eMedicine Specialties > Emergency Medicine > Neurology

Spinal Cord Infections

Andrew K Chang, MD, Associate Professor, Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center

Updated: Sep 14, 2009

Introduction

Background

Infections involving the spinal canal include epidural abscesses (infection in the epidural space), meningitis (infection of the meninges), subdural abscesses (infections of the subdural space), and intramedullary abscesses (infections within the spinal cord). Because the first 3 infections are discussed elsewhere in this journal (see Epidural and Subdural Infections, Meningitis), this article addresses only intramedullary abscesses.

Intramedullary spinal cord abscesses are extremely rare lesions. Since the original description in 1830 by Hart, approximately 100 cases have been reported. Their rarity, compared with brain abscesses, has been attributed to the relatively lower volume of the spinal cord and its particular blood supply.

Pathophysiology

Mechanisms of infection include (1) hematogenous spread from an extraspinal focus of infection, (2) contiguous spread from an adjacent focus of infection, (3) direct inoculation (ie, penetrating trauma, postneurosurgery), and (4) cryptogenic mechanisms (ie, no documented extraspinal focus of infection). In a 1998 review of 25 cases, hematogenous spread accounted for 8%, contiguous spread accounted for 24%, direct inoculation accounted for 4%, and 64% were cryptogenic.¹ In children, the abscesses are associated with prior anatomic spinal canal defects, such as dermal sinus tracts, which result from the incomplete partition of epithelial ectoderm and neuroectoderm in early fetal life.

Bacteria, such as staphylococci and streptococci, are the most common organisms responsible for these infections. Infections may also be caused by viral, fungal, or parasitic organisms. A diverse list of pathogens include, but are not limited to, cysticercosis, Mycobacterium tuberculosis, Listeria monocytogenes, Toxoplasma gondii, Nocardia asteroides, Histoplasma capsulatum, brucellosis, and the tapeworm spargana.

Initially, the area of the bacterial nidus is infiltrated with polymorphonuclear cells, leading to a suppurative myelitis. This evolves into central necrosis and liquefaction, which can spread along the long spinal tracts. Although the average extent of the process before 1975 was 6 vertebral levels, the average current length appears to be 3 levels. This change may be due to earlier detection and more effective antibiotics. At the periphery of this infectious process, fibroblasts proliferate and the central purulent area eventually becomes encapsulated by fibrous granulation tissue. The most commonly affected area is the dorsal thoracic spinal cord.

Frequency

International

Various reviews of the literature describe different numbers, with a range of approximately 80-100 cases since the first description in 1830. In a 2003 review, only 38 pediatric cases were identified in the medical literature since 1830.²

Mortality/Morbidity

Although the first reported cases had high mortality rates, prognosis has improved significantly with the advent of antibiotics.

• The mortality rate without surgical intervention is practically 100%, and those patients who died despite surgery almost exclusively were affected in the preantibiotic era.
• The current mortality rate (cases reported in the last 2 y) is 8-12%, although 70% of survivors had persistent neurologic deficits.
• In a review of 38 pediatric cases, 20% died, 60% had residual neurologic deficits, and only 20% recovered without sequelae.²

Race

Ethnic preference does not appear to exist, although some geographic differences are present. All intramedullary paracoccidioidomycosis cases were reported in Brazil.

Sex

In one study in which sex was reported, spinal cord infections were 2.5 times more common in males than in females.

Age

• All ages are affected though children younger than 5 years are more likely affected.
• Female patients are affected mainly in the first 4 decades of life, whereas the incidence among male patients is distributed more evenly, with a peak in the third decade of life (see Media file 1).

Graph showing age distribution of 91 patients with intramedullary spinal cord abscess. The age or gender of 14 patients is unknown.

Clinical

History

Menezes and VanGilder have classified patients by the duration of symptoms into acute, subacute, and chronic categories.³ In one study, the average time from the onset of symptoms to diagnosis was 46 days, with a range of 0-540 days.

• Patients in the acute category present with symptoms lasting less than 1 week.
  • Patients who present acutely have a clinical picture of transverse myelitis (with rapid onset of motor and sensory loss) and sphincter disturbances.
  • Pain is common, and fever with signs of concomitant infection typically is present.
• Patients in the subacute category present with symptoms that are 1-6 weeks old. The clinical picture resembles that of a chronic presentation.
• Those in the chronic category present with symptoms of greater than 6 weeks' duration.
  • Patients with chronic spinal cord abscesses present with signs and symptoms that are more consistent with an intramedullary tumor (ie, with a slowly progressive and stuttering neurologic deficit).
  • Patients may complain of a radicular-type pain and are frequently afebrile.
• Radiculopathic pain can present in the back, neck, extremities, or, occasionally, as abdominal or chest pain of undetermined origin. At least one reported case exists in which abdominal surgery was performed and later diagnosis proved intramedullary abscess of the spinal cord to be the origin of the problem.
• A review of 25 patients, published in 1998, revealed fever in 40%, back or radicular pain in 60%, and a triad of fever, pain, and neurologic deficits in 24%.¹

Physical

A thorough physical examination to determine the extent of the motor and sensory deficit and its levels is of primary importance to guide diagnostic modalities later. Examine the cervical, dorsal, and lumbar regions carefully looking for dermal sinuses, suggestive lesions, and signs of local infection.

