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Acute Compartment Syndrome

Author: Abraham T Rasul Jr, MD; Chief Editor: Consuelo T Lorenzo, MD more...

Updated: May 9, 2013
Background
Acute compartment syndrome occurs when the tissue pressure within a closed muscle compartment exceeds the
perfusion pressure and results in muscle and nerve ischemia. It typically occurs subsequent to a traumatic event,
most commonly a fracture.
The cycle of events leading to acute compartment syndrome begins when the tissue pressure exceeds the venous
pressure and impairs blood outflow. Lack of oxygenated blood and accumulation of waste products result in pain and
decreased peripheral sensation secondary to nerve irritation.
Late manifestations of compartment syndrome include the absence of a distal pulse, hypoesthesia, and extremity
paresis, because the cycle of elevating tissue pressure eventually compromises arterial blood flow. If left untreated or
if inadequately treated, the muscles and nerve within the compartment undergo ischemic necrosis, and a limb
contracture, called a Volkmann contracture, results. Severe cases may lead to renal failure and death.
The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and
recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Crush syndrome is distinct
from compartment syndrome; it is defined as a severe systemic manifestation (eg, rhabdomyolysis) of trauma and
ischemia involving soft tissues, principally skeletal muscle, as a result of prolonged severe crushing. Crush
syndrome trauma or rhabdomyolysis may also lead to an acute compartment syndrome.
Chronic compartment syndrome (CCS) is a recurrent syndrome during exercise or work. CCS is characterized by
pain and disability that subside when the precipitating activity is stopped but that return when the activity is resumed.
Although CSS is more common in the anterior compartment of the lower leg, it has been described in the forearm of
motocross racers and other athletes.
[1, 2, 3]
For more information, see the Medscape Reference article Chronic
Exertional Compartment Syndrome.
The incidence of compartment syndrome depends on the patient population studied and the etiology of the
syndrome. In a study by Qvarfordt and colleagues, 14% of patients with leg pain were noted to have anterior
compartment syndrome
[4]
; compartment syndrome was seen in 1-9% of leg fractures.
Compartment syndrome may affect any compartment, including the hand, forearm, upper arm, abdomen, buttock,
[5]
and entire lower extremity. Almost any injury can cause this syndrome, including injury resulting from vigorous
exercise. Clinicians need to maintain a high level of suspicion when dealing with complaints of extremity pain.
[6]
The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with
subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is
restoration of muscle perfusion within 6 hours. (See Treatment.)
Historical aspects
The original description of the consequences of unchecked rising intracompartmental pressures is widely attributed
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to Richard von Volkmann. His 1872 publication documented nerve injury and subsequent contracture from
compartment syndrome following supracondylar fracture.
[7]
That injury remains known as Volkmann contracture.
Although long bone fractures are a common cause of compartment syndrome, other injuries are also a common
antecedent to compartment syndrome. Approximately 50 years after von Volkmann's seminal paper, Jepson
described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous
obstruction.
[8]
Wilson first described the initial case of exertional compartment syndrome in 1912. Mavor, in 1956, first reported a
case of chronic compartment syndrome. Since then, various cases of compartment syndrome have been reported in
the literature, and pathophysiology and treatment options have been discussed.
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 compartment syndrome. 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 various circumstances.
[9]
Almost simultaneously, Matsen published his
findings, which are the most commonly annotated group of articles in present literature.
[10]
Anatomy
Compartment syndrome may develop wherever a compartment is present. Possible sites include the lower leg,
forearm, wrist, and hand.
Lower leg
The lower leg is divided into 4 compartments. A fifth compartment has been documented, but the clinical significance
of this compartment has yet to be established. The 5 compartments are as follows:
Anterior
Lateral
Superficial posterior
Deep posterior
Tibialis posterior
Anterior compartment
Muscles in the anterior compartment are as follows:
Tibialis anterior
Extensor digitorum longus
Extensor hallucis longus
Peroneus tertius
The borders of the anterior compartment are as follows:
Tibia
Fibula
Interosseous membrane
Anterior intermuscular septum
Lateral compartment
The lateral compartment includes the peroneus longus and brevis. Within the compartment lie the common peroneal
nerve and its superficial and deep branches. The borders of this compartment are as follows:
Anterior intermuscular septum
Fibula
Posterior intermuscular septum
Deep fascia
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Superficial posterior compartment
The superficial posterior compartment contains the gastrocnemius, soleus, and plantaris. It is surrounded by the
deep fascia of the leg.
