Foot compartment syndrome 


Compartment syndrome of the foot is uncommon, accounting for < 5% of lower limb compartment syndromes. High index of suspicion is needed after a high energy injury to foot.  Raised interstitial pressure in any of the tightly bound osseofascial compartments of the foot can can be higher than the capillary closing pressure, resulting in myo-neural ischaemia. Left untreated, necrosis of intrinsic foot muscles occur leading to soft tissue atrophy and clawing of foot. Patients may experience constant discomfort, insensate foot, ankle stiffness, neuropathic pain and ulceration.


Traditional teaching divides the foot into four myofascial compartments – interosseous, medial, central and lateral. Infusion studies have now reported 10 compartments:

  • Central compartment divided into three parts.
  • Interossei compartment increased from one to four parts.
  • Medial and lateral compartments remain unaltered.
  • Dorsal compartment is newly described containing extensor digitorum and extensor hallucis brevis.

Conflicting reports suggest only central, interosseous and lateral compartments are bound by fascia on all sides, whilst others have shown isolated medial compartment syndromes.
Communication between the compartments can occur following traumatic disruption to facial membranes. This includes tibial fracture with communication of posterior compartment of leg and calcaneal compartment of foot.  
The calcaneal compartment has the highest risk of developing compartment syndrome, whereas interosseous is the lowest. 



  • High energy injuries e.g. crush injuries, midfoot and forefoot trauma, Lisfranc fracture dislocations and calcaneal fractures.  
  • Tibial fracture with communication of posterior compartment of leg and calcaneal compartment of foot.
  • Coagulopathy.
  • Acute revascularisation of the limb.
  • Overexertion from sporting activity.
  • Iatrogenic – tight casts and dressings.



Trauma, bleeding and oedema all raise interstitial pressure and cause vascular stasis from occlusion of blood vessles. Secondary ischaemia damages nerves and intrinsics muscle. If left untreated, claw toes result from contraction of unopposed extrinsic muscles and cavus deformity results from fibrotic plantar components. Neuropathic pain and ulcers may occur secondary to irreversible peripheral nerve damage if also left untreated.  

Clinical presentation


  • Pain out of proportion to severity of injury – most reliable but often late clinical finding.
  • Burning, deep and aching pain encompassing the entire foot.
  • Progressive pain despite foot immobilisation and increased analgesia requirements. 
  • Tense feeling in foot.

Examination findings:

  • Pain with passive stretching and active dorsiflexion of toes.
  • Loss of two point discrimination and decreased light touch on plantar aspect of foot and toes (most sensitive finding for sensory changes).
  • Swelling of foot.
  • Firmness of involved compartments.
  • Intrinsic muscle weakness.
  • NB: Warm and well perfused foot with palpable dorsalis pedis and posterior tibial pulses does not exclude the diagnosis.

Specific examination: 

  • Weak dorsiflexion (anterior compartment).
  • Weak eversion (lateral compartment).
  • Weak plantar flexion (posterior compartment).




Compartment syndrome is a clinical diagnosis. Compartment pressure monitoring can be used to support the diagnosis especially when clinical examination is compromised (e.g. an unconscious patient) using needle manometry under the base of first metatarsal (medial and central compartments) or through dorsal intermetatarsal approach (interosseous and central). Under physiological conditions, compartment pressure is 8 to 15mmHg. At 25mmHg, venous perfusion obliterated within musculoskeletal compartments. Pressures above 30mmHg or within 30mmHg of diastolic pressure are pathological and fasciotomy indicated.



Split any dressings or casts to skin. Controversy exist whether decompression is always necessary and beneficial. Contractures, toe deformities, paralysis, and sensory neuropathy can result if decompression is not carried out but there is significant morbidity associated with surgery as well. If decompression is decided on either a three incision or a single dorsal incision approach can be used. Three incision approach incorporates the nine osseofascial compartments through a medial incision and two dorsal incisions.

Surgical technique 

Medial incision: Medial, central and lateral compartments released through this.Once neurovascular bundle retracted, fascia overlying abductor hallucis (medial) and flexor digitorum brevis (FDB) (third level of central) released. Medial intermuscular septum opened longitudinally. Remaining compartment (lateral) entered through blunt dissection and retracting FBD out the way.  

Dorsal incision: Interosseous compartments released through 2 dorsal incisions.  Superficial fascia is divided and interosseous are elevated off the metatarsals to decompress the compartments.  

Single dorsal incision: Central in foot. Compartments entered elevating the interossei off the metatarsals then dividing the plantar interosseous fascia to decompress the deeper layers. 

Additional Treatment


  • Stabilisation of the skeletal injury with definitive or temporary means.
  • Secondary closure of wounds +/- skin grafts if large defects persist.
  • Definitive or temporary reduction and stabilisation of the skeletal injury is likely to reduce swelling and pain and should be considered if the expertise is available.
  • The wounds may be secondarily closed with split-thickness skin grafts 5-7 days post-operatively.

Post-operative management 

  • Ice and non-steroidal anti-inflammatories to reduce swelling.
  • Massage to aid lymphatic drainage.
  • Increase range of motion and mobility of joints through passive mobilisation of ankle joint. 



  • Cavus deformity.
  • Neuropathic pain.
  • Clawed toes.

Complications can be managed with (1) passive mobilisation and stretching for toe and cavus deformity; (2) orthotics to control foot position; (3) skin care for neuropathic pain. Surgical management may include tibial nerve neurolysis and its distributaries for neuropathic symptoms after confirmation from nerve conduction studies; tenotomies, tendon lengthening and joint fusions for clawed toes, and tarsectomy or arthrodesis for cavus deformity.

In all patients, it must be explained that normal function may not be restored although improvements in pain and function can be achieved.  



The following clinical findings are consistent with compartment syndrome in the foot:

  1. Pain, swelling, weakness of eversion and dorsiflexion, sensory loss, palpable pulses 
  2. Pain, swelling, loss of active foot movement, pain on passive stretch, loss of Doralis pedis pulse 
  3. Swelling, plantar ecchymosis, weakness of the intrinsic muscles, sensory disturbance, pain on passive stretch, palpable pulses 
  4. Pain, rasied compartment pressure to 35mmHg, absent DP pulse, pale skin 
  5. All of the above 

(Answer 5) 


The following muscles are found in the medial compartment of the foot:

  1. Flexor Hallucis Brevis, Abductor Hallucis, Adductor Hallucis 
  2. Abductor Hallucis, Flexor Hallucis brevis, Plantar inteossei 
  3. Abductor Hallucis, Plantar interossei, Flexor digitorum brevis 
  4. Flexor digitorum brevis, Abductor digit minimi, Adductor Hallucis 
  5. Flexor digiti minimi, Opponens digiti minimi, Adductor Hallucis 

(Answer 2) 


If compartment pressures are measured the following readings would suggest decompression is necessary:

  1. A reading of 30mmHG and 25mmHg above the systolic blood pressure 
  2. A reading of 20mmHG or within 50mmHg of the systolic blood pressure 
  3. A reading of 20mmHg or within 50mmHg of the diastolic blood pressure 
  4. A reading of 30mmHG or within 30mmHg of the diastolic blood pressure 
  5.  A reading of 30mmHG or within 30mmHg of the systolic blood pressure 

(answer 4) 



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