eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Compartment Syndrome, Extremity

Author: Richard Paula, MD, Director of Research, Assistant Professor of Emergency Medicine, University of South Florida
Contributor Information and Disclosures

Updated: Dec 10, 2008

Introduction

Background

Compartment syndrome (CS) is a limb-threatening and life-threatening condition observed when perfusion pressure falls below tissue pressure in a closed anatomic space. The current body of knowledge unequivocally reflects that untreated CS leads to tissue necrosis, permanent functional impairment, and, if severe, renal failure and death.

The original description of the consequences of unchecked rising intracompartmental pressures is widely attributed to Richard vonVolkmann. His 1872 publication documented nerve injury and subsequent contracture from CS following supracondylar fracture.¹ That injury remains known as Volkmann contracture.

Although long bone fractures are a common cause of CS, other injuries are also a common antecedent to CS. Approximately 50 years after vonVolkmann's seminal paper, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction. In 1941, Bywaters and Beall reported on the significance of crush injury while working with victims of the London Blitz. These pioneers revealed mechanisms and consequences of CS. It was not until 30 years later, in the 1970s, the importance of measuring intracompartmental pressures became apparent.

Owen et al published a series of articles describing the use of the wick catheter for pressure measurement and then documented high compartmental pressures in a variety of circumstances.² Almost simultaneously, Matsen published his findings, which are the most commonly annotated group of articles in present literature.

CS has been found wherever a compartment is present: hand, forearm, upper arm, abdomen, buttock, and entire lower extremity. Almost any injury can cause this syndrome, including injury resulting from vigorous exercise.

This article presents current thoughts and findings regarding CS. Most importantly, it urges physicians to maintain a high level of suspicion when dealing with complaints of extremity pain.

Pathophysiology

CS pathophysiology follows the path of ischemic injury. Intracompartmental structures cannot withstand infinite pressure. When fluid is introduced into a fixed volume, or when volume decreases with fixed volume, pressure rises. Various osseofascial compartments have a relatively fixed volume; introduction of excess fluid or extraneous constriction increases pressure and decreases tissue perfusion, until no oxygen is available for cellular metabolism.

Elevated perfusion pressure is the physiologic response to rising intracompartmental pressure. As intracompartmental pressure rises, autoregulatory mechanisms are overwhelmed and a cascade of injury develops. Tissue perfusion is determined by measuring capillary perfusion pressure (CPP) minus the interstitial fluid pressure. When this pressure falls below a critical threshold, injury results.

Normal cellular metabolism requires 5-7 mm Hg oxygen tension; this is easily maintained with the CPP averaging 25 mm Hg and interstitial pressure 4-6 mm Hg. However, rising interstitial pressure overwhelms perfusion pressure.

Matsen demonstrated that as intracompartmental pressure rises, venous pressure rises. When venous pressure is higher than CPP, capillaries collapse. The pressure at which this occurs is under debate; however, intracompartmental pressures greater than 30 mm Hg are generally agreed to require intervention.

At this point, blood flow through the capillaries stops. In the absence of flow, oxygen delivery stops. Hypoxic injury causes cells to release vasoactive substances (eg, histamine, serotonin), which increase endothelial permeability. Capillaries allow continued fluid loss, which increases tissue pressure and advances injury. Nerve conduction slows, tissue pH falls due to anaerobic metabolism, surrounding tissue suffers further damage, and muscle tissue suffers necrosis, releasing myoglobin. The end result is loss of the extremity and, possibly, the loss of life.

Frequency

United States

Anterior distal lower extremity is the most common studied cause of CS. Tibial fracture is quoted as the most common, likely secondary to its frequency of injury. Ranges of 2-12% have been published. Another frequency rate cited is that 30% of limbs develop CS following vascular injury; however, this is not well documented and is most likely an estimate. McQueen (2000) retrospectively looked at 164 patients with diagnosed CS; 69% were associated with a fracture, one half of those being the tibia.³

Mortality/Morbidity

• CS outcome depends on both the diagnosis and the time from injury to intervention.
• Rorabeck and Macnab reported almost complete recovery of limb function if fasciotomy was performed within 6 hours.⁴
• Matsen found necrosis after 6 hours of ischemia, which currently is the accepted upper limit of viability.