Deep posterior compartment
The muscles within the deep posterior compartment are as follows:
Flexor digitorum longus
Flexor hallucis longus
Popliteus
Tibialis posterior
Also within this compartment lie the posterior tibial artery and vein and the tibial nerve.
The borders of the deep posterior compartment are as follows:
Tibia
Fibula
Deep transverse fascia
Interosseous membrane
Tibialis posteriorcompartment
The tibialis posterior compartment is a more recently described subdivision of the deep posterior compartment. It
consists of the tibialis posterior, which has been shown to have its own fascial layer.
Forearm
Four interconnected compartments of the forearm are recognized, as follows:
Superficial volar (flexor)
Deep volar
Dorsal (extensor) compartment
Compartment containing the mobile wad of Henry
The deep volar compartment contains the flexor digitorum profundus, flexor pollicis longus, and pronator quadratus
muscles and tendons. The mobile wad of Henry comprises the brachioradialis, extensor carpi radialis brevis (ECRB),
and extensor carpi radialis longus muscles and tendons.
Elevated pressures most commonly affect the volar compartments, but the dorsal and mobile wad compartments
may also be involved, alone or in addition to the volar compartments. It is usually difficult to clinically differentiate
isolated or combined involvement of the deep and superficial volar compartments.
Wrist
In the wrist, most of the soft tissues are bound within rigid compartments. The volar wrist tendons, for the most part,
are tightly constrained within the carpal tunnel (thumb and finger long flexor tendons), except for the flexor carpi
radialis, flexor carpi ulnaris, and palmaris longus tendons, which are in separate compartments. The dorsal
compartments are primarily channels for tendons and are rarely afflicted by compartment syndrome.
The dorsal extensor tendons pass under an extensor retinaculum and are divided into 6 compartments, as follows:
Radial wrist abductor (abductor pollicis longus tendon) and thumb extensor (extensor pollicis brevis tendon)
dorsal to the trapezium bone
Radial wrist extensors (extensor carpi radialis longus and ECRB tendons) dorsal and radial to the trapezoid
bone
Extensor pollicis longus tendon
Common finger extensors (extensor digitorum communis [EDC] tendon) dorsal to the capitotrapezoid
articulation
Extensor digiti minimi tendon to the fifth digit
Ulnar wrist extensor (extensor carpi ulnaris tendon) in a groove adjacent to the ulnar styloid
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Hand
The hand has 10 compartments, as follows:
Dorsal interossei (4 compartments)
Palmar interossei (3 compartments)
Adductor pollicis compartment
Thenar compartment
Hypothenar compartment
Pathophysiology
Compartment syndrome results primarily from increased intracompartmental pressure. The mechanism involved in
the development of increased pressure depends on the precipitating event.
Two distinct types of compartment syndrome have been recognized. The first type is associated with trauma to the
affected compartment, as seen in fractures or muscle injuries. The second form, called exertional compartment
syndrome, is associated with repetitive loading or microtrauma related to physical activity.
[11, 12, 13, 14, 15, 16, 17, 18]
Thus, compartment syndrome may be acute or chronic in nature.
Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial
fluid pressure, which is stated by the following formula:
LBF = (PA - PV)/R
In the formula above, LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local
vascular resistance.
Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25
mm Hg and an interstitial tissue pressure of 4-6 mm Hg.
[19]
When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises.
When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary
collapse and muscle and tissue ischemia occur.
Skeletal muscle responds to ischemia by releasing histaminelike substances that increase vascular permeability.
Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the
ischemia. The myocytes begin to lyse, and the myofibrillar proteins decompose into osmotically active particles that
attract water from arterial blood.
One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in
osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular
pressure. When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This
vicious cycle of worsening tissue perfusion continues to propagate.
Some reduction in the local AV gradient can be compensated for by changes in local vascular resistance
(autoregulation). However, compartment tamponade occurs as arterial blood flow is occluded. Shrier and Magder
questioned this traditional hypothesis for the pathophysiology of compartment syndrome and postulated that within
muscle compartments, a critical closing pressure exists (similar to West zone II in lung physiology).
