eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Carpal Tunnel Syndrome

Jeffrey G Norvell, MD, Clinical Assistant Professor of Emergency Medicine, University of Kansas School of Medicine
Mark Steele, MD, Associate Dean for Truman Medical Center Programs, Professor, Department of Emergency Medicine, University of Missouri-Kansas City

Updated: Sep 10, 2009

Introduction

Background

Carpal tunnel syndrome (CTS) is a compressive neuropathy of the median nerve at the wrist. The carpal tunnel is located at the base of the palm and is bounded on 3 sides by carpal bones and anteriorly by the transverse carpal ligament. Inside run the median nerve, flexor tendons, and their synovial sheaths.

Pathophysiology

Carpal tunnel syndrome (CTS) is caused predominantly by compression of the median nerve at the wrist because of hypertrophy or edema of the flexor synovium. Pain is thought to be secondary to nerve ischemia rather than direct physical damage of the nerve.

Carpal tunnel syndrome. Carpal and Guyon tunnels. Drawing showing the proximal level of the carpal tunnel delimited by the pisiform (P) and the scaphoid (S). The flexor retinaculum (medium gray region) forms the roof of the carpal tunnel and the floor of the Guyon tunnel. The palmar carpal ligament (dark gray region) forms the volar boundary of the Guyon tunnel. * = flexor pollicis longus tendon, * = flexor carpi radialis tendon. From Martinoli C, Bianchi S, et al. US of nerve entrapments in osteofibrous tunnels of the upper and lower limbs. Radiographics 2000; 20:S199-S217. Used by permission of the authors and RSNA.

Carpal tunnel syndrome. Carpal and Guyon tunnels. Transverse 5-12-MHz ultrasound scan corresponding to Image 1 shows the proximal level of the carpal tunnel delimited by the pisiform (P) and the scaphoid (S). The flexor tendons and median nerve (MN) extend through the carpal tunnel, with the nerve lying palmar and radial. The flexor retinaculum (open arrowheads) forms the roof of the carpal tunnel and the floor of the Guyon tunnel. At the level of the pisiform, the ulnar nerve (U) courses medial to the ulnar artery (solid arrowhead) within the Guyon tunnel. * = flexor pollicis longus tendon. From Martinoli C, Bianchi S, et al. US of nerve entrapments in osteofibrous tunnels of the upper and lower limbs. Radiographics 2000; 20:S199-S217. Used by permission of the authors and RSNA.

Frequency

United States

Carpal tunnel syndrome is the most frequently encountered peripheral compressive neuropathy. The prevalence of carpal tunnel syndrome in the United States is estimated to at 3.7%, and the annual incidence is estimated at 0.4%.^1,2

Mortality/Morbidity

Early in the course of carpal tunnel syndrome (CTS), the neurologic findings are reversible. If untreated, CTS can result in thenar atrophy, chronic hand weakness, and numbness in the median nerve distribution of the hand.

Sex

CTS is more prevalent in females than in males.^3,4

Age

CTS is most common in middle-aged persons.

Clinical

History

Patients typically complain of an intermittent "pins-and-needles" paresthesia in the median nerve distribution of the hand. Pain is generally worse at night than during the day. Patients may awaken with a burning pain or tingling that may be relieved with shaking their hands. Classic carpal tunnel syndrome (CTS) is associated with symptoms that affect at least 2 of the first through third digits; symptoms affecting the fourth and fifth digits, wrist pain, and radiation of pain proximal to the wrist may also occur, but classic CTS is not associated with symptoms on the palm or dorsum of the hand.⁵

Symptoms of probable CTS are the same as classic CTS except palmar symptoms may be present, unless confined solely to the ulnar aspect. Possible CTS involves symptoms in at least one of the first 3 digits. The sensitivity of classic or probable CTS symptoms for diagnosing CTS is 80%. CTS is unlikely if no symptoms are present in any of the first 3 digits.⁵

• Symptoms are most often bilateral, insidious in onset, and progressive in nature.
• With advanced nerve compression, an aching sensation is persistent and static and may radiate to the forearm and elbow.
• Inquire with regard to repetitive strain risk, such as waitperson, assembly packing, computer keyboard work, playing a musical instrument, or craftwork.
• Determine if any significant trauma has occurred.
• Inquire with regard to presence of any other predisposing factors listed below under Causes.

