Updated: Aug 22, 2008
Scaphoid fracture is the most common type of bone fracture in the carpus (ie, wrist). Frequently, however, the diagnosis of this scaphoid injury is delayed; a delay in the diagnosis and treatment of a scaphoid fracture may alter the prognosis for union, increase the risk of avascular necrosis, and dramatically increase the long-term likelihood of arthritis.
Related eMedicine topics:
Avascular Necrosis
Fracture, Wrist
Hand, Fractures and Dislocations: Wrist
Scapholunate Advanced Collapse
Wrist, Scaphoid Fractures and Complications
Related Medscape topic:
Resource Center Fracture
Anatomic considerations
The carpus contains 8 small bones, which are arranged in 2 rows, proximal and distal. The proximal bones, from the radial to the medial side, are the scaphoid, lunate, triquetrum, and pisiform. Only the scaphoid and lunate articulate with the radius; thus, these 2 bones transmit the entire force of a fall on the hand to the forearm. The distal bones are, starting from the radial side, the trapezium, trapezoid, capitate, and hamate.
Blood supply
Anatomically, the scaphoid may be divided into proximal, middle (termed the waist), and distal thirds. Most of the blood supply to the scaphoid enters distally. The proximal part of the scaphoid has no blood vessels entering it, depending instead on vessels that pierce the midportion. Fractures of the proximal third of the scaphoid account for 20% of scaphoid fractures, those of the middle portion account for 60%, and fractures of the distal part make up the remaining 20%. Diminished blood flow to the proximal pole is noted in about one third of fractures at the waist level. This reduced blood supply may result in avascular necrosis of the proximal pole of the scaphoid. Almost 100% of proximal pole fractures result in aseptic necrosis. Displaced scaphoid fractures have a nonunion rate of 55-90%.
Fall onto outstretched hand
The usual mechanism of injury is a fall onto the outstretched hand (FOOSH) that results in forceful dorsiflexion and impaction of the scaphoid against the dorsal rim of the radius. This mechanism explains why snuffbox tenderness is so common, even in the absence of a scaphoid fracture. Conventional medical wisdom dictates that snuffbox tenderness should be equated with a scaphoid fracture unless radiographs prove otherwise. If initial radiographs do not show fracture, follow-up radiographs should be obtained in 7-14 days, because the fracture line may be more visible after some resorption.
Scaphoid fracture has been reported in people aged 10-70 years, although it is most common in young adult men following a fall, athletic injury, or motor vehicle accident.
The scaphoid has no ligamentous or tendinous attachments, but joint compressive forces, trapezial-scaphoid shear stress, and capitolunate rotation moments exert control on the scaphoid. Therefore, scaphoid fractures have a high incidence of nonunion (8-10%), frequent malunion, and late sequelae of carpal instability and posttraumatic arthritis.
No known correlation exists between race and scaphoid fracture.
Scaphoid injuries are more common in men than in women.
Scaphoid fracture is uncommon in children because the physis of the distal radius usually fails first, resulting in Salter type I or II fractures of the distal radius. Similarly, in elderly patients, the distal radial metaphysis usually fails before the scaphoid can fracture.
Scaphoid fracture can occur through 2 different mechanisms: a compression injury or a hyperextension (ie, bending) injury.
The patient with a scaphoid fracture often presents complaining of wrist pain and may be diagnosed as having a sprain of the wrist. In sports-related injuries, it is not uncommon for a fractured scaphoid to go unnoticed. Pain and tenderness are often on the radial side of the wrist. Pain often is exacerbated with wrist motion. The importance of increasing the number of clinical tests for this injury is vital; one study found that emergency department residents had difficulty naming diagnostic maneuvers beyond "snuffbox tenderness."
Special provocation maneuvers
Scaphoid fractures usually are an injury of young men and women, occurring after a fall, athletic injury, or motor vehicle accident.
De Quervain Tenosynovitis
Osteoarthritis
Radius, Distal Fractures
Tendonitis
Tenosynovitis
Wrist Dislocation
Fracture of the forearm
Fracture of the hand
Scapholunate dissociation
Rehabilitation considerations immediately following injury to 1 week
Rehabilitation considerations in 2 weeks
Rehabilitation considerations in 4-6 weeks
Rehabilitation considerations in 8-12 weeks
The patient usually needs retraining in the performance of activities of daily living (ADL). The occupational therapist provides the patient with compensatory strategies to use when completing ADL tasks. Either physical or occupational therapy is necessary for regaining strength and ROM of the affected wrist and hand. The guidelines for rehabilitation are discussed above in the Physical Therapy section.
