(Left) Clinical photograph of a foot with compartment syndrome due to multiple metatarsal fractures from the AP and sagittal planes. (Right) AP Radiograph of the foot with multiple metatarsal fractures.


Published 1/1/2007
Steven L. Haddad, MD

Managing risk: Compartment syndromes of the foot

Heightened awareness will assist the observant orthopaedic surgeon in avoiding litigation for the sequela of a missed compartment syndrome.

Acute compartment syndrome of the foot was first described in the literature in 1981. It is similar in pathophysiology to compartment syndrome of the lower leg and results in ischemic changes to both nerves and muscles due to elevated interstitial pressures within tight osseofascial compartments. Prolonged ischemia may lead to irreversible destruction of myoneural tissue and subsequent fibrosis. Thus, a heightened awareness of this condition will assist the observant orthopaedic surgeon in avoiding litigation for the sequela of a missed compartment syndrome.


Initially, researchers believed there were the following four separate compartments within the foot:

Medial–consisting of the abductor hallucis and flexor hallucis brevis; bounded medially and inferiorly by the plantar aponeurosis, laterally by the intermuscular septum, and dorsally by the first metatarsal

Lateral–consisting of the abductor digiti mini, flexor digitorum brevis (fifth toe), and opponens for the fifth digit; bounded by the fifth metatarsal dorsally, the plantar aponeurosis inferiorly and laterally, and the intermuscular septum medially

Central–consisting of the flexor digitorum brevis, lumbricals, quadratus plantae, and adductor hallucis; bounded by the plantar aponeurosis inferiorly, the intermuscular septum medially and laterally, and the osseofascial tarsometatarsal structures dorsally

Interosseous–consisting of seven interosseus muscles and bounded by the interosseus fascia and the metatarsals

Others have expanded on this anatomic division, discerning as many as nine separate compartments. In particular, a calcaneal compartment, including the quadratus plantae and lateral plantar nerve was described and suspected as the source for forefoot deformity following calcaneus fractures. Direct communication between the deep posterior compartment of the leg and the calcaneal compartment has been suggested, encouraging the clinician to pay particular attention to the foot for potential compartment syndrome in those individuals with known compartment syndrome of the leg.

Guyton et. al. questioned whether there are more than four compartments, refuting prior gelatin injection studies as inaccurate and invalid due to a flawed experimental design without control and/or the absence of pressure monitoring of the injections done by hand. Using computed tomography (CT) guidance, they injected fluid into isolated compartments and monitored the resulting interstitial pressures. The so-called calcaneal compartment merged with the central compartment of the foot with as little as 10 mm Hg interstitial pressure. Because interstitial pressure measurements of 30 mm Hg are the minimum value required to quantify an extremity as afflicted by compartment syndrome, it is impractical to subdivide the foot into more than four compartments based on the location of a variety of fascial planes.

Mechanism and pathophysiology

Although the inciting event may differ, all compartment syndromes of the foot share the same pathophysiological pathway. Edema or hemorrhage creates increased interstitial pressures within the soft tissues, lowering capillary perfusion and creating ischemia and potential necrosis. Increasing pressure further hampers tissue perfusion, for flow ceases once diastolic blood pressure is reached. Correlation exists between the mean arterial blood pressure and the compartment pressure with respect to insult to both muscle metabolism and neural dysfunction. The decreased perfusion pressure—not the mechanical compression—causes the nerve dysfunction in compartment syndrome.

Crush injuries to the foot create the majority of compartment syndromes. Hematoma formation through metatarsal fractures, in combination with interstitial edema through direct cellular damage, is a contributing factor. From 5 percent to 17 percent of all calcaneus fractures result in compartment syndrome; one study found all high-energy calcaneus fractures (falls from a height greater than 8 meters) created compartment pressures greater than 40 mm Hg, and every patient had myoneural damage. Other causes include elective foot surgery, Lisfranc fracture/dislocation, cast immobilization, abnormal or prolonged extremity positioning, snake bites, and even a severe ankle sprain that creates a pseudoaneurism or ruptures the dorsalis pedis artery.