Physical

• Weakness of resisted thumb abduction (ie, movement of the thumb at right angles to the palm) is helpful determining which patients will have an electrodiagnosis of CTS.⁶
• Sensory hypalgesia as demonstrated by diminished ability to perceive painful stimuli applied along the palmar aspect of the index finger when compared with the ipsilateral little finger also is associated with the electrodiagnosis of CTS.⁶
• Hyperflexion of the wrist for 60 seconds may elicit paresthesia in the median nerve distribution (ie, Phalen sign). A literature review showed the average sensitivity and specificity of the Phalen sign to be 68% and 73%, respectively.⁷
• Tapping the volar wrist over the median nerve (ie, Tinel sign) may produce paresthesia in the median distribution of the hand. Pooled data show the sensitivity and specificity of the Tinel sign to be 50% and 77%, respectively.⁷
• Shaking or flicking one's hands for relief during maximal symptoms (ie, Flick sign) has been shown to have a sensitivity of 47% and specificity of 62%.⁷
• The loss of 2-point discrimination in the median nerve distribution or abductor pollicis brevis atrophy has a high specificity (>90%) but low sensitivity (<25%).⁷

Causes

• Inflammation of the flexor tendon sheath caused by activities involving repetitive wrist flexion (eg, assembly packing, computer keyboard work, playing a musical instrument, craftwork)
• Edema from trauma of any type (eg, fractures), which can compress the median nerve
• Compression of the median nerve from pregnancy⁸  or oral contraceptive-related edema
• Strong association between being overweight or obese and the presence of CTS
• Acromegaly
• Rheumatoid arthritis
• Gout or pseudogout
• Tuberculosis
• Renal failure and hemodialysis
• Hypothyroidism
• Amyloidosis
• Has been associated with diabetes mellitus

Differential Diagnoses

Tendonitis
Tenosynovitis

Other Problems to Be Considered

Compressive neuropathies of the nerve roots and brachial plexus
Proximal median neuropathy
Polyneuropathy

Workup

Imaging Studies

• Currently, there is no universally accepted criterion standard for the diagnosis of carpal tunnel syndrome (CTS). The diagnosis of CTS is made from the ED presumptively. The clinician who follows the patient after the acute presentation usually orders the imaging studies and other tests discussed below.
  • Magnetic resonance imaging (MRI) is reasonably accurate in diagnosing CTS. Currently, this imaging modality is only recommended when the clinical picture is confusing or when nerve conduction studies are equivocal or contradictory. Dynamic MRI imaging may be useful in identifying dynamic CTS (CTS symptoms brought on only by repetitive wrist motion).⁹ MRI may also identify causative lesions in carpal tunnel.¹⁰

Carpal tunnel syndrome. Axial fast spin-echo T2-weighted MRI with fat saturation. Note the increased T2-weighted signal within the median nerve (arrow). A slightly increased cross sectional area of the nerve is noted but the nerve architecture is preserved, consistent with early or mild inflammation.

Carpal tunnel syndrome. Fast spin-echo T2-weighted MRI illustrates more pronounced increased signal within the median nerve (arrow). Note the small amount of fluid within the carpal tunnel, a secondary sign of inflammation. Slightly less optimal fat saturation is noted than on other images, which is a common occurrence.

Carpal tunnel syndrome. Axial fast spin-echo T2-weighted MRI with greater increase in signal and loss of definition within the nerve (arrow). Inflammatory change is noted within the carpal tunnel, adjacent to the flexor digitorum superficialis tendons. The appearance is consistent with pronounced inflammatory change within the carpal tunnel.

• Plain radiography is low-yield.¹¹
• High-resolution ultrasonography (US) has received increased attention in the evaluation of CTS. US as a modality is more widely available than electrodiagnostic studies and is noninvasive and has lower costs. Recent US studies have shown that patients with CTS have an increased cross-sectional area of the median nerve in the carpal tunnel than controls. Ultrasonography may be useful as an alternative to nerve conduction studies for an initial diagnostic test for CTS.¹² One study concluded that sonography is not accurate enough to replace nerve conduction studies for diagnosing CTS.¹³

Other Tests

• Electromyographic (EMG) and nerve conduction studies
  • EMG and nerve conduction studies help to confirm the diagnosis of CTS.
  • They are most helpful in the determination of the site and severity of nerve compression.
  • Electrodiagnostic testing has been found to have an 85% sensitivity and specificity greater than 95% for diagnosing CTS.¹⁴
  • Clinically symptomatic CTS may have normal nerve conduction findings.¹⁵