Immediate consultation with a hand specialist or an orthopedic surgeon should be obtained for an open or unstable scaphoid fracture or for a scaphoid fracture that requires fixation.
Please see the Physical Therapy section.
Related eMedicine topic:
Splinting, Thumb Spica
Drugs used for pain management include analgesics. The agents used for mild to moderate pain, such as aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs (NSAIDs), are nonopioids. These agents usually suffice; if they do not, however, the clinician can prescribe opiate agonists, such as codeine or propoxyphene.
Related Medscape topics:
CME/CE Acute Pain Management: Overcoming Barriers and Enhancing Treatment
Resource Center Pharmacologic Management of Pain
Effective management of pain is essential to quality patient care. Pain management improves the patient's quality of life, as well as his/her ability to work productively and to participate in self-care and physical therapy activities.
Effective in relieving mild to moderate acute pain; however, acetaminophen has no peripheral anti-inflammatory effects. It may be preferred in elderly patients because of fewer GI and renal side effects.
325-650 mg PO q4-6h prn; alternatively, 1000 mg PO tid/qid; not to exceed 4 g/d; daily dose not to exceed 6 extended-release tab
10-15 mg/kg PO or PR q4-6h; not to exceed 5 doses in 24 h
Extended-release dose not established for this population
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; known G-6-P deficiency; alcoholic hepatic disease, viral hepatitis, alcoholism
A - Fetal risk not revealed in controlled studies in humans
Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose
Synthetic analog of codeine; however, tramadol has a lower affinity for opioid receptors than does codeine. It has less potential for abuse or respiratory depression than do other opiate agonists, but both may occur. Tramadol is equivalent in analgesic relief to codeine, but it is less potent than are acetaminophen-codeine and acetaminophen-hydrocodone combinations. A lack of significant cardiac effects and no association with peptic ulcer disease make tramadol an alternative in patients who may not tolerate NSAIDs.
50-100 mg PO q4-6h; not to exceed 400 mg/d
Not established
Can cause additive CNS depression when used with other CNS depressants like ethanol, opiate agonists, phenothiazines, benzodiazepines, barbiturates, other tranquilizers or sedative hypnotics; concomitant use with opiate agonists may increase risk of seizures; international recommendations contraindicate the concurrent use with MAOIs or use of tramadol within 14 d of discontinuing MAOI therapy; increases INRs in patients previously stabilized on warfarin
Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 d; use of SSRIs, TCAs, opioids, acute alcohol intoxication
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Can cause dizziness, nausea, constipation, sweating, pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, hypoadrenalism; pregnancy, breastfeeding; seizure; development of tolerance or dependency with extended use
Used to treat moderate to severe pain. The combination produces additive analgesia compared with the same doses of either agent alone; however, dosage escalation of this combination is limited by the side effects of propoxyphene and by the toxicity and ceiling effect of acetaminophen.
1 tab PO q4-6h prn; not to exceed propoxyphene 600 mg/d and acetaminophen 4000 mg/d (6 tab)
Not established
May increase serum concentrations of MAOIs, tricyclic antidepressants, carbamazepine, phenobarbital, and warfarin
Documented hypersensitivity; history of substance abuse, alcoholism, or suicidal ideation; alcohol and other CNS depressants may increase toxic effects
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients dependent on opiates, substitution may result in acute opiate withdrawal symptoms; caution in severe renal or hepatic dysfunction
Used to treat moderate to severe pain. Tylenol #3 produces additive analgesia compared with the same doses of either agent alone. Dosage escalation of this combination is limited by the ceiling effect of acetaminophen.
30-60 mg based on codeine content PO q4-6h or 1-2 tab q4h; not to exceed 12 tab/d
1-1.5 mg/kg/d codeine PO q4-6h prn; not to exceed 75 mg/kg/d of acetaminophen
Toxicity increased when administered with other CNS depressants or tricyclics; antacids or food can delay and decrease the oral absorption; concurrent use of antidiarrheals and opiate agonists can lead to severe constipation and possibly additive CNS depression; antihypertensive agents can produce an exaggerated response; concomitant use with other CNS depressants can potentiate respiratory depression effects of both
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients with COPD or decreased pulmonary reserve; renal and hepatic dysfunction; abrupt discontinuation can result in withdrawal symptoms; patients with asthma who also have salicylate hypersensitivity
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.
Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek the lowest dose of celecoxib for each patient.