In addition, compartment syndrome of the foot may not be temporally immediately apparent. Myerson et al found isolated medial compartment syndrome that developed 36 hours after a suspected football injury. Finally, children are subject to foot compartment syndrome similar to their adult counterparts, and any child experiencing high-energy trauma or crush injury to the foot or leg should be evaluated for this condition.


Diagnosis of foot compartment syndrome begins with a heightened level of clinical suspicion based on mechanism of injury. Because not all situations are clinically obvious, the clinician should be aware of signs and symptoms associated with the condition.

Pain out of proportion to the injury is a primary indication of evolving compartment syndrome. Passive dorsiflexion of the toes stretches the intrinsic musculature of the foot, exacerbating this pain, but be careful if there are concurrent metatarsal fractures, because they may alter the validity of the test.

An absent pulse or complete anesthesia are late findings in compartment syndrome, and may be difficult to diagnose under circumstances of massive swelling. In one series, just one in 17 patients with diagnosed compartment syndrome had an absent pulse.

The only objective method to diagnose compartment syndrome is to measure the absolute compartment pressures. Most institutions use a simple intra-compartmental pressure monitoring system. Pressures are measured as follows:

Central compartment–insertion site: base of first metatarsal, directing the needle lateral and plantar, through the abductor hallucis muscle

(Left) Clinical photograph of a foot with compartment syndrome due to multiple metatarsal fractures from the AP and sagittal planes. (Right) AP Radiograph of the foot with multiple metatarsal fractures.
Intraoperative photographs of intraosseous compartment decompression seven day postoperative (left). Patient returned to the operating room at seven days post initial decompression, where the tension was evaluated following closure of one of the dorsal incisions (middle), followed by split-thickness skin grafting (right).

Medial compartment–insertion site: base of first metatarsal, advancing approximately 2 cm, within abductor hallucis muscle

Interosseous compartment–insertion site: second, third, fourth webspaces, advancing plantarward approximately 2 cm, puncturing extensor fascia

Lateral compartment–insertion site: fifth metatarsal midshaft, advancing 1 cm medial and plantar

Calcaneal compartment–insertion site: 5 cm distal and 2 cm inferior to medial malleolus, advancing through abductor hallucis, directed inferior to posterior tuberosity of calcaneus. Note that the clinical relevance of this compartment remains in question (see above). Evaluation, however, remains appropriate until a definitive answer is reached by investigators

Nerve tissue is more sensitive to ischemia than muscle, tendon, ligament, or bone. Central and calcaneal compartment syndromes generally affect the lateral plantar nerve first, because it lies in a more constrictive portion of the compartment adjacent to the quadratus plantae and underlying the fourth and fifth metatarsals. The medial plantar nerve may also be affected, although it is not within an osseofibrous compartment and is thus less subject to ischemia.

Nerve tissue maintains normal conduction velocity for up to one hour of ischemia. Though neuropraxia remains reversible at one to four hours of ischemia, it becomes irreversible axonotmesis following eight hours of complete ischemia.


A patient with a potential compartment syndrome should first elevate the extremity to the level of the heart. Studies suggest that elevation above this level lowers the mean arterial pressure, reducing oxygen perfusion. In addition, the use of a pneumatic intermittent impulse compression device may decrease interstitial pressure and lower the incidence of compartment syndrome of the foot. Such devices potentially improve venous return and enhance arterial flow, increasing the osmotic resorption of the interstitial fluid (osmotic fluid resorption at this level normally accounts for 90 percent of resorbed interstitial fluid). Intuitively, better fluid resorption lowers the compartment pressure.

Fasciotomy should be performed within 24 hours of injury. Some studies suggest that after this time, ischemic changes become irreversible. In fact, recommendations concerning fasciotomy in patients who are seen after 24 hours of injury become less defined. Infection risk from fasciotomy incisions potentially outweighs the risks of further neural or muscle ischemia, and most suggest that fibrosis due to ischemia is inevitable in patients with delayed presentation. The patient’s own skin provides the best biologic dressing and should not be violated under these circumstances.

Fasciotomy should be performed when compartment pressures are 30 mm Hg or greater, or 10 mm Hg to 30 mm Hg below the diastolic blood pressure in hypotensive trauma patients.

