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CRUSH SYNDROM and SUDECK'S ATROPHY

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CRUSH SYNDROME

Definition

Crush syndrome is the systemic manifestation that results from prolonged crushing of muscle tissue and the subsequent release of toxic intracellular contents into the circulation when blood flow is restored (reperfusion). It was first described in victims trapped during the London Blitz in World War II.
  • Bailey and Love's Short Practice of Surgery, 28th Ed.
  • Rosen's Emergency Medicine, Concepts and Clinical Practice

Pathophysiology

When a large volume of muscle is crushed and then released, a reperfusion injury occurs. The key mechanisms are:
  1. Rhabdomyolysis - massive muscle destruction releases myoglobin, potassium, phosphate, and uric acid into the circulation.
  2. Myoglobinuria - myoglobin precipitates in renal tubules (especially in acid urine), causing tubular obstruction and acute tubular necrosis (ATN) - the main cause of renal failure.
  3. Fluid sequestration - many litres of fluid are trapped in the crushed compartment, causing hypovolemia and renal vasoconstriction further worsening ischaemia.
  4. Electrolyte disturbances - hyperkalaemia (from dying cells), hypocalcaemia (Ca²⁺ influx into damaged muscle), hyperphosphataemia, and metabolic acidosis (anion-gap type) all develop.
  5. Vasoactive mediators released from crushed tissue contribute to systemic effects.
  6. DIC (disseminated intravascular coagulation) can also occur.
The severity increases with the extent of body area crushed. Under extreme conditions crush syndrome can develop within 1 hour; typically it takes 4-6 hours. It occurs in 3-20% of earthquake victims and up to 40% of survivors of multi-storey building collapses.

Causes / Settings

  • Earthquakes, mining accidents, battlefield casualties
  • Industrial crush injuries
  • Prolonged immobility (e.g., drug-induced unconsciousness on a hard floor)
  • Vascular occlusion causing large tissue ischaemia (e.g., femoral artery occlusion)
  • Untreated compartment syndrome
  • Burns (over large surface areas)

Clinical Presentation

Early (on extrication):
  • Patient may appear stable initially but deteriorates rapidly after release
  • Lacerations, fractures, bruising at the crush site
  • Compartment syndrome features
Systemic (after release):
  • Hypovolemic shock (fluid sequestration/third spacing)
  • Oliguria or anuria - dark, cola/tea-coloured urine (myoglobinuria)
  • Dysrhythmias due to severe hyperkalaemia and metabolic acidosis
  • Acute kidney injury (AKI) / acute renal failure
Delayed (days later):
  • Acute renal failure requiring dialysis
  • ARDS (acute respiratory distress syndrome)
  • Sepsis
  • Ischaemic organ injury
  • Multi-organ failure
Extensive crush injury showing depth of soft tissue devitalisation
Extensive crush injury in a man trapped in a fallen house. The depth of soft tissue devitalisation is clearly visible. - Bailey and Love's Surgery, p. 479

Treatment

The golden rule: begin treatment BEFORE extrication.

Pre-hospital / Field

  • Aggressive IV fluid resuscitation (normal saline 1000-1500 mL/h in adults) should begin as soon as the victim is found, before release, to prevent tubular myoglobin precipitation
  • Continuous cardiac monitoring (even in confined spaces) for hyperkalaemia-induced dysrhythmias
  • Manage hyperkalaemia: insulin + glucose, calcium gluconate, ion exchange resins, β-agonists
  • Urinary catheter to measure urine output (target: forced diuresis of up to 8 L/day)

Hospital Management

  • Continue aggressive fluid loading (up to 12 L/day in an average adult)
  • Mannitol - reduces the reperfusion injury component and promotes osmotic diuresis
  • Urinary alkalinisation - sodium bicarbonate to keep urinary pH > 6.5, preventing myoglobin precipitation in tubules (mannitol-alkaline diuresis up to 8 L/day until urine is clear of myoglobin)
  • Early fasciotomy - decompresses muscle compartments, prevents severe limb loss
    • Caution: A late fasciotomy (>12 hours of entrapment) is likely to cause a massive release of myoglobin and risk introducing infection into dead tissue - it should NOT be performed
  • Intensive care with close fluid balance monitoring
  • Renal dialysis if AKI develops (anticipating recovery of renal function over several days)
  • Amputation of a non-viable limb may prevent renal damage from further myoglobin release

Summary (Bailey & Love's, p. 480)

  • Arises as a result of reperfusion
  • Acute kidney injury and renal failure from myoglobinuria is a complication
  • A late fasciotomy may make things worse, not better

SUDECK'S ATROPHY (Complex Regional Pain Syndrome Type I)