200 mg PO qd or 100 mg PO bid
Not established
Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity or hypersensitivity to sulfonamides or salicylates; severe hepatic impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; severe heart failure and hyponatremia, because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction, or in abnormal liver lab results
Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit COX activity and prostaglandin synthesis. Other mechanisms may exist as well, such as the inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.
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 the therapeutic effects. Administer high doses with caution and closely observe the patient for a response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
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
Documented hypersensitivity
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
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain; naproxen inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease in prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
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
Documented hypersensitivity, peptic ulcer disease, recent GI bleeding or perforation, and renal insufficiency
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
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
Oral NSAID with analgesic and antipyretic properties. Ibuprofen is useful for the alleviation of mild to moderate pain.
400-800 mg PO tid/qid; not to exceed 3200 mg/d; use lowest effective dose
30-40 mg/kg PO tid/qid in divided doses; not to exceed 50 mg/kg/d
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
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
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
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
A retrospective study of 22 pediatric scaphoid fractures (17 managed conservatively and 5 managed with screw fixation) revealed that 94% of patients had “good or excellent” results, with 1 reported malunion.15
Cheung GC, Lever CJ, Morris AD. X-ray diagnosis of acute scaphoid fractures. J Hand Surg [Br]. Feb 2006;31(1):104-9. [Medline].
Toth F, Sebestyen A, Balint L, et al. Positioning of the wrist for scaphoid radiography. Eur J Radiol. Oct 2007;64(1):126-32. [Medline].
Beeres FJ, Hogervorst M, Rhemrev SJ, et al. A prospective comparison for suspected scaphoid fractures: bone scintigraphy versus clinical outcome. Injury. Jul 2007;38(7):769-74. [Medline].
Beeres FJ, Hogervorst M, den Hollander P, et al. Outcome of routine bone scintigraphy in suspected scaphoid fractures. Injury. Oct 2005;36(10):1233-6. [Medline].
Beeres FJ, Hogervorst M, Rhemrev SJ, et al. Reliability of bone scintigraphy for suspected scaphoid fractures. Clin Nucl Med. Nov 2007;32(11):835-8. [Medline].
Karantanas A, Dailiana Z, Malizos K. The role of MR imaging in scaphoid disorders. Eur Radiol. Nov 2007;17(11):2860-71. [Medline].
Jenkins PJ, Slade K, Huntley JS, et al. A comparative analysis of the accuracy, diagnostic uncertainty and cost of imaging modalities in suspected scaphoid fractures. Injury. Jul 2008;39(7):768-74. [Medline].
Brooks S, Cicuttini FM, Lim S, et al. Cost effectiveness of adding magnetic resonance imaging to the usual management of suspected scaphoid fractures. Br J Sports Med. Feb 2005;39(2):75-9. [Medline]. [Full Text].
Moller JM, Larsen L, Bovin J, et al. MRI diagnosis of fracture of the scaphoid bone: impact of a new practice where the images are read by radiographers. Acad Radiol. Jul 2004;11(7):724-8. [Medline].
Finkenberg JG, Hoffer E, Kelly C, et al. Diagnosis of occult scaphoid fractures by intrasound vibration. J Hand Surg [Am]. Jan 1993;18(1):4-7. [Medline].
Brotzman SB, Wilk KE, eds. Handbook of Orthopaedic Rehabilitation. 2nd ed. Philadelphia, Pa: Elsevier; 2007.
Dinah AF, Vickers RH. Smoking increases failure rate of operation for established non-union of the scaphoid bone. Int Orthop. Aug 2007;31(4):503-5. [Medline]. [Full Text].
Dias JJ, Dhukaram V, Abhinav A, et al. Clinical and radiological outcome of cast immobilisation versus surgical treatment of acute scaphoid fractures at a mean follow-up of 93 months. J Bone Joint Surg Br. Jul 2008;90(7):899-905. [Medline].
Munk B, Larsen CF. Bone grafting the scaphoid nonunion: a systematic review of 147 publications including 5,246 cases of scaphoid nonunion. Acta Orthop Scand. Oct 2004;75(5):618-29. [Medline]. [Full Text].
Huckstadt T, Klitscher D, Weltzien A, et al. Pediatric fractures of the carpal scaphoid: a retrospective clinical and radiological study. J Pediatr Orthop. Jun 2007;27(4):447-50. [Medline].
Katzung BG, ed. Basic and Clinical Pharmacology. 9th ed. New York, NY: Lange Medical Books/McGraw Hill; 1995.
