eMedicine Specialties > Infectious Diseases > Bone and Joint Infections

Pott Disease (Tuberculous Spondylitis): Treatment & Medication

Author: Jose A Hidalgo, MD, Assistant Professor, Universidad de San Marcos Medical School; Attending Physician, Department of Internal Medicine, Division of Infectious Diseases, Guillermo Almenara Hospital
Coauthor(s): George Alangaden, MD, Staff Physician, Associate Professor, Department of Internal Medicine, Division of Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine
Contributor Information and Disclosures

Updated: Aug 29, 2008

Treatment

Medical Care

  • Before the advent of effective antituberculosis chemotherapy, Pott disease was treated with immobilization using prolonged bed rest or a body cast. At the time, Pott disease carried a mortality rate of 20%, and relapse was common (30%).
  • The duration of treatment, surgical indications, and inpatient care have since evolved.
  • Studies performed by the British Medical Research Council indicate that tuberculous spondylitis of the thoracolumbar spine should be treated with combination chemotherapy for 6-9 months.4
  • According to the most recent recommendations issued in 2003 by the US Centers for Disease Control and Prevention, the Infectious Diseases Society of America, and the American Thoracic Society, a 4-drug regimen should be used empirically to treat Pott disease.1  
  • Isoniazid and rifampin should be administered during the whole course of therapy. Additional drugs are administered during the first 2 months of therapy. These are generally chosen among the first-line drugs, which include pyrazinamide, ethambutol, and streptomycin. The use of second-line drugs is indicated in cases of drug resistance.
  • Regarding the duration of therapy, the British Medical Research Council studies did not include patients with multiple vertebral involvement, cervical lesions, or major neurologic involvement. Because of these limitations, many experts still recommend chemotherapy for 9-12 months.
  • Opinions differ regarding whether the treatment of choice should be conservative chemotherapy or a combination of chemotherapy and surgery. The treatment decision should be individualized for each patient. Routine surgery does not to seem to be indicated. Most common indications for surgical procedures are discussed below.

Surgical Care

  • Indications for surgical treatment of Pott disease generally include the following:22,23
    • Neurologic deficit (acute neurologic deterioration, paraparesis, paraplegia)
    • Spinal deformity with instability or pain
    • No response to medical therapy (continuing progression of kyphosis or instability)
    • Large paraspinal abscess
    • Nondiagnostic percutaneous needle biopsy sample
  • Resources and experience are key factors in the decision to use a surgical approach.
  • The lesion site, extent of vertebral destruction, and presence of cord compression or spinal deformity determine the specific operative approach (kyphosis, paraplegia, tuberculous abscess).
  • Vertebral damage is considered significant if more than 50% of the vertebral body is collapsed or destroyed or a spinal deformity of more than 5° exists.
  • The most conventional approaches include anterior radical focal debridement and posterior stabilization with instrumentation.24,10
  • In Pott disease that involves the cervical spine, the following factors justify early surgical intervention:
    • High frequency and severity of neurologic deficits
    • Severe abscess compression that may induce dysphagia or asphyxia
    • Instability of the cervical spine
  • Contraindications: Vertebral collapse of a lesser magnitude is not considered an indication for surgery because, with appropriate treatment and therapy compliance, it is less likely to progress to a severe deformity.

Consultations

  • Orthopedic surgeons
  • Neurosurgeons
  • Rehabilitation teams

Activity

  • Despite questionable efficacy, prolonged recumbence and the use of frames, plaster beds, plaster jackets, and braces are still used.
  • Cast or brace immobilization was a traditional form of treatment but has generally been discarded. Patients with Pott disease should be treated with external bracing.

Medication

  • A 4-drug regimen should be used empirically to treat Pott disease. Treatment can be adjusted when susceptibility information becomes available. 
  • Isoniazid and rifampin should be administered during the whole course of therapy. Additional drugs are administered during the first 2 months of therapy. These are generally chosen among the first-line drugs, which include pyrazinamide, ethambutol, and streptomycin.
  • A 3-drug regimen usually includes isoniazid, rifampin, and pyrazinamide.
  • The use of second-line drugs is indicated in cases of drug resistance.
  • The duration of treatment is somewhat controversial. Although some studies favor a 6- to 9-month course, traditional courses range from 9 months to longer than 1 year. The duration of therapy should be individualized and based on the resolution of active symptoms and the clinical stability of the patient.

Antituberculous drugs

These agents inhibit growth and proliferation of causative organism.


Isoniazid (Laniazid, Nydrazid)

Highly active against Mycobacterium tuberculosis. Has good GI absorption and penetrates well into all body fluids and cavities.