[20]
These authors
showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial
resistance, results in decreased blood flow.
The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure;
the pressure at which this occurs is still under debate. However, in general, compartmental pressures higher than 30
mm Hg require surgical intervention. If such high compartmental pressures are left untreated, within 6-10 hours,
muscle infarction, tissue necrosis, and nerve injury occur. For unclear reasons, compartment syndrome that is
associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer
postoperatively.
[21]
Pressure-induced functional deficits are likely caused by decreased tissue perfusion rather than a direct mechanical
effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure,
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hemorrhage, and arterial occlusion. In addition to local morbidity caused by muscle necrosis and tissue ischemia,
cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation.
This circulating myoglobin results in renal injury. Advanced compartment syndrome may result in rhabdomyolysis,
and conversely, rhabdomyolysis may result in compartment syndrome.
[22]
Mortality is usually due to renal failure or
sepsis from difficult wound management.
The mechanism of compartment syndrome following vascular trauma may differ slightly from the above scenario
because most cases occur with reperfusion. This reperfusion syndrome is likely related to the ischemic depletion of
high-energy phosphate forms and ischemic muscle injury.
Muscle has considerable ability to regenerate by forming new muscle cells. Therefore, it is extremely important to
decompress ischemic muscle as early as possible. Compartment pressures return to normal after a fasciotomy.
[23]
Etiology
Any internal or external event that increases pressure within a compartment can cause compartment syndrome.
Thus, increased fluid content or decreased compartment size can lead to the condition.
[24]
Increased fluid content can be caused by the following:
Intensive muscle use (eg, tetany, vigorous exercise, seizures)
[25]
Everyday exercise activities (eg, stationary bicycle use, horseback riding
[26]
)
Burns
[27]
Envenomation
Decreased serum osmolarity (eg, nephrotic syndrome)
Hemorrhage (particularly from a large vessel injury)
[28, 29]
Postischemic swelling
Drug/alcohol abuse and coma
Rhabdomyolysis
[30]
Gastrocnemius or peroneus muscle tear (lower extremity)
Ruptured Baker cyst
Influenza myositis
[31]
Autoimmune vasculitis
[32]
Androgen abuse/muscle hypertrophy
Deep venous thrombosis
[33]
Fractures or gunshot wounds may be the source of hemorrhage underlying compartment syndrome.
[3]
Upper
extremity fractures most frequently associated with compartment syndrome are supracondylar fractures of the
humerus, but cases have also been reported in conjunction with fractures of the radial or ulnar diaphysis, fractures of
the surgical neck of the humerus, and Colles fractures.
Although trauma is the most common etiology, compartment syndrome has been shown to occur in neonates from
intrauterine malposition or strangulation of the extremity by the umbilical cord.
Lying on a limb can cause compartment syndrome. In 1979, Owen et al published a landmark study in which
researchers measured intracompartmental pressures in various positions common in drug overdoses.
[9]
Average
pressures were 48 mm Hg with the head resting on the forearm; 178 mm Hg when the forearm was under the
ribcage; and 72 mm Hg when one leg was folded under the other.
Iatrogenic causes
Iatrogenic causes of compartment syndrome include the following:
Military antishock trousers
[34]
Tight splints, casts, dressings
[35]
Lithotomy position (lower extremity cases)
[36]
Malfunctioning sequential compression devices
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Intramuscular, intra-arterial, or intracompartmental injection
[37]
Intraosseous infusion
Massive hypertonic IV fluid infusion
Pressurized intravenous (IV) infusion of parenteral hypertonic contrast agent
Attempts at cannulating veins and arteries of the arm in patients on systemic anticoagulants or patients
treated with thrombolytic drugs
Intraoperative use of a pressurized pulsatile irrigation system
Use of a pump for infusion of fluids into the joint during an arthroscopic procedure
Chemotherapy drugs can produce true compartment syndrome. Alternatively, extravasation of these drugs can
cause pain and swelling that mimics compartment syndrome.
Compartment syndrome may follow operations for orthopedic fixation (eg, open reduction and internal fixation).
