Summary
Compartment syndrome is a condition in which increased pressure within a muscle compartment (containing nerves and vasculature, enclosed by unyielding fascia) leads to impaired tissue perfusion. It most commonly affects the lower legs, but can also occur in other parts of the extremities or the abdomen. Compartment syndrome may be acute (e.g., after trauma) or chronic (e.g., collectively excessive training in athletes). Acute compartment syndrome is a surgical emergency that initially presents with rapidly progressive pain, paresthesia, and pallor. Pronounced neurological symptoms with motor deficits, absent pulses, and poikilothermia occur later on and indicate irreversible damage. This diagnosis should be suspected in the presence of typical clinical findings and then confirmed via measurement of compartment pressures. Acute compartment syndrome requires early fasciotomy (an incision through the fascia) within six hours of onset to prevent severe ischemic necrosis. Chronic compartment syndrome is also often associated with pain; it can be exacerbated by exercise and relieved by rest, and is usually managed with conservative treatment. The prognosis of compartment syndrome is generally good with early and appropriate management.
Etiology
The etiology of compartment syndrome | ||
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Causes of external compression | Causes of internal compression | |
Trauma-related causes |
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Non-trauma-related causes |
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Because shock leads to reduced peripheral circulation, patients with polytrauma are at a high risk of compartment syndrome with muscle ischemia.
Classification
- Acute compartment syndrome: predominantly trauma-induced; a surgical emergency
- Chronic compartment syndrome: also known as exertional compartment syndrome; usually not a medical emergency
Pathophysiology
Clinical features
Compartment syndrome may occur in any enclosed muscle compartment inside the body. The most common sites are the lower legs and arms. Less common sites include the feet, hands, thighs, and gluteal region.
Acute compartment syndrome (ACS)
Typically presents with a rapid progression of symptoms
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Early presentation
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Pain
- Often out of proportion to the extent of injury
- Worse with passive stretching or extension of muscles
- Very tight, wood-like muscles that are extremely tender to touch
- Paresthesia (e.g., pins and needles)
- Soft tissue swelling
- Initially, peripheral circulation and distal pulses are maintained.
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Pain
- Late presentation
6 P's of acute limb ischemia: Pain, Pallor, Paresthesias, Poikilothermia, Pulselessness, and Paralysis
Arterial pulse is usually still palpable; pulselessness is a sign of very severe compartment syndrome.
Chronic compartment syndrome
- More common in young athletes and runners
- Usually affects the lower legs
- Muscle pain, weakness, and swelling exacerbated by exercise and relieved with rest
- Paresthesia and numbness may occur.
Subtypes and variants
Anterior compartment syndrome of the lower leg
- Prevalence: most common type of acute compartment syndrome
- Etiology: : usually trauma to anterior compartment of the leg (See “Etiology” above.)
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Clinical features
- Motor: limited dorsiflexion, inversion, and eversion
- Sensory: loss of sensation/paresthesia in the nerve territory
- See “Clinical features” above.
- Treatment: surgery (dermato-fasciotomy)
Abdominal compartment syndrome [1]
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Classification
- Primary: conditions associated with intra-abdominal injuries that usually result in massive intra-abdominal bleeding or hematoma
- Secondary: conditions associated with massive intraperitoneal fluid accumulation not due to intra-abdominal injury
- Recurrent: conditions that reoccurred after surgical or medical treatment of primary or secondary abdominal compartment syndrome
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Etiology
- Primary
- Penetrating abdominal trauma
- Abdominal surgery
- Pelvic trauma
- Rupture of abdominal aortic aneurysm
- Secondary peritonitis
- Massive retroperitoneal hematoma
- Liver transplantation
- Intra-abdominal masses
- Secondary
- Massive volume resuscitation (e.g., postoperative patients, treatment of hypovolemic shock, severe burns)
- Severe ascites
- Sepsis
- Others
- Primary
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Pathophysiology: ↑ intra-abdominal pressure → organ dysfunction
- Cardiovascular: ↓ cardiac output
- Renal: ↓ glomerular perfusion and urine output
- Gastrointestinal: intestinal hypoperfusion and ischemia
- Pulmonary: ↓ pulmonary volume; ↑ peak airway pressures
- Cerebral: ↑ intracranial pressure
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Clinical features: may develop within hours or over days
- Critically ill patient
- Cardiovascular: signs of increased central venous pressure (e.g., distended jugular veins), hypotension, tachycardia
- Renal: from oliguria to progressive renal failure
- Gastrointestinal: tight and distended abdomen, nausea, vomiting
- Pulmonary: tachypnea, wheezing
- Cerebral (See “Signs of increased intracranial pressure.”)