Adult

300 mg PO qd; alternatively, 15 mg/kg IV qd

Pediatric

10 mg/kg PO qd

Higher incidence of isoniazid-related hepatitis can occur with daily alcohol ingestion; aluminum salts may decrease isoniazid serum levels (administer 1-2 h before taking aluminum salts); may increase anticoagulants effects with coadministration; may inhibit metabolic clearance of benzodiazepines; carbamazepine toxicity or isoniazid hepatotoxicity may result from concurrent use (monitor carbamazepine concentrations and liver function); coadministration with cycloserine may increase adverse CNS effects (eg, dizziness); acute behavioral and coordination changes may occur with coadministration of disulfiram; coadministration with rifampin after halothane anesthesia may result in hepatotoxicity and hepatic encephalopathy; may inhibit hepatic microsomal enzymes and increase toxicity of hydantoin

Documented hypersensitivity; previous isoniazid-associated hepatic injury or other severe adverse reactions

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

Monitor patients with active chronic liver disease or severe renal dysfunction; periodic ophthalmologic examinations during INH therapy are recommended even when visual symptoms do not occur


Rifampin (Rifadin, Rimactane)

For use in combination with at least one other antituberculous drug; inhibits DNA-dependent bacterial but not mammalian RNA polymerase. Cross-resistance may occur.

Adult

10 mg/kg PO qd; not to exceed 600 mg/d

Pediatric

10-20 mg/kg PO qd; not to exceed 600 mg/d

Induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with INH may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFTs occur)

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

Obtain CBC counts and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with reversible thrombocytopenia if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur


Pyrazinamide

Bactericidal against M tuberculosis in an acid environment (macrophages). Has good absorption from the GI tract and penetrates well into most tissues, including CSF.

Adult

15-30 mg/kg PO qd

Pediatric

Not established

Documented hypersensitivity; severe hepatic damage, acute gout

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

Use only in combination with other effective antituberculous agents; inhibits renal excretion of urates; may result in hyperuricemia (usually asymptomatic); perform baseline serum uric acid determinations; discontinue drug if signs of hyperuricemia with acute gouty arthritis; perform baseline LFTs (closely monitor in liver disease); discontinue pyrazinamide if signs of hepatocellular damage appear; caution in history of diabetes mellitus


Ethambutol (Myambutol)

Has bacteriostatic activity against M tuberculosis. Has good GI absorption. CSF concentrations remain low, even in the presence of meningeal inflammation.

Adult

15-25 mg/kg PO qd

Pediatric

15-25 mg/kg PO qd
Not recommended for young children because of difficulty monitoring vision

Aluminum salts may delay and reduce absorption (administer several hours before or after ethambutol dose)

Documented hypersensitivity; optic neuritis (unless clinically indicated)

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

Reduce dose in impaired renal function; may have reversible visual adverse effects if promptly discontinued


Streptomycin

Bactericidal in an alkaline environment. Because it is not absorbed from the GI tract, must be administered parenterally. Exerts action mainly on extracellular tubercle bacilli. Only about 10% of the drug penetrates cells that harbor organisms. Enters the CSF only in the presence of meningeal inflammation. Excretion is almost entirely renal.

Adult

15 mg/kg IM qd; not to exceed 1 g/d

Pediatric

20-40 mg/kg IM qd; not to exceed 1 g/d

Nephrotoxicity may be increased with aminoglycosides, cephalosporins, penicillins, amphotericin B, and loop diuretics

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Pregnancy

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

Precautions

Narrow therapeutic index; not intended for long-term therapy; caution in renal failure not on dialysis; caution with myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission

More on Pott Disease (Tuberculous Spondylitis)

Overview: Pott Disease (Tuberculous Spondylitis)
Differential Diagnoses & Workup: Pott Disease (Tuberculous Spondylitis)
Treatment & Medication: Pott Disease (Tuberculous Spondylitis)
Follow-up: Pott Disease (Tuberculous Spondylitis)
Multimedia: Pott Disease (Tuberculous Spondylitis)
References

References

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Further Reading

Keywords

Pott’s disease, Pott disease, tuberculous spondylitis, spinal tuberculosis, spinal TB, TB, disk disease, vertebral collapse, kyphosis, kyphotic deformity, musculoskeletal tuberculosis, cold abscess, bone tuberculosis, soft-tissue tuberculosis, tuberculosis of the spine, osteomyelitis, arthritis, spinal deformity

Contributor Information and Disclosures

Author

Jose A Hidalgo, MD, Assistant Professor, Universidad de San Marcos Medical School; Attending Physician, Department of Internal Medicine, Division of Infectious Diseases, Guillermo Almenara Hospital
Jose A Hidalgo, MD is a member of the following medical societies: HIV Medicine Association of America and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

George Alangaden, MD, Staff Physician, Associate Professor, Department of Internal Medicine, Division of Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine
George Alangaden, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

Thomas Herchline, MD, Professor of Medicine, Wright State University Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio
Thomas Herchline, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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