Sex

In the retrospective study by McQueen (2000), CS was diagnosed more often in men than in women; however, this likely represents selection bias, since men are more often patients with traumatic injuries.³

Clinical

History

• Suspect compartment syndrome (CS) whenever significant pain occurs in an extremity.  
• Pressure rises and ischemic injury begins to impair nerve function.
• Nerve impairment will cause the patient to complain of severe pain, out of proportion to examination, often described as a burning sensation or tightness.
• The traditional 5 Ps (ie, pain, paraesthesia, pallor, poikilothermia, pulselessness) are not diagnostic of CS. Literature warns that, with the exception of pain and paraesthesia, these traditional signs are not reliable, and the presence or absence of them should not affect injury management.
  • Importantly, note that these symptoms assume a conscious patient who did not suffer any additional injury that hinders sensory input (eg, spinal cord injury).
  • In young children, the ability to gather a history of complaints is limited.
• Maintain a high level of suspicion in any injury that causes limb pain.
• High-velocity injuries are particularly worrisome.
• Determine the mechanism of injury.
  • Long bone fractures
  • High-energy trauma
  • Penetrating injuries (eg, gunshot wounds, stabbings) - Often cause arterial injury, which can quickly lead to CS
  • Venous injury - May cause CS (do not be misled by palpable pulses)
  • Crush injuries
• Anticoagulation therapy significantly increases the likelihood of CS; remember to ask if patients are anticoagulated for any reason.
  • CS requiring fasciotomy has been observed after simple venipuncture in an anticoagulated patient
  • Vigorous exertion may lead to CS.
  • CS has been found in soldiers and athletes without any trauma. This can be acute or chronic with acute compartment pressures as high as those found in severe trauma.
  • If CS is suspected, check intracompartmental pressure, even with no presence of any trauma.

Physical

• Certain physical signs are associated with CS. After initial symptoms of pain or burning, decreased strength and eventually paralysis of the affected extremity occur. Follow-up physical examinations are important to determine if any progression of symptoms exists.
• Severe pain at rest or with any movement should raise suspicion.
• Pain with certain movements, particularly passive stretching of the muscles, is the earliest clinical indicator of CS.
• A patient may report pain with active flexion.
• If a patient complains of pain, determine if any neural compromise exists.
  • Sensory nerves begin to lose conductive ability, followed by motor nerves.
  • Some nerves may reveal effects of increasing pressure before others.
  • For example, in the anterior compartment of the lower leg, the deep peroneal nerve is quickly affected, and sensation in the web space between first 2 toes may be lost.
• The affected limb may begin to feel tense or hard, as if filling with fluid.
• Compare the affected limb to the unaffected limb.
• Any discharged patient should be given these specific signs and return immediately if they develop.

Causes

• A myriad of precipitating injuries leading to CS share some pathophysiology.
• The cause of CS is extremely simple: the pressure is too high.
• The underlying reason for increasing pressure, as proposed by Mubarak and Hargens (1983), is increased fluid content or decreased compartment size.⁵
• Increased fluid content can be caused by the following:
  • Intensive muscle use (eg, tetany, vigorous exercise, seizures)
  • Everyday exercise activities (eg, stationary bicycle use, horseback riding)
  • Burns
  • Intraarterial injection (frequently iatrogenic)
  • Envenomation
  • Decreased serum osmolarity (eg, nephrotic syndrome)
  • Infiltrated infusion
  • Hemorrhage (particularly from a large vessel injury)
• Decreased compartment size can be caused by the following:
  • Military antishock trousers (MAST)
  • Burns
  • Casts
• Lying on a limb can cause CS. In 1979, Owen et al published a landmark study in which researchers measured intracompartmental pressures in various positions common in drug overdoses.² Average pressures of 48 mm Hg with the head resting on forearm, 178 mm Hg when the forearm was under ribcage, and 72 mm Hg when one leg was folded under the other were reported.

• Search for CME/CE on This Topic »

• Compartment Syndrome, Upper Extremity (Orthopedic Surgery)
• Compartment Syndrome, Lower Extremity (Orthopedic Surgery)
• Tibial Shaft Fractures (Orthopedic Surgery)
• Upper Extremity Occlusive Disease (Vascular Surgery)

• Biomarkers Predict Outcomes in Lower Extremity Revascularization Patients
• Many Women May Not Be Using the Safest Brands of Oral Contraceptives
• Upper Arm Exercises Improve Vigor in COPD Patients

• Bites That Bleed: Crotalid Envenomation
• Management of Access Site and Systemic Complications of Percutaneous Coronary and Peripheral Interventions
• Treatment Options for Limited or Symptomatic Metastatic Melanoma