Treatment

Emergency Department Care

• The mainstay of treatment for carpal tunnel syndrome (CTS) is rest, wrist immobilization with a splint, and nonsteroidal anti-inflammatory drugs (NSAIDs). Corticosteroid injections, oral steroids, and diuretics are other treatment modalities that have been used. 
  • A volar splint should be placed in neutral position because flexion and extension of the wrist increases carpal intracanal pressure. Splinting has been shown to have a statistically significant decrease in symptoms compared with controls. Studies comparing nocturnal only splinting to full-time splinting have not revealed a clear difference, although the studies may have been underpowered.^16,17  
  • No data support that NSAIDs are superior to placebo in the treatment of CTS.¹⁷ However, in absence of contraindications, a trial of NSAIDs may be appropriate.
  • Oral steroids have been shown to have an advantage in treating CTS over placebo. The benefit appears short lived, and the studies do not assess the long-term effectiveness or complications of oral steroids used in treating CTS.^16,17
  • Although not typically performed in the emergency department, corticosteroid injections have been shown to have a statistically significant benefit in CTS at 1 month compared with placebo. The effects of corticosteroid injection appear to be time limited, and the benefit beyond 1 month is unclear. Two steroid injections do not appear to add significant clinical benefit to one injection.¹⁸ Local injections have been shown to be superior to systemic corticosteroids.¹⁶ Steroid injection combined with splinting has been shown to be superior to splinting alone.¹⁹  
  • Diuretics have not been shown to be superior to placebo in the treatment of CTS.¹⁷
• Surgery
  • Definitive therapy consists of surgical release of the transverse carpal ligament.
  • The surgical approach may be open or endoscopic. Both approaches have similar efficacy. A randomized controlled trial showed that patients who underwent endoscopic surgery for carpal tunnel syndrome had less postoperative pain than patients who underwent open surgery; however, the difference was small.²⁰  The authors of this study extended the follow-up period to 5 years, and it demonstrated an equivalent improvement in CTS symptoms between an open and an endoscopic carpal tunnel release.²¹ An article in the Cochrane Database of Systematic Reviews states that endoscopic surgery allows an earlier return to work and fewer wound problems, but possible disadvantages may be higher complication rates and cost.²²
  • Surgery for CTS has a long-term success rate of greater than 75%.²³

Consultations

Referral to a hand specialist (plastic surgeon or orthopedic surgeon) for follow-up care is recommended.

Medication

The goal of therapy is to reduce inflammation and prevent complications.

Nonsteroidal anti-inflammatory agents

Most commonly are used for the relief of mild-to-moderate pain. Although the effects of NSAIDs in the treatment of pain tend to be patient specific, ibuprofen usually is the DOC for the initial therapy. Other options include flurbiprofen, ketoprofen, and naproxen.

Flurbiprofen (Ansaid)

May inhibit cyclo-oxygenase enzyme, which in turn inhibits prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Dosing

Adult

200-300 mg/d PO divided bid/qid

Pediatric

Not established

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion, risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Ketoprofen (Actron, Orudis, Oruvail)

For relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease.
Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Ibuprofen (Ibuprin, Advil, Motrin)

Usually the DOC for the treatment of mild-to-moderate pain if no contraindications exist.
Inhibits inflammatory reactions and pain, probably by decreasing the activity of cyclooxygenase enzyme, which results in the inhibition of prostaglandin synthesis.
Taking medication with at least 4 oz of water may minimize adverse effects.

Dosing

Adult

400 mg PO q4-6h; or 600 mg PO q6h; or 800 mg PO q8h; not to exceed 2400 mg/d

Pediatric

<6 months: Not established
6 months to 12 years: 20-40 mg/kg/d PO divided tid or qid
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Naproxen (Anaprox, Naprelan, Naprosyn, Aleve)

Used for the relief of mild-to-moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase enzyme, which results in a decrease of prostaglandin synthesis. Inexpensive and effective.

Dosing

Adult

250 mg PO q6-8h; or 500 mg PO q12h; not to exceed 1 g/d

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; diathesis; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Follow-up

Further Outpatient Care

• Perform EMG and nerve conduction studies to help confirm diagnosis of carpal tunnel syndrome.

Complications

• Chronic hand pain
• Chronic hand weakness and numbness
• Chronic disability

Prognosis

• Prognosis is excellent with definitive therapy.
• CTS during pregnancy seems to be less severe than idiopathic CTS and has milder course with fewer cases requiring surgical treatment.
• Risks factors for poorer-than-average prognosis include the following:
  • Advanced disease
  • Atypical symptoms (normal nerve conduction studies, symptoms in fifth digit)
  • Longer symptom duration
  • Older age
  • Coexisting disease (diabetes, other peripheral neuropathy)
  • Heavy manual occupation
• Despite treatment, some patients may have residual fingertip numbness.

Patient Education

• For excellent patient education resources, visit eMedicine's Hand, Wrist, Elbow, and Shoulder Center and Arthritis Center. Also, see eMedicine's patient education article Carpal Tunnel Syndrome.

Miscellaneous

Medicolegal Pitfalls

• Median nerve injury following steroid injection has been reported.

Multimedia

Media file 1: Carpal tunnel syndrome. Carpal and Guyon tunnels. Drawing showing the proximal level of the carpal tunnel delimited by the pisiform (P) and the scaphoid (S). The flexor retinaculum (medium gray region) forms the roof of the carpal tunnel and the floor of the Guyon tunnel. The palmar carpal ligament (dark gray region) forms the volar boundary of the Guyon tunnel. * = flexor pollicis longus tendon, * = flexor carpi radialis tendon. From Martinoli C, Bianchi S, et al. US of nerve entrapments in osteofibrous tunnels of the upper and lower limbs. Radiographics 2000; 20:S199-S217. Used by permission of the authors and RSNA.

