
Carefully graded use reverses disuse and altered motor processing, while prolonged protection can deepen disability.
Distress is not causation
Anxiety and depression commonly follow persistent severe pain and should be treated without invalidating the physical syndrome.
A label can hide new disease
Infection, DVT, nerve compression or fixation failure can arise later and must be investigated when the pattern changes.
Surgery needs coordination
Necessary procedures are not absolutely contraindicated, but analgesia, handling and early rehabilitation should be planned across teams.
Common pitfalls
01
Diagnosing CRPS from pain and swelling alone without documenting the full Budapest requirements.
02
Ordering routine bone scintigraphy and delaying functional treatment while waiting for confirmation.
03
Immobilising indefinitely because movement hurts despite a structurally safe limb.
04
Escalating multiple sedating medicines without measuring functional benefit or planning withdrawal.
05
Attributing symptoms to anxiety and overlooking objective vasomotor, sensory or motor findings.
06
Assuming every later symptom is CRPS and missing infection, thrombosis, nerve injury or hardware failure.
Practice
Two practice questions
Your practice draft is saved in this browser.
Question 1 of 2
0 correct
Musculoskeletal medicine and orthopaedicsOriginal SBA
Budapest diagnostic pattern
A patient has continuing regional pain disproportionate to a wrist fracture. They report symptoms in all four Budapest categories and have signs in sensory and vasomotor categories today. No alternative diagnosis fits better. Which interpretation is correct?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
CRPS is a clinical diagnosis. Plain radiographs can assess fracture healing, alignment and alternative pathology; MRI may exclude infection, osteonecrosis, tendon or structural disease; ultrasound assesses DVT; nerve conduction may define a nerve lesion. Regional osteopenia or increased scintigraphic uptake is neither necessary nor specific, and routine three-phase bone scanning can delay treatment. Blood tests investigate infection, inflammatory disease or metabolic alternatives only when indicated.
Explain that pain is real, the limb is usually safe to use within structural limits and gradual restoration is central. Refer to a therapist familiar with CRPS for desensitisation, oedema control, active range, graded loading, functional tasks and body-perception or graded motor-imagery techniques where appropriate. Set meaningful goals such as washing, handwriting, stairs or work rather than waiting for pain to disappear. Avoid forceful passive treatment, unnecessary immobilisation and adversarial language when progress fluctuates.
Use medicines as one support for rehabilitation, not the sole intervention. NICE neuropathic-pain options include amitriptyline, duloxetine, gabapentin or pregabalin, selected around comorbidity and adverse effects. Establish baseline pain interference and function, titrate one change at a time and stop ineffective treatment gradually. Long-term strong opioids are rarely appropriate. Specialist pain teams can offer interdisciplinary programmes and, for refractory disabling disease after integrated care, assess neuromodulation or other specialist procedures.
Address sleep, anxiety, depression, trauma and work participation through psychologically informed care while avoiding the false claim that CRPS is caused by personality. Involve pain psychology when fear, distress or avoidance blocks rehabilitation. Plan necessary future operations with the surgeon, anaesthetist, pain and therapy teams, minimising immobilisation and restarting movement when safe. Reassess the diagnosis when the pattern changes, because a later infection, nerve compression or hardware problem can occur in a limb already labelled CRPS.
Key points
CRPS is continuing regional pain disproportionate to the inciting event with sensory, vasomotor, sudomotor or oedema and motor or trophic abnormalities.
Use Budapest criteria: continuing disproportionate pain, symptoms in at least three of four categories, signs on examination in at least two categories and no better diagnosis.
First-line assessment is clinical examination and exclusion of dangerous mimics; no blood test, MRI or bone scan confirms CRPS.
Type I has no confirmed major nerve injury and type II follows nerve injury, but the rehabilitation principles are similar.
Refer early to physiotherapy or occupational therapy and pain services when symptoms are persistent, severe, diagnostically uncertain or function is deteriorating.
Management combines clear explanation, desensitisation, graded functional use, oedema and range work, laterality or motor imagery where appropriate and psychological strategies for living with pain.
For neuropathic pain, amitriptyline may start at 10 to 25 mg orally in the evening and increase by 10 to 25 mg every 3 to 7 days toward 25 to 75 mg daily as tolerated; review function and adverse effects.
Pregabalin may start at a total 150 mg daily in two or three divided doses, rise to 300 mg after 3 to 7 days and at most 600 mg after another 7 days, with renal adjustment and a discontinuation plan.
Scalding pain confined to one named nerve distribution after surgery or trauma may indicate acute nerve injury or entrapment requiring urgent surgical review.
New whole-limb swelling, venous tenderness, chest pain or breathlessness requires DVT or PE assessment rather than a CRPS assumption.
Suicidal thoughts, severe depression, medication dependence or catastrophic functional collapse requires urgent mental-health or specialist pain support alongside physical care.
05Nerve conduction and specialist neurological assessment
Why
Define a suspected nerve lesion, entrapment, radiculopathy or plexopathy and help distinguish CRPS type II.
Interpretation and limitations
Normal testing does not exclude CRPS type I; use it when the neurological distribution or weakness creates a genuine question.
2
Begin graded desensitisation, active movement, oedema care and progressive functional loading with skilled therapy.
3Address sleep, mood, fear and work barriers and involve family without reinforcing complete avoidance.
4EscalationReview within weeks and escalate early when pain or disability prevents participation.
03Pain treatmentUse medicine to enable rehabilitationPain intensity or allodynia blocks sleep, therapy or daily function.+
1Select one NICE neuropathic-pain option around age, cardiac, renal, mental-health and medicine risks.
2Start low, titrate at supported intervals and record functional benefit and adverse effects alongside pain.
3Plan gradual withdrawal before prescribing pregabalin or other dependence-associated medicine and avoid routine long-term strong opioids.
4Refer to specialist pain care for severe symptoms, diagnostic uncertainty or failure of a meaningful trial.
04Refractory disabilityEscalate interdisciplinary rehabilitationEscalationIntegrated community treatment does not restore participation or fixed motor and psychological barriers develop.+
1Recheck diagnosis and image or test any new focal mechanical, vascular, infectious or neurological feature.
2Use an interdisciplinary pain-management or specialist rehabilitation programme with therapy and psychology.
3Consider neuromodulation only through an experienced specialist service after appropriate integrated management.
4Coordinate vocational, equipment and social support and maintain self-management beyond procedure-focused care.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Can reduce neuropathic pain and improve sleep sufficiently to support desensitisation, movement and daily function.
Amitriptyline for neuropathic pain
Start 10 to 25 mg orally in the evening and increase by 10 to 25 mg every 3 to 7 days as tolerated; the usual neuropathic-pain range is 25 to 75 mg daily.
Use lower doses in older or cardiovascular patients; review anticholinergic effects, sedation, falls, urinary retention, glaucoma, arrhythmia, overdose risk and interacting serotonergic medicines.
May reduce neuropathic pain when selected as part of a rehabilitation plan and response is reviewed against function.
Pregabalin for neuropathic pain
Start a total 150 mg orally each day in two or three divided doses; increase to 300 mg daily after 3 to 7 days and, if needed, to no more than 600 mg after another 7 days.
Adjust for renal impairment and monitor dizziness, somnolence, oedema, respiratory depression with opioids and misuse; agree gradual discontinuation before starting and never stop abruptly.