| Patient Education |
|
Click here for patient education.
|
|
You are in: eMedicine Specialties >
Emergency Medicine > TRAUMA AND ORTHOPEDICS
Compartment Syndrome, Extremity
Article Last Updated: Jun 22, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Richard Paula, MD, Director of Research, Emergency Medicine Residency Program, Tampa General Hospital, University of South Florida at Tampa
Richard Paula is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Editors: William K Chiang, MD, Associate Professor, Department of Emergency Medicine, Department of Emergency Medicine, New York University School of Medicine; Consulting Staff, Bellevue Hospital Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Eric Legome, MD, Residency Director, Assistant Professor of Emergency Medicine, Department of Emergency Medicine New York University, New York University Hospital, Bellevue Hospital Center, Manhattan VA; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Author and Editor Disclosure
Synonyms and related keywords:
CS, compartmental syndrome, Volkmann contracture, Volkmann's contracture, intracompartmental pressure, extremity pain, perfusion pressure, capillary perfusion pressure, CPP, venous pressure, long bone fractures, vascular injury, ischemic injury, fasciotomy, paraesthesia, limb pain, high-energy trauma, penetrating injuries, venous injury, crush injuries, tetany, vigorous exercise, seizures, stationary bicycle use, horseback riding, burns, intraarterial injection, envenomation, decreased serum osmolarity, nephrotic syndrome, infiltrated infusion, hemorrhage, military antishock trousers, MAST, casts
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. That injury remains known as Volkmann contracture.
Although long bone fractures are a common cause of CS, vascular injury is also a common antecedent to CS. Approximately 50 years after vonVolkmann, Jepson described ischemic contractures in dog hind legs resulting from 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. Almost 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. 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. If fluid is introduced into a 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.
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 studied CS. It is quoted as the most common, 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.
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.
- 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.
History
- Suspect CS whenever significant pain occurs in an extremity following an injury.
- Pressure rises and ischemic injury begins to impair nerve function.
- Nerve impairment will often cause the patient to complain of severe pain, out of proportion to examination, and 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.
- 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. 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.
Cellulitis
Coelenterate and Jellyfish Envenomations
Deep Venous Thrombosis and Thrombophlebitis
Gas Gangrene
Necrotizing Fasciitis
Peripheral Vascular Injuries
Rhabdomyolysis
Other Problems to be Considered
Differentials listed above often occur concurrently with CS.
Lab Studies
- Complete metabolic profile (CMP)
- Complete blood count (CBC) with differential
- Creatine phosphokinase (CPK) and urine myoglobin
- Serum myoglobin
- Urine toxicology screen: This subsequently may help define the etiology, but it rarely is helpful in patient treatment.
- Initial urinalysis: This may be positive for blood but negative for RBC on microscopic analysis, which may indicate myoglobin in the urine (rhabdomyolysis).
- Prothrombin time (PT) and activated partial thromboplastin time (aPTT)
Imaging Studies
- Radiography of the affected extremity
- Ultrasonography
- Ultrasonography aids in evaluating arterial flow as well as in visualizing any deep venous thrombosis (DVT).
- Ultrasonography is not helpful in diagnosis of CS; however, it aids in the elimination of differential diagnoses.
Other Tests
- Compartment pressure measurement
- This measure should be at the top of the list when searching for CS; perform it as soon as the diagnosis of CS is considered.
- A number of commercial model tonometers are available (eg, Stryker, ACE). A number of "build-it-yourself" techniques, without evidence of reliability, are also available; their use is not recommended.
Prehospital Care
- CS can develop rapidly after an arterial injury. Therefore, speed of transport is essential. Perform only the necessary lifesaving procedures in the field if CS is suspected.
Emergency Department Care
Time is of the essence in diagnosing and treating compartment syndrome. Irreversible nerve damage begins after 6 hours of intracompartmental hypertension. If CS is suspected, pressure measurements and appropriate consultation must be performed quickly.
- Many cases of CS are due to trauma. Follow advanced trauma life support (ATLS) guidelines to stabilize the patient before attempting to address CS.
- Ischemic injury is the basis for CS. Additional oxygen should be administered because it slightly increases partial pressure of oxygen (PO2).
- Keeping extremities level with the body decreases limb mean arterial pressure without changing intracompartmental pressure.
- Do not elevate the affected extremity. Styf and Wiger (1998) measured, after an elevation of 35 cm, a decrease in the mean arterial perfusion pressure of 23 mm Hg and no change in intracompartmental pressure.