Media file 2: Carpal tunnel syndrome. Carpal and Guyon tunnels. Transverse 5-12-MHz ultrasound scan corresponding to Image 1 shows the proximal level of the carpal tunnel delimited by the pisiform (P) and the scaphoid (S). The flexor tendons and median nerve (MN) extend through the carpal tunnel, with the nerve lying palmar and radial. The flexor retinaculum (open arrowheads) forms the roof of the carpal tunnel and the floor of the Guyon tunnel. At the level of the pisiform, the ulnar nerve (U) courses medial to the ulnar artery (solid arrowhead) within the Guyon tunnel. * = flexor pollicis longus tendon. From Martinoli C, Bianchi S, et al. US of nerve entrapments in osteofibrous tunnels of the upper and lower limbs. Radiographics 2000; 20:S199-S217. Used by permission of the authors and RSNA.

Media file 3: Carpal tunnel syndrome. Carpal and Guyon tunnels. Drawing showing the distal level of the carpal tunnel delimited by the hook of the hamate (H) and the tubercle of the trapezium (T). The flexor retinaculum (medium gray region) forms the roof of the carpal tunnel. From Martinoli C, Bianchi S, et al. US of nerve entrapments in osteofibrous tunnels of the upper and lower limbs. Radiographics 2000; 20:S199-S217. Used by permission of the authors and RSNA.

Media file 4: Carpal tunnel syndrome. Carpal and Guyon tunnels. Transverse 5-12-MHz ultrasound scan corresponding to Image 3 shows the distal level of the carpal tunnel delimited by the hook of the hamate (H) and the tubercle of the trapezium (T). The flexor retinaculum (open arrowheads) forms the roof of the carpal tunnel. The flexor tendons and median nerve (MN) extend through the carpal tunnel, with the nerve lying palmar and radial. At the level of the pisiform, the ulnar nerve courses medial to the ulnar artery (solid arrowhead) within the Guyon tunnel. At the level of the hamate, the ulnar nerve divides into two terminal branches, a deep motor branch (curved arrow) and a superficial sensory branch (straight arrow). From Martinoli C, Bianchi S, et al. US of nerve entrapments in osteofibrous tunnels of the upper and lower limbs. * = flexor pollicis longus tendon. Radiographics 2000; 20:S199-S217. Used by permission of the authors and RSNA.

Media file 5: Carpal tunnel syndrome. Normal findings on an axial spin-echo T1 MRI of the carpal tunnel showing the intermediate signal intensity of the median nerve (arrow).

Media file 6: Carpal tunnel syndrome. Normal findings of isointense-to-hypointense appearance of the median nerve on fast spin-echo T2-weighted MRI (arrow). Note the fairly well-defined nerve fascicles within the median nerve sheath.

Media file 7: Carpal tunnel syndrome. Axial fast spin-echo T2-weighted MRI with fat saturation. Note the increased T2-weighted signal within the median nerve (arrow). A slightly increased cross sectional area of the nerve is noted but the nerve architecture is preserved, consistent with early or mild inflammation.

Media file 8: Carpal tunnel syndrome. Fast spin-echo T2-weighted MRI illustrates more pronounced increased signal within the median nerve (arrow). Note the small amount of fluid within the carpal tunnel, a secondary sign of inflammation. Slightly less optimal fat saturation is noted than on other images, which is a common occurrence.

Media file 9: Carpal tunnel syndrome. Axial fast spin-echo T2-weighted MRI with greater increase in signal and loss of definition within the nerve (arrow). Inflammatory change is noted within the carpal tunnel, adjacent to the flexor digitorum superficialis tendons. The appearance is consistent with pronounced inflammatory change within the carpal tunnel.

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Keywords

carpal tunnel syndrome, CTS, median nerve compression at the wrist, median neuropathy, nerve compression syndrome, carpal tunnel syndrome symptoms, carpal tunnel syndrome causes, compressive neuropathy, median nerve, peripheral compressive neuropathy, hand weakness, numbness in the hand, thenar atrophy, hand pain, wrist pain

Contributor Information and Disclosures

Author

Jeffrey G Norvell, MD, Clinical Assistant Professor of Emergency Medicine, University of Kansas School of Medicine
Jeffrey G Norvell, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Mark Steele, MD, Associate Dean for Truman Medical Center Programs, Professor, Department of Emergency Medicine, University of Missouri-Kansas City
Mark Steele, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eric L Legome, MD, Chair, Department of Emergency Medicine, St Vincent's Hospital Manhattan; 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.

CME Editor

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
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
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

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