Fasciotomy incisions are as follows:

  1. Dorsal–two incisions, overlying the second and fourth metatarsals. Maintain the widest skin bridge possible, and make a blunt approach directly to the metatarsal bones. Do not undermine any skin, due to its tenuous nature. Continue blunt dissection into the web spaces, and decompress the hematoma while simultaneously performing boney stabilization.
  2. Medial–one incision, along the inferior border of the first metatarsal, but superior to the abductor muscle. Expose the muscle by incising the fascia from its superior portion, and enter the central compartment with further lateral penetration.
  3. Calcaneal–one incision, beginning medially, from the inferior border of the posterior tuberosity extending towards the inferior surface of the first metatarsal. Retract the abductor muscle superiorly (along with a fascial release, if necessary) and enter the quadratus compartment through the medial intermuscular septum. The calcaneus fracture is normally not reconstructed at this time. Instead, standard protocols are used to delay the lateral approach until skin conditions are reasonable. The standard lateral calcaneal approach is not sufficient in itself to release the calcaneal compartment. The tight plantar aponeurosis remains a constrictive block, requiring medial incision to eliminate it.

In general, all incisions are used if all compartments are involved. The medial and calcaneal approaches are sufficient for isolated calcaneus fractures and subsequent central or calcaneal compartment syndrome.

All fasciotomy incisions are left open for at least five days, to enable sufficient dissipation of edema and swelling to determine whether direct closure is available, or a split-thickness skin graft is required. Some authors have suggested applying a split-thickness skin graft at decompression, to serve as both a biologic dressing (allowing drainage simultaneously) and long-term coverage. If the graft is taken from the edge of the dorsal incision, bleeding from the donor site defines the limits of viable skin surrounding the surgical approach.


Untreated compartment syndrome may lead to a disabling outcome. The patient may have chronic, debilitating pain. Forefoot deformity (commonly seen as clawtoes) may result from neural insult, because the muscles will atrophy after ischemia to the nerves. An intrinsic-minus deformity arises from interosseous and lumbrical muscle atrophy and subsequent fibrosis. In addition, fibrosis of the short flexors (due to neural insult) accentuates the fixed flexion deformity of the digits.

Fixed flexion deformity requires the release of both the flexor digitorum brevis and longus at the level of the digits. This may be done in combination with arthrodesis of the proximal interphalangeal joints. If necessary, generous excision of fibrotic muscle tissue is required.

Paresis and anesthesia to the plantar foot may be permanent, and managed similar to the plantar foot experienced by a neuropathic diabetic.


Compartment syndrome of the foot is a potentially disabling condition, but treatable if promptly recognized. Litigation surrounding this condition centers on the sequela resulting from a missed diagnosis, rather than surgical decompression. Thus, a heightened clinical suspicion—along with objective evidence through pressure monitoring—lessens the liability that could result if the condition goes untreated.


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  2. Kamel, R. and Sakla, FB.: Anatomical compartments of the sole of the human foot. Anat. Rec., 140:57-64, 1961.
  3. Manoli, A. and Weber TG: Fasciotomy of the foot: an anatomical study with special reference to release of the calcaneal compartment. Foot Ankle 10:267-275, 1990.
  4. Guyton, GP., Shearman, CM., Saltzman, CL., The compartments of the foot revisited: rethinking the validity of cadaver infusion experiments. JBJS Vol. 83-B(2):245-249, March 2001.
  5. Mittlmeier T, Mächler G., Lob G, et.al. Compartment syndrome of the foot after intraarticular calcaneal fracture. Clin Orthop 269: 241-248, August, 1991.
  6. Myerson MS and Berger B, Isolated medial compartment syndrome of the foot: a case study. FAI, Vol 17(3): 183-185, March 1996.
  7. Silas, SI, Herzenberg JE, Myerson MS, et.al: Compartment syndrome of the foot in children. JBJS 77-A (3): 356-361, March, 1995.
  8. Finklestein JA, Hunter GA, Hu RW, Lower limb compartment syndrome: course after delayed fasciotomy. Journal of Trauma, Injury, Infection, and Critical Care. 40(3): 342-344, 1996.

Steven L. Haddad, MD, is a member of the AAOS Medical Liability Committee. He can be reached at slhaddad@earthlink.net.