First findings of intramedullary spinal cord abscess include fever (in acute forms), radiculopathic pain, and neurologic deficit.

• Root pain can present along a well-defined dermatome or, occasionally, as abdominal or chest pain of undetermined origin.
• Palpation of the spinous processes or straight-leg raising is unlikely to elicit pain on examination.
• Motor deficit usually progresses from slight paresis of one or more limbs to a flaccid paraplegia or tetraplegia with sensory loss below the level of the lesion and eventual sphincter disturbances (urinary retention or incontinence and/or loss of rectal tone).
• A review of 25 patients, published in 1998, revealed the following¹ :
  • Motor deficits only (24%)
  • Sensory deficits only (4%)
  • Motor and sensory deficits (68%)
  • Brainstem dysfunction (4%)
  • Urinary incontinence (56%)
  • Meningismus (12%)

Causes

• Presence of spinal dysraphism (congenital midline neuroectodermal defects) with persistent dermal sinus can lead to development of an intramedullary abscess by contiguity.
  • These abscesses usually are observed early in life. In a review of 25 patients, 36% had spinal dysraphisms.¹
  • Tethered cord syndrome can lend itself to iatrogenic spinal cord infection and damage via a lumbar puncture.
• The existence of chronic conditions (eg, alcoholism, diabetes, intravenous drug use) can predispose patients to the development of this rare pathology of intramedullary abscess.
• Immunosuppression (eg, AIDS) alters the bacteriology of spinal abscesses.
• Organisms also can cause spinal cord infections.

Differential Diagnoses

Epidural and Subdural Infections

Other Problems to Be Considered

Transverse myelitis
Intervertebral disk herniation
Intraspinal tumor
Spinal cord compression

Workup

Laboratory Studies

• A complete blood count (CBC) demonstrates leukocytosis only in the acute presentation (with or without neutrophilia).
• Cerebrospinal fluid (CSF) analysis demonstrates the following:
  • Marked pleomorphic leukocytosis, increased protein level, and decreased glucose and chloride level may be noted in the rare patients in whom the abscess has ruptured into the subarachnoid space.
  • Often, mild leukocytosis (mostly polymorphonucleocytes) and protein level increase are observed.
• Results from blood cultures occasionally are positive, showing the bacteriology of the underlying disease (eg, bacterial endocarditis, urosepsis).
• CSF cultures usually are sterile.

Imaging Studies

• Cervical, thoracic, or lumbar spine radiographs
  • Plain films are not helpful in diagnosing spinal cord abscesses and usually are normal.
  • If plain films show diskitis, osteomyelitis, or paraspinal infection, then one should suspect spread of contiguous infection into the spinal cord.
  • However, in patients in whom the abscess is associated with dysraphism, spina bifida can be demonstrated.
• Myelography with contrast
  • A positive myelogram reveals an expanded spinal cord or a complete block.
  • Until recently, myelography was the most reliable diagnostic tool; MRI largely has replaced it.
• Magnetic resonance imaging
  • To date, in the cases reported using MRI, the T1-weighted images exhibit decreased signal intensity. Peripheral enhancement, similar to that observed with abscesses of the brain, has been found with gadolinium.
  • MRI has become the preferred imaging technique, yielding not only the diagnosis but also the extent of the process.

Procedures

• Lumbar puncture
  • Do not attempt lumbar puncture if a dermal sinus is found in the lumbar area. Delay the procedure until a tethered cord syndrome has been excluded using computed tomography of the lumbar spinal canal.
  • Abdominal and jugular compression maneuvers with proper manometry may be indicated to establish the presence of a block to CSF flow. CSF manometer has been supplanted by neuroimaging, particularly MRI.
  • Jugular compression for manometric testing never should be performed if an intracranial mass is present.