- Intravenous (IV) hydration is essential.
- Fasciotomy remains the definitive therapy for CS because of its well-documented, limb-saving results.
- Recently, timing and use of fasciotomy have been questioned. Fasciotomy extends hospital stay and changes a closed injury to an open injury, greatly increasing the chance of infection.
- As mentioned previously, debate exists regarding the threshold for fasciotomy. A number of authors recommend 30 mm Hg, while others cite 45 mm Hg. Still others urge prophylactic fasciotomy at normal pressures to prevent CS.
- Convincing evidence reflects that debate should center on delta-p. Delta-p is a measure of perfusion pressure (diastolic blood pressure minus intracompartmental pressure). Originally used in dogs, delta-p measurements of less than 30 mm Hg were used by McQueen (1996) for fasciotomy. As a result, several patients with intracompartmental pressures of 40 mm Hg or greater were observed because the delta-p was greater than 30 mm Hg. Criteria were used in 116 patients without sequelae. The converse also is true, since patients with intracompartmental pressures less than 30 mm Hg but with high delta-p values have developed CS.
- A special note about envenomations: Recent studies have confirmed previously postulated theories that myonecrosis associated with compartment syndrome after envenomation is multifactorial and that fasciotomy may not prevent myonecrosis. Myonecrosis is thought to be due to a direct toxic effect of the venom and the inflammatory response. Therefore, these patients should be aggressively treated with antivenom if available, as this has been shown to decrease limb hypoperfusion.
Consultations
- General surgeon
- Orthopedic surgeon
- Vascular surgeon
- Toxicologist
Some authors have advocated the use of mannitol for CS. While its use in rhabdomyolysis is well documented, its use in acute CS is new. More recently, Daniels and Reichman treated an Israeli soldier who developed CS with mannitol. After resolution, he was discharged without a fasciotomy. Unfortunately, intracompartmental pressures were not measured, since the diagnosis was based on limb circumference and nerve conduction studies. Further investigation is warranted in this area.
Hyperbaric oxygen (HBO) therapy is a logical choice for CS because it addresses the primary concern of ischemic injury. HBO has many beneficial effects. It reduces edema through oxygen-induced vasoconstriction while maintaining oxygen perfusion and supports tissue healing in a similar mechanism by allowing oxygen delivery when perfusion pressure is low. Reperfusion injury following CS often is voiced as an argument against HBO. However, HBO actually protects against reperfusion injury.
Bouachour performed a well-controlled randomized study with 31 patients following crush injury and demonstrated significant increase in complete healing (p <0.0005) with HBO. Wattel et al have given an appraisal of the current literature regarding HBO therapy for CS and justifiably conclude that studies demonstrate HBO effectiveness in improving wound healing, reducing amputation rate, and lowering surgical procedure rate.
Although HBO currently is only adjunctive therapy because of its limited availability, it should not be ignored. It may extend treatment duration and it may not reverse the CS etiology, but it has been shown to be beneficial.
Transfer
- Transfer if CS is suspected and any of the following are present:
- Severe or multiple limb involvement that requires intensive care facilities
- Inadequate surgical coverage
- Inability to accurately diagnose CS because of lack of equipment or diagnostic imaging
Complications
- Permanent nerve damage
- Infection
- Loss of limb
- Death
- Cosmetic deformity from fasciotomy
Prognosis
- The prognosis is excellent to poor, depending on how quickly CS is treated and whether complications develop.
Patient Education
- Include the following discharge instructions for patients with injuries that predispose them to CS:
- Timely follow-up examination with appropriate physician is necessary.
- Immediately call or return to the hospital if severe pain, numbness, burning sensation, or weakness in the affected extremity develops.
Medical/Legal Pitfalls
- Failure to measure compartment pressures
- In 1993, Templeman reported an average litigation award of $280,000 for 8 cases of missed CS.
- In all 8 cases, compartment pressures were never measured.
- Failure to investigate rhabdomyolysis if suspected.
- Failure to consider potential errors in compartment pressure measurements
- Equipment errors occur, and needles are misplaced into tendons, fascia, or a wrong compartment.
- Interpret all pressure readings within the context of the clinical presentation.
| Media file 1:
Compartment Syndrome, Extremity. Picture of compartment pressure measuring device for use when commercial devices are unavailable. |
 |  View Full Size Image | |
Media type: Graph
|
| Media file 2:
Compartment syndrome, extremity. Stryker STIC Monitor. Image courtesy of Stryker Corporation, used with permission. |
 | View Full Size Image | |
Media type: Photo
|
- Berlemann U, al-Momani Z, Hertel R. Exercise-induced compartment syndrome in the flexor-pronator muscle group. A case report and pressure measurements in volunteers. Am J Sports Med. May-Jun 1998;26(3):439-41. [Medline].