Breederveld RS, Tuinebreijer WE. Investigation of computed tomographic scan concurrent criterion validity in doubtful scaphoid fracture of the wrist. J Trauma. Oct 2004;57(4):851-4. [Medline].
Canale ST, ed. Campbell's Operative Orthopaedics. 10th ed. St Louis, Mo: Mosby; 2003.
Cuenod P, Charriere E, Papaloizos MY. A mechanical comparison of bone-ligament-bone autografts from the wrist for replacement of the scapholunate ligament. J Hand Surg [Am]. Nov 2002;27(6):985-90. [Medline].
[Best Evidence] Dias JJ, Wildin CJ, Bhowal B, et al. Should acute scaphoid fractures be fixed? A randomized controlled trial. J Bone Joint Surg Am. Oct 2005;87(10):2160-8. [Medline].
Hoppenfeld S, Murthy VL. Treatments and Rehabilitation of Fractures. Philadelphia, Pa: Lippincott Williams & Wilkins; 2000.
Hunter JM, Mackin EJ, Callahan AD. Rehabilitation of the Hand: Surgery and Therapy. 4th ed. St Louis, Mo: Mosby; 1995.
Kumar S, O'Connor A, Despois M, et al. Use of early magnetic resonance imaging in the diagnosis of occult scaphoid fractures: the CAST Study (Canberra Area Scaphoid Trial). N Z Med J. Feb 11 2005;118(1209):U1296. [Medline].
Magee DJ. Orthopedic Physical Assessment. 4th ed. Philadelphia, Pa: Saunders; 2002.
Oka K, Murase T, Moritomo H, et al. Patterns of bone defect in scaphoid nonunion: a 3-dimensional and quantitative analysis. J Hand Surg [Am]. Mar 2005;30(2):359-65. [Medline].
Pao VS, Chang J. Scaphoid nonunion: diagnosis and treatment. Plast Reconstr Surg. Nov 2003;112(6):1666-76; quiz 1677; discussion 1678-9. [Medline].
Bucholz RW, Heckman JD, Court-Brown CM. Rockwood and Green's Fractures in Adults. 6th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2006.
Senall JA, Failla JM, Bouffard JA, et al. Ultrasound for the early diagnosis of clinically suspected scaphoid fracture. J Hand Surg [Am]. May 2004;29(3):400-5. [Medline].
Richmond JC, Shahady EJ, eds. Sports Medicine for Primary Care. Cambridge, Mass: Blackwell Science; 1996.
Temple CL, Ross DC, Bennett JD, et al. Comparison of sagittal computed tomography and plain film radiography in a scaphoid fracture model. J Hand Surg [Am]. May 2005;30(3):534-42. [Medline].
scaphoid injury, scaphoid, scaphoid fracture, scaphoid fractures, broken wrist, wrist fracture, scaphoid bone, wrist surgery, scaphoid waist fracture, avascular necrosis, aseptic necrosis, os scaphoideum, scaphoideum, scaphoid necrosis, os naviculare manus, navicular, navicular bone of hand, navicular bone injury
Scott R Laker, MD, Staff Physician, Department of Rehabilitation, University of Colorado Health Sciences Center
Scott R Laker, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Deborah Saint-Phard, MD, Associate Professor, Department of Physical Medicine and Rehabilitation, Department of Orthopedic Surgery, Director, Active Women's Health at CU Sports Medicine Program, University of Colorado Denver
Deborah Saint-Phard, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Colorado Medical Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Maria Carmen E Espiritu, MD, PT, Consulting Staff, Espiritu Clinic, Clinch Valley Medical Center
Maria Carmen E Espiritu, MD, PT is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Medical Association
Disclosure: Nothing to disclose.
Robert Irwin, MD, Consulting Staff, Florida Orthopaedic Institute
Robert Irwin, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American College of Physicians, Association of Academic Physiatrists, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
J Michael Wieting, DO, MEd, Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Principles and Practices, Director of Sports Medicine, Associate Director of Physician Assistant Training Program, Department of Osteopathic Principles and Practice, Lincoln Memorial University-DeBusk College of Osteopathic Medicine
J Michael Wieting, DO, MEd is a member of the following medical societies: American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Sports Medicine, American College of Sports Medicine, American Osteopathic Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Osteopathic College of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, Association of Academic Physiatrists, and International Society of Physical and Rehabilitation Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service, University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM 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.
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center
Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association
Disclosure: Nothing to disclose.
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