Treatment

Prehospital Care

• Because the course of this condition is measured in days and not in hours (some patients take several months to present to medical care), patients' arrival by Emergency Medical Services (EMS) transport is unlikely.
• If presented with a patient who requires EMS transport, oxygen, analgesia, and a position of comfort are the only treatments needed in the prehospital arena.
• In patients in whom meningismus is involved, antiemetics and gentle handling are indicated.

Emergency Department Care

• Because this is such a rare entity, making the diagnosis in the ED is likely difficult. The emergency physician should consider the diagnosis when an infectious picture is present along with neurologic deficits originating at the spinal cord level.
• Treatment goals include making an accurate diagnosis and starting antibiotics as early as possible.⁴
• Determining the extent of the motor and sensory deficit and its levels is important to guide diagnostic modalities later. Examine the cervical, dorsal, and lumbar regions carefully looking for dermal sinuses, suggestive lesions, and signs of local infection.
• Plain radiography of the involved spinal levels occasionally can offer a clue when abnormal.
• A lumbar puncture always is considered in a patient with a septic picture with neurologic involvement; however, remember that besides cell count, protein, glucose, and bacteriologic studies, manometric maneuvers can establish the diagnosis of CSF block. Again, neuroimaging (especially MRI) of the spine has made CSF manometry largely obsolete for detecting spinal canal block. If a dermal sinus is found in the lumbar region, deferring the lumbar puncture until the absence of a tethered cord syndrome can be ascertained is prudent.
• Start antibiotics as soon as the bacteriologic workup samples have been obtained. Concomitant risk factors determine the most optimal antibiotic coverage for each individual patient.
• The use of steroids to treat spinal cord swelling should be made in consultation with neurosurgery.
• For additional information, see Spinal Cord Abscess and Spinal Cord Tumors - Management of Intradural Intramedullary Neoplasms.

Consultations

• The neurosurgeon should be involved early to guide the diagnostic flow toward surgery.
• An infectious disease consultant can offer invaluable help regarding the best antimicrobial combination.
• Consult a neuroradiologist to read the MRI with gadolinium study.

Medication

The goal of therapy is to eradicate infections. The empiric antimicrobial therapy should take into account the mechanism of infection, which helps predict the most likely infection organism or organisms.

For example, for contiguous spread through a sinus tract opening, one suggested regimen is vancomycin plus cefotaxime plus metronidazole.

For postneurosurgical complication, a suggested regimen consists of vancomycin plus ceftazidime with or without metronidazole.

For cryptogenic infection (ie, no identified primary source), a suggested regimen is ampicillin plus cefotaxime plus metronidazole. Ampicillin must be administered to cover L monocytogenes.

For hematogenous spread, the choice of antibiotics obviously depends on the primary source of infection. The optimal duration of antimicrobial therapy is not well defined. One review recommended a minimum of 4-6 weeks of parenteral therapy, with consideration of an additional 2-3 months of oral antimicrobial therapy.

Antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Vancomycin (Vancocin, Vancoled, Lyphocin)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci.

Dosing

Adult

500 mg to 2 g/d IV divided tid/qid for 7-10 d

Pediatric

40 mg/kg/d IV divided tid/qid for 7-10 d

Interactions

Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants

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

Precautions

Caution in renal failure and neutropenia; "red man" syndrome is caused by too-rapid IV infusion (dose given over a few min) but rarely happens when dose administered IV over 2-h administration or as PO or IP administration; "red man" syndrome is not an allergic reaction

Cefotaxime (Claforan)

Arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth. Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.

Dosing

Adult

Moderate-to-severe infections: 1-2 g IV/IM q6-8h
Life-threatening infections: 1-2 g IV/IM q4h

Pediatric

Infants and children: 50-180 mg/kg/d IV/IM divided q4-6h
>12 years: Administer as in adults

Interactions

Probenecid may increase cefotaxime levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; has been associated with severe colitis

Metronidazole (Flagyl IV, Metro IV)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for Clostridium difficile enterocolitis).

Dosing

Adult

Loading dose: 15 mg/kg or 1 g for 70-kg adult IV over 1 h
Maintenance dose: 6 h following loading dose; infuse 7.5 mg/kg or 500 mg IV over 1 h for 70-kg adult q6-8h; not to exceed 4 g/d

Pediatric

Administer as in adults using body weight

Interactions

May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity of metronidazole; disulfiramlike reaction may occur with orally ingested ethanol

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy

Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.

Dosing

Adult

250-500 mg to 2 g IV/IM q8-12h

Pediatric

Neonates: 30 mg/kg IV q12h
Infants and children: 30-50 mg/kg/dose IV q8h; not to exceed 6 g/d
Adolescents: Administer as in adults

Interactions

Nephrotoxicity may increase with aminoglycosides, furosemide, and ethacrynic acid; probenecid may increase ceftazidime levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy

Ampicillin (Marcillin, Omnipen, Principen, Polycillin-N)

Bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.