These cases may result from postoperative hematoma, muscle edema, or tight closure of the deep fascia. These
risks can usually be minimized by releasing the tourniquet before wound closure to ensure that hemostasis is
adequate and by closing only the subcutaneous tissue and skin.
Epidemiology
The anterior distal lower extremity is the most common studied site of compartment syndrome. Tibial fracture is the
most common precipitating event, accounting for 2-12% of all compartment syndrome cases, according to the
literature. In a retrospective study by McQueen and Court-Brown in 164 patients with diagnosed compartment
syndrome, 69% of cases were associated with a fracture, and half of those involved the tibia. In the study,
compartment syndrome was diagnosed more often in men than in women. This finding likely represents selection
bias, however, because most patients with traumatic injuries are male.
[38]
In a 10-year study, McQueen et al studied
850 patients and concluded that continuous intracompartmental pressure monitoring should be considered following
tibial diaphyseal fracture because these patients are at risk for acute compartment syndrome.
[39]
The incidence of acute compartment syndrome varies depending on the inciting event. DeLee and Stiehl found that
6% of patients with open tibial fractures developed compartment syndrome, compared with only 1.2% of patients
with closed tibial fractures.
[40]
The reported incidence of compartment syndrome may underestimate the true
incidence because the syndrome may go undetected in severely traumatized patients.
The frequency of compartment syndrome is much higher in patients who have an associated vascular injury.
Feliciano et al reported that 19% of patients with vascular injury required fasciotomy
[41]
; an incidence of 30% has
also been suggested, but this figure is not well documented and is most likely an estimate. The true incidence of
cases associated with vascular trauma may not be known because many vascular surgeons perform a prophylactic
fasciotomy at the time of the vascular repair in high-risk patients.
Prognosis
Compartment syndrome 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.
[42]
Matsen found necrosis after 6 hours of ischemia, which currently is the accepted upper limit of viability.
[43]
When fasciotomy was performed within 12 hours after the onset of acute compartment syndrome, Sheridan and
Matsen reported that normal limb function was regained in 68% of patients.
[44]
However, when fasciotomy was
delayed 12 hours or longer, only 8% of patients had normal function. Thus, little or no return of function can be
expected when the diagnosis and treatment are delayed. Tendon transfers and stabilization may be indicated as late
treatment for CS.
Long-term follow-up of patients who have undergone fasciotomies has shown good results, with a return to
premorbid activity level. Pain also has been found to significantly improve.
In the lower leg, the results of fasciotomies for posterior compartment syndrome are not as good as those for the
anterior compartment. A possible explanation is that it is difficult to do a complete decompression of the deeper
posterior compartment, because of the morbidity associated with this procedure. In general, however, early
diagnosis, with institution of the appropriate treatment, results in a good outcome.
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With late diagnosis, irreversible tissue ischemia can develop in the acute setting. Thus, permanent muscle and nerve
damage, along with chronic pain, may occur. In the lower leg, peroneal nerve palsy, in particular, may develop.
Volkmann contracture is the residual limb deformity that results over weeks to months following untreated acute
compartment syndrome or ischemia from an uncorrected arterial injury. Approximately 1-10% of patients develop a
Volkmann contracture.
[45]
Calcific myonecrosis of lower extremity muscles has been identified as an uncommon late
complication of posttraumatic compartment syndrome.
Recurrent compartment syndrome has been reported in athletes. It is thought to be related to severe scarring and
the subsequent closing of the initial compartment release.
Infection is a serious complication of compartment syndrome. In a retrospective review by Matsen et al, 11 of 24
extremities that had late surgical decompression developed infections, and 5 of these infections led to an
amputation.
[46]
Infection after fasciotomy may become chronic. Patients, especially those with multiple traumatic
injuries, may die because of infections or metabolic complications. Renal failure or multiple organ failure may occur
preoperatively or postoperatively. Most fatalities are due to prolonged intensive care admissions with sepsis and
multisystem organ failure.


Contributor Information and Disclosures
Author
Abraham T Rasul Jr, MD Medical Director for Rehabilitation, Specialty Hospital of Washington; Founder, Arizona
Golf Medicine Institute
Abraham T Rasul Jr, MD is a member of the following medical societies: American Academy of Physical Medicine
and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of
Sports Medicine, and American Medical Association
Disclosure: Nothing to disclose.