- Better OS, Zinman C, Reis DN, et al. Hypertonic mannitol ameliorates intracompartmental tamponade in model compartment syndrome in the dog. Nephron. 1991;58(3):344-6. [Medline].
- Bywaters EG, Beall D. Crush injuries with impairment of renal function. 1941. J Am Soc Nephrol. Feb 1998;9(2):322-32. [Medline].
- Daniels M, Reichman J, Brezis M. Mannitol treatment for acute compartment syndrome. Nephron. Aug 1998;79(4):492-3. [Medline].
- Field CK, Senkowsky J, Hollier LH, et al. Fasciotomy in vascular trauma: is it too much, too often?. Am Surg. Jun 1994;60(6):409-11. [Medline].
- Garfin SR, Castilonia RR, Mubarak SJ. Rattlesnake bites and surgical decompression: results using a laboratory model. Toxicon. 1984;22(2):177-82. [Medline].
- Gutyon AC. Textbook of Medical Physiology. 8th ed. Harcourt Brace & Company; 1991:171-184.
- Hach W, Prave F, Hach-Wunderle V, et al. The chronic venous compartment syndrome. Vasa. May 2000;29(2):127-32. [Medline].
- Hargens AR, Akeson WH, Mubarak SJ, et al. Fluid balance within the canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg Am. Jun 1978;60(4):499-505. [Medline].
- Heppenstall RB, Sapega AA, Scott R, et al. The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop. Jan 1988;(226):138-55. [Medline].
- Jepson PN. The classic. Ischemic contracture experimental study by Paul N. Jepson, M.D. Clin Orthop Relat Res. Nov-Dec 1975;3-7. [Medline].
- Matsen FA, Winquist RA, Krugmire RB. Diagnosis and management of compartmental syndromes. J Bone Joint Surg Am. Mar 1980;62(2):286-91. [Medline].
- Matsen FA. Compartment Syndrome. New York: Grune and Stratton;1980.
- McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br. Jan 1996;78(1):99-104. [Medline].
- McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk?. J Bone Joint Surg Br. Mar 2000;82(2):200-3. [Medline].
- Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am. Jun 1983;63(3):539-65. [Medline].
- Owen CA, Mubarak SJ, Hargens AR, et al. Intramuscular pressures with limb compression clarification of the pathogenesis of the drug-induced muscle-compartment syndrome. N Engl J Med. May 24 1979;300(21):1169-72. [Medline].
- Roberge RJ, McLane M. Compartment syndrome after simple venipuncture in an anticoagulated patient. J Emerg Med. Jul-Aug 1999;17(4):647-9. [Medline].
- Rorabeck CH, Macnab I. The pathophysiology of the anterior tibial compartmental syndrome. Clin Orthop. Nov-Dec 1975;(113):52-7. [Medline].
- Styf J, Wiger P. Abnormally increased intramuscular pressure in human legs: comparison of two experimental models. J Trauma. Jul 1998;45(1):133-9. [Medline].
- Tanen DA, Danish DC, Clark RF. Crotalidae polyvalent immune Fab antivenom limits the decrease in perfusion pressure of the anterior leg compartment in a porcine crotaline envenomation model. Ann Emerg Med. Mar 2003;41(3):384-90. [Medline].
- Tanen DA, Danish DC, Grice GA, et al. Fasciotomy worsens the amount of myonecrosis in a porcine model of crotaline envenomation. Ann Emerg Med. Aug 2004;44(2):99-104. [Medline]. [Full Text].
- Tornetta P, Templeman D. Compartment syndrome associated with tibial fracture. Instr Course Lect. 1997;46:303-8. [Medline].
- Wattel F, Mathieu D, Neviere R, Bocquillon N. Acute peripheral ischaemia and compartment syndromes: a role for hyperbaric oxygenation. Anaesthesia. May 1998;53 Suppl 2:63-5. [Medline].
- vonVolkmann R. Verletzungen und krannkheiten der bewwgungsorgane. Handbuch der Allegemeinen und Speziellen Chirurgie. Vol 2. 1872;234-920. [Medline].
Compartment Syndrome, Extremity excerpt Article Last Updated: Jun 22, 2006
|