Dosing

Adult

250-500 mg PO q6h
500 mg to 3 g IV q4-6h; not to exceed 12 g/d
500 mg to 1.5 g IM q4-6h

Pediatric

50-100 mg/kg/d PO divided q4-6h
100-400 mg/kg/d IV/IM divided q4-6h

Interactions

Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction

Follow-up

Further Inpatient Care

• Laminectomy is the treatment of choice once the provisional diagnosis is made.
  • Then, opening of the dura, needle aspiration of the abscess (with pus bacteriology), midline myelotomy with drainage of the cavity, abundant irrigation, and closure by layers are performed.
  • The dura mater preferably is closed with a graft, if needed, once decompression has been accomplished.
  • Although marsupialization has been tried occasionally, it generally is not recommended.
• In children, all cases of abscesses with concomitant isolated dermal sinus presented when the child was older than 6 months of age, which suggests that complete resection of the dermal sinus before 6 months of age may prevent the formation of intramedullary spinal cord abscess and its significant morbidity and mortality.

Complications

• Sepsis
• Neurologic sequelae (70%)
• Death

Prognosis

• Prognosis of spinal cord infection was grim in the preantibiotic era. Currently, with prompt diagnosis, early surgery, and correct antibiotic therapy, the chances for full or almost full recovery often are very good.
• Early surgery is the key to recovery for patients in the acute category.
• Prognosis generally is better for patients in the chronic and subacute categories.

Miscellaneous

Special Concerns

• In children, intramedullary abscess of the spinal cord is predominantly secondary to direct contiguous spread of infection from the skin.
• In children, unlike adults, the abscesses are associated with prior anatomic spinal canal defects.
  • Fifty-three percent of all children and 63% of children younger than age 5 years have prior anatomic spinal canal defects of which more than two thirds have been identified before the development of neurologic deficits.
  • Spinal dermal sinuses, seen in association with the abscesses, result from defective separation of the epithelium ectoderm from the neural ectoderm and subsequent communication between the skin and deeper structures. They can terminate in soft tissue or in the epidural space, or they can form a connection with the dura and the spinal cord, leading to abscesses that arise at any point along the sinus tract.

Multimedia

Media file 1: Graph showing age distribution of 91 patients with intramedullary spinal cord abscess. The age or gender of 14 patients is unknown.

References

1. Chan CT, Gold WL. Intramedullary abscess of the spinal cord in the antibiotic era: clinical features, microbial etiologies, trends in pathogenesis, and outcomes. Clin Infect Dis. Sep 1998;27(3):619-26. [Medline].

2. Simon JK, Lazareff JA, Diament MJ, Kennedy WA. Intramedullary abscess of the spinal cord in children: a case report and review of the literature. Pediatr Infect Dis J. Feb 2003;22(2):186-92. [Medline].

3. Menezes AH, VanGilder JC. Spinal cord abscess. In: Wilkins RH, Rengachary SS. Neurosurgery. New York: McGraw-Hill; 1985:1969.

4. Al Barbarawi M, Khriesat W, Qudsieh S, Qudsieh H, Loai AA. Management of intramedullary spinal cord abscess: experience with four cases, pathophysiology and outcomes. Eur Spine J. May 2009;18(5):710-7. [Medline].

5. Bartels RH, Gonera EG, van der Spek JA, Thijssen HO, Mullaart RA, Gabreels FJ. Intramedullary spinal cord abscess. A case report. Spine. May 15 1995;20(10):1199-204. [Medline].

6. Benzil DL, Epstein MH, Knuckey NW. Intramedullary epidermoid associated with an intramedullary spinal abscess secondary to a dermal sinus. Neurosurgery. Jan 1992;30(1):118-21. [Medline].

7. Byrne RW, von Roenn KA, Whisler WW. Intramedullary abscess: a report of two cases and a review of the literature. Neurosurgery. Aug 1994;35(2):321-6; discussion 326. [Medline].

8. Cokca F, Meco O, Arasil E, Unlu A. An intramedullary dermoid cyst abscess due to Brucella abortus biotype 3 at T11-L2 spinal levels. Infection. Sep-Oct 1994;22(5):359-60. [Medline].

9. Darouiche RO. Spinal epidural abscess. N Engl J Med. Nov 9 2006;355(19):2012-20. [Medline].

10. David C, Brasme L, Peruzzi P, Bertault R, Vinsonneau M, Ingrand D. Intramedullary abscess of the spinal cord in a patient with a right-to-left shunt: case report. Clin Infect Dis. Jan 1997;24(1):89-90. [Medline].