Definition and Nomenclature

Sudeck's atrophy is now classified under Complex Regional Pain Syndrome Type I (CRPS-I), formerly called Reflex Sympathetic Dystrophy (RSD). Other older names include:
  • Shoulder-hand syndrome
  • Causalgia (CRPS Type II - with a definable nerve lesion)
  • Transient osteoporosis
  • Acute atrophy of bone
The unifying CRPS classification requires: regional pain and sensory changes following a noxious event, with pain disproportionate to the inciting injury, plus vasomotor/sudomotor/trophic changes.
  • Bradley and Daroff's Neurology in Clinical Practice
  • Pye's Surgical Handicraft, 22nd Ed.
  • Andrews' Diseases of the Skin

Inciting Events

  • Fractures (especially around the wrist/distal radius) - 25% of CRPS cases
  • Soft tissue injury - ~40% of cases
  • Myocardial infarction - ~12%
  • Almost any fracture in adults
  • Minor trauma, surgery, immobilization

Pathophysiology

The exact cause is unknown. Current understanding:
  • An abnormal reflex arc following the sympathetic nervous system pathway, modulated by cortical centres
  • Decreased sympathetic outflow to the affected limb
  • Autonomic manifestations previously attributed to sympathetic overactivity are now thought to be due to catecholamine hypersensitivity in peripheral tissues
  • Significant emotional disturbance and psychological stress at onset are common precipitating factors
  • The pain creates a vicious circle: pain → disuse → further bony atrophy → more pain

Clinical Features and Stages

CRPS progresses through three classical stages:
StageDurationFeatures
Stage I (Acute)Weeks-monthsDiffuse burning/throbbing/aching pain, hypersensitivity to touch or cold, localised oedema, vasomotor disturbance (altered skin colour and temperature)
Stage II (Dystrophic)3-6 monthsProgressive soft tissue oedema, skin and periarticular soft tissue thickening, muscle wasting
Stage III (Atrophic)Months-yearsLimitation of movement, frozen shoulder, digital contractures, waxy trophic skin changes, brittle ridged nails, severe demineralisation on X-ray
Characteristic signs on examination:
  • Diffuse severe non-segmental pain with cyanosis or mottling
  • Increased sweating (hyperhidrosis) and shiny skin
  • Swollen, non-articular tissue
  • Coldness to touch
  • Hypersensitivity to pinprick
  • Associated myofascial trigger points and shoulder tendonitis
  • Radiograph: diffuse, patchy, "moth-eaten" type osteoporosis (hallmark of Sudeck's)
Motor impairment (weakness, tremor, dystonia) may be present but is NOT required for diagnosis.
Skin changes in CRPS - shiny, discoloured, swollen hand
Skin changes in Complex Regional Pain Syndrome (Sudeck's Atrophy): discolouration, swelling, and shiny appearance of the affected hand compared to normal. - Bradley and Daroff's Neurology, p. 551

Diagnosis

  • Primarily clinical (no single objective diagnostic test for CRPS Type I)
  • Bone scintigraphy - most sensitive in Stage I, less useful in later stages
  • Autonomic testing - resting sweat output + quantitative sudomotor axon reflex test: 94% sensitive, 98% specific; excellent predictor of response to sympathetic block
  • X-ray - patchy periarticular osteoporosis in later stages
  • Stellate ganglion block - useful both diagnostically and therapeutically

Treatment

Non-pharmacological

  • Vigorous physiotherapy and active movement - the cornerstone; improvement occurs over many months despite pain
  • Psychological support (significant emotional component)

Pharmacological

  • Bisphosphonates - prevent bone resorption and help with pain control
  • Calcium channel blockers (nifedipine, verapamil) - for vasomotor symptoms
  • Alpha-blockers (prazosin, phenoxybenzamine)
  • Guanethidine (sympatholytic)
  • Beta-blockers (propranolol)
  • Antidepressants
  • Thyrocalcitonin (calcitonin) injections - some evidence of shortening the time course (Pye's, p. 157)

Interventional

  • Stellate ganglion block (or regional sympathetic block) - therapeutic and diagnostic; can be repeated if successful
  • Sympathectomy - reserved for progressive disease in patients who previously responded to sympathetic block

Key Differences and Comparison

FeatureCrush SyndromeSudeck's Atrophy (CRPS-I)
NatureSystemic/metabolic emergencyRegional neurogenic pain syndrome
MechanismReperfusion + rhabdomyolysisAbnormal sympathetic reflex
Key organ affectedKidneys (AKI/ARF)Bone + skin + joints (affected limb)
TimingAcute (hours after injury)Subacute to chronic (weeks-months post-injury)
X-ray finding-Patchy "moth-eaten" osteoporosis
Key lab findingMyoglobinuria, hyperkalaemia, metabolic acidosisNone specific
Treatment priorityAggressive IV fluids + forced diuresisPhysiotherapy + sympathetic blockade
SurgeryEarly fasciotomy (if <12h)Sympathectomy (severe progressive cases)
Sources: Bailey and Love's Short Practice of Surgery 28th Ed. | Rosen's Emergency Medicine | Bradley and Daroff's Neurology in Clinical Practice | Pye's Surgical Handicraft 22nd Ed. | Andrews' Diseases of the Skin
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