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Diagnostics
- Best initial test: indirect measurement of intra-abdominal pressure
- CT scan: increased abdominal diameter, compression of the inferior vena cava, intestinal wall thickening, bilateral inguinal herniation
- Abdominal x-ray: not useful for detecting abdominal compartment syndrome
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Treatment
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Abdominal decompression
- Laparotomy for decompression
- Temporary abdominal closure (e.g., patch technique, vacuum-assisted closure)
- Definitive closure
- Supportive management
- Hemodynamic stabilization (e.g., fluid resuscitation, transfusions)
- Percutaneous drainage of intra-abdominal fluid
- Ventilation
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Abdominal decompression
Diagnostics
Diagnosis of acute compartment syndrome is primarily clinical. [2][3]
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Compartment pressure measurement (initial and confirmatory test) [2]
- Measurement of tissue pressure with a manometer and calculation of delta pressures (delta pressure = diastolic – (compartment) tissue pressure)
- Delta pressure ≤ 30 mm Hg assists in diagnosis.
- Laboratory tests: used to assess for rhabdomyolysis (e.g., creatine phosphokinase, renal function tests)
- Imaging
- Pulse oximetry: not diagnostic but can help identify limb hypoperfusion
Differential diagnoses
Differential diagnoses of compartment syndrome | ||||
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Features | Acute compartment syndrome | Deep vein thrombosis | Acute limb ischemia | Rhabdomyolysis |
History |
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Clinical features |
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Diagnosis |
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Treatment |
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Others
The differential diagnoses listed here are not exhaustive.
Treatment
Surgical treatment [3]
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Indication
- Required for all cases of acute compartment syndrome
- Chronic compartment syndrome if conservative treatment fails
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Techniques
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Fasciotomy (tissue and fascia incisions): relieves the pressure, thus restoring perfusion
- Should be conducted within 6 hours after the onset of the condition to prevent necrosis
- Followed by open wound treatment
- Fibulectomy: if fasciotomy fails; to decompress all compartments of the lower leg
- Escharotomy: in the case of circumferential compression by a burn eschar
- Last resort: amputation
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Fasciotomy (tissue and fascia incisions): relieves the pressure, thus restoring perfusion
Supportive treatment [3]
- Indicated as perioperative care
- May be considered as sole treatment for chronic compartment syndrome
- Eliminate any underlying cause, i.e., remove restrictive cast/dressing
- Cooling and positioning of the limb at heart level to relieve pressure
- Close monitoring with frequent examination of the affected limb
- Correct any fluid imbalances
- Supplemental oxygen
- Analgesia
Elevated positioning may worsen ischemia by reducing blood flow.
Acute compartment syndrome is a surgical emergency and requires an early fasciotomy.
Complications
- Muscle and soft tissue necrosis with a higher risk of infection [3]
- Nerve lesions (esp. the tibial nerve and peroneal nerve) with sensory and motor deficits or paralysis
- Rhabdomyolysis with potential crush syndrome
- Malunion fractures
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Volkmann ischemic contracture
- Definition: permanent shortening of the forearm muscles resulting in a claw-like deformity of the fingers, hand, and wrist
- Etiology
- Undiagnosed compartment syndrome (especially due to tight casts/bandages and crush injuries)
- Supracondylar humeral fracture
- Pathophysiology: blood vessel (e.g., brachial artery) or nerve (e.g., radial nerve) damage ; (e.g., due to forearm fracture, repositioning of the bones, restrictive cast) → sustained ischemia and necrosis → fibrosis and contracture of the forearm flexor muscles → atrophy of the flexors of the hand and fingers
- Clinical features
- Thumb adduction
- Flexed fingers and wrist
- Pain on passive extension of affected fingers and wrist
- Elbow flexion and forearm pronation
- Decreased sensation
- Intrinsic minus deformation (advanced cases): overextended metacarpophalangeal joints and flexed interphalangeal joint
- Diagnostics: clinical diagnosis
- Differential diagnosis: Dupuytren contracture
- Treatment
- Conservative: physical therapy, dynamic elbow splint
- Surgical: tendon transfer procedures, nerve decompression (severely impaired hand function)
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Rebound compartment syndrome
- Onset: occurs 6–12 hours after surgical reperfusion
- Etiology: increased capillary permeability and edema, often due to insufficient fasciotomy incisions
We list the most important complications. The selection is not exhaustive.
Prognosis
The prognosis depends on the amount of time that has elapsed prior to performing the fasciotomy: [3]
- ≤ 4–6 h: almost complete recovery
- 6–12 h: first necroses
- ≥ 12 h: necroses; little or no return of function