11. Desai KI, Muzumdar DP, Goel A. Holocord intramedullary abscess: an unusual case with review of literature. Spinal Cord. Dec 1999;37(12):866-70. [Medline].

12. Dev R, Husain M, Gupta A, Gupta RK. MR of multiple intraspinal abscesses associated with congenital dermal sinus. AJNR Am J Neuroradiol. Apr 1997;18(4):742-3. [Medline].

13. DiTullio MV Jr. Intramedullary spinal abscess: a case report with a review of 53 previously described cases. Surg Neurol. Jun 1977;7(6):351-4. [Medline].

14. Hanci M, Sarioglu AC, Uzan M, Islak C, Kaynar MY, Oz B. Intramedullary tuberculous abscess: a case report. Spine. Mar 15 1996;21(6):766-9. [Medline].

15. Hardwidge C, Palsingh J, Williams B. Pyomyelia: an intramedullary spinal abscess complicating lumbar lipoma with spina bifida. Br J Neurosurg. 1993;7(4):419-22. [Medline].

16. Hart J. Case of encysted abscess in the centre of the spinal cord. Dublin Hosp Rep. 1830;5:522-524.

17. Hoil-Parra JA, Lazareff JA. [Lumbar dermal sinus as a cause of intramedullary and subdural abscess. Report of 2 cases]. Bol Med Hosp Infant Mex. May 1993;50(5):341-6. [Medline].

18. Hott JS, Horn E, Sonntag VK, Coons SW, Shetter A. Intramedullary histoplasmosis spinal cord abscess in a nonendemic region: case report and review of the literature. J Spinal Disord Tech. Apr 2003;16(2):212-5. [Medline].

19. Lahdou JB, Gilliard C, de Coene BD, Vandercam B, Deltombe T, Hanson P. [Streptococcus milleri subacute spinal cord abscess. Apropos of a case]. Neurochirurgie. 1996;42(2):100-4. [Medline].

20. Lindner A, Becker G, Warmuth-Metz M, Schalke BC, Bogdahn U, Toyka KV. Magnetic resonance image findings of spinal intramedullary abscess caused by Candida albicans: case report. Neurosurgery. Feb 1995;36(2):411-2. [Medline].

21. Manfredi M, Bozzao L, Frasconi F. Chronic intramedullary abscess of the spinal cord. Case report. J Neurosurg. Sep 1970;33(3):352-5. [Medline].

22. Martin RJ, Yuan HA. Neurosurgical care of spinal epidural, subdural, and intramedullary abscesses and arachnoiditis. Orthop Clin North Am. Jan 1996;27(1):125-36. [Medline].

23. Miranda Carus ME, Anciones B, Castro A, Lara M, Isla A. Intramedullary spinal cord abscess. J Neurol Neurosurg Psychiatry. Mar 1992;55(3):225-6. [Medline].

24. Rogg JM, Benzil DL, Haas RL, Knuckey NW. Intramedullary abscess, an unusual manifestation of a dermal sinus. AJNR Am J Neuroradiol. Nov-Dec 1993;14(6):1393-5. [Medline].

25. Tacconi L, Arulampalam T, Johnston FG, Thomas DG. Intramedullary spinal cord abscess: case report. Neurosurgery. Oct 1995;37(4):817-9. [Medline].

26. Vajramani GV, Nagmoti MB, Patil CS. Neurobrucellosis presenting as an intra-medullary spinal cord abscess. Ann Clin Microbiol Antimicrob. 2005;4:14. [Medline].

27. Weng TI, Shih FY, Chen WJ, Lin FY. Intramedullary abscess of the spinal cord. Am J Emerg Med. Mar 2001;19(2):177-8. [Medline].

Keywords

spinal cord injury, SCI, anterior cord syndrome, Brown-Séquard syndrome, central cord syndrome, conus medullaris syndrome, cauda equina syndrome, incomplete SCI syndromes, spinal cord concussion, spinal cord injury syndromes, SCIWORA, spinal cord injury without radiologic abnormality

injuries of the spinal cord, neurogenic shock, spinal shock, spinal fractures, spinal dislocations, spinal epiduralhematomas, spinal epidural abscesses, spinal cord compression, complete cord syndromes, incomplete cord syndromes, hemorrhagic shock

Contributor Information and Disclosures

Author

Andrew K Chang, MD, Associate Professor, Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center
Andrew K Chang, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Professor, Department of Emergency Medicine, University of Texas-Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center, San Antonio, Texas
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Talecris Biotherapeutics Honoraria Speaking and teaching

Pharmacy Editor

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

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, 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, 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
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