Chief Editor
Consuelo T Lorenzo, MD Executive Health Resources
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine
and Rehabilitation
Disclosure: Nothing to disclose.
Additional Contributors
Samuel Agnew, MD, FACS Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of
Orthopedic Trauma, University of Florida at Jacksonville College of Medicine; Consulting Surgeon, Department of
Orthopedic Surgery, McLeod Regional Medical Center
Samuel Agnew, MD, FACS is a member of the following medical societies: American Association for the Surgery
of Trauma, American College of Surgeons, Orthopaedic Trauma Association, and Southern Orthopaedic
Association
Disclosure: Nothing to disclose.
Jason H Calhoun, MD, FACS Frank J Kloenne Chair in Orthopedic Surgery, Professor and Chair, Department of
Orthopedics, The Ohio State University Medical Center
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7 of 15 2/13/14 6:43 AM
Jason H Calhoun, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic
Surgeons, American College of Surgeons, American Diabetes Association, American Medical Association,
American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Missouri State Medical
Association, Musculoskeletal Infection Society, Southern Medical Association, Southern Orthopaedic Association,
Texas Medical Association, and Texas Orthopaedic Association
Disclosure: Nothing to disclose.
William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of
Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology,
American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Patrick M Foye, MD Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal
Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service:
www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and
Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic
Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.
Stuart B Goodman, MD, PhD, FRCS(C), FACS, FBSE Robert L and Mary Ellenburg Professor of Surgery,
Professor, Department of Orthopedic Surgery, Fellowship Director, Orthopedic Adult Reconstruction, Affiliated
Faculty, Department of Bioengineering, Affiliated Faculty, Stanford Center on Longevity, Stanford University
School of Medicine, Stanford University Medical Center
Stuart B Goodman, MD, PhD, FRCS(C), FACS, FBSE is a member of the following medical societies: American
Academy of Orthopaedic Surgeons, American College of Surgeons, California Medical Association, Canadian
Medical Association, College of Physicians and Surgeons of Ontario, Orthopaedic Trauma Association, and Royal
College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.
Mary Ann E Keenan, MD Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic
Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of
Orthopedic Surgery, Hospital of the University of Pennsylvania
Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy
of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society,
American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association
Disclosure: Nothing to disclose.
Rick Kulkarni, MD
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Emergency Medicine, American College of Emergency Physicians, American Medical Association, American
Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment
Eric L Legome, MD Chief, Department of Emergency Medicine, Kings County Hospital Center; Associate
Professor, Department of Emergency Medicine, New York Medical College
Eric L Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency
Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Acute Compartment Syndrome http://emedicine.medscape.com/article/307668-overview
8 of 15 2/13/14 6:43 AM
Richard Paula, MD Assistant Professor of Emergency Medicine, Director of Research, University of South Florida
College of Medicine
Richard Paula, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Steven I Rabin, MD Clinical Associate Professor, Loyola University Medical Center; Chair, Department of
Orthopedic Surgery, Dreyer Medical Clinic
Steven I Rabin, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons,
American Fracture Association, AO Foundation, and Orthopaedic Trauma Association
Disclosure: Nothing to disclose.
Douglas G Smith, MD Associate Professor, Department of Orthopedic Surgery, Harborview Medical Center,
University of Washington School of Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Drug Reference Salary Employment
Jeffrey L Visotsky, MD Assistant Professor, Department of Clinical Orthopedic Surgery, Northwestern University,
The Feinberg School of Medicine
Jeffrey L Visotsky, MD is a member of the following medical societies: American Academy of Orthopaedic
Surgeons, American Association for Hand Surgery, American College of Physician Executives, American College
of Surgeons, American Medical Association, American Society for Surgery of the Hand, Arthroscopy Association
of North America, Chicago Medical Society, and Illinois State Medical Society
Disclosure: Depuy Consulting fee Speaking and teaching; Pegasus Honoraria Board membership
Stephen Wallace, MD Staff Physician, Department of Emergency Medicine, Memorial Hospital of Sweetwater
County
Stephen Wallace, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Rajesh R Yadav, MD Associate Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer
Center, University of Texas Medical School at Houston
Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and
Rehabilitation
Disclosure: Nothing to disclose.
Additional Contributors
Samuel Agnew, MD, FACS Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of
Orthopedic Trauma, University of Florida at Jacksonville College of Medicine; Consulting Surgeon, Department of
Orthopedic Surgery, McLeod Regional Medical Center
Samuel Agnew, MD, FACS is a member of the following medical societies: American Association for the Surgery
of Trauma, American College of Surgeons, Orthopaedic Trauma Association, and Southern Orthopaedic
Association
Disclosure: Nothing to disclose.
Jason H Calhoun, MD, FACS Frank J Kloenne Chair in Orthopedic Surgery, Professor and Chair, Department of
Orthopedics, The Ohio State University Medical Center
Jason H Calhoun, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic
Acute Compartment Syndrome http://emedicine.medscape.com/article/307668-overview
9 of 15 2/13/14 6:43 AM
Surgeons, American College of Surgeons, American Diabetes Association, American Medical Association,
American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Missouri State Medical
Association, Musculoskeletal Infection Society, Southern Medical Association, Southern Orthopaedic Association,
Texas Medical Association, and Texas Orthopaedic Association
Disclosure: Nothing to disclose.
William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of
Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology,
American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Patrick M Foye, MD Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal
Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service:
www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and
Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic
Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.
Stuart B Goodman, MD, PhD, FRCS(C), FACS, FBSE Robert L and Mary Ellenburg Professor of Surgery,
Professor, Department of Orthopedic Surgery, Fellowship Director, Orthopedic Adult Reconstruction, Affiliated
Faculty, Department of Bioengineering, Affiliated Faculty, Stanford Center on Longevity, Stanford University
School of Medicine, Stanford University Medical Center
Stuart B Goodman, MD, PhD, FRCS(C), FACS, FBSE is a member of the following medical societies: American
Academy of Orthopaedic Surgeons, American College of Surgeons, California Medical Association, Canadian
Medical Association, College of Physicians and Surgeons of Ontario, Orthopaedic Trauma Association, and Royal
College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.
Mary Ann E Keenan, MD Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic
Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of
Orthopedic Surgery, Hospital of the University of Pennsylvania
Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy
of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society,
American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association
Disclosure: Nothing to disclose.
Rick Kulkarni, MD
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Emergency Medicine, American College of Emergency Physicians, American Medical Association, American
Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment
Eric L Legome, MD Chief, Department of Emergency Medicine, Kings County Hospital Center; Associate
Professor, Department of Emergency Medicine, New York Medical College
Eric L Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency
Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Richard Paula, MD Assistant Professor of Emergency Medicine, Director of Research, University of South Florida
Acute Compartment Syndrome http://emedicine.medscape.com/article/307668-overview
10 of 15 2/13/14 6:43 AM
College of Medicine
Richard Paula, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Steven I Rabin, MD Clinical Associate Professor, Loyola University Medical Center; Chair, Department of
Orthopedic Surgery, Dreyer Medical Clinic
Steven I Rabin, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons,
American Fracture Association, AO Foundation, and Orthopaedic Trauma Association
Disclosure: Nothing to disclose.
Douglas G Smith, MD Associate Professor, Department of Orthopedic Surgery, Harborview Medical Center,
University of Washington School of Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Drug Reference Salary Employment
Jeffrey L Visotsky, MD Assistant Professor, Department of Clinical Orthopedic Surgery, Northwestern University,
The Feinberg School of Medicine
Jeffrey L Visotsky, MD is a member of the following medical societies: American Academy of Orthopaedic
Surgeons, American Association for Hand Surgery, American College of Physician Executives, American College
of Surgeons, American Medical Association, American Society for Surgery of the Hand, Arthroscopy Association
of North America, Chicago Medical Society, and Illinois State Medical Society
Disclosure: Depuy Consulting fee Speaking and teaching; Pegasus Honoraria Board membership
Stephen Wallace, MD Staff Physician, Department of Emergency Medicine, Memorial Hospital of Sweetwater
County
Stephen Wallace, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Rajesh R Yadav, MD Associate Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer
Center, University of Texas Medical School at Houston
Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and
Rehabilitation
Disclosure: Nothing to disclose.
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