eMedicine Specialties > Emergency Medicine > Infectious Diseases

Osteomyelitis

Author: Randall W King, MD, Assistant Clinical Professor of Emergency Medicine, Medical College of Ohio; Program Director, Associate Chair, Department of Emergency Medicine, St Vincent Mercy Medical Center
Coauthor(s): David Johnson, MD, Assistant Clinical Professor, Department of Surgery, Medical University of Ohio; Associate Chair, Department of Emergency Services, Director, Lucas County Emergency, St Vincent's Mercy Medical Center
Contributor Information and Disclosures

Updated: Nov 4, 2008

Introduction

Background

Osteomyelitis is an acute or chronic inflammatory process of the bone and its structures secondary to infection with pyogenic organisms.

Pathophysiology

The infection associated with osteomyelitis may be localized or it may spread through the periosteum, cortex, marrow, and cancellous tissue. The bacterial pathogen varies on the basis of the patient's age and the mechanism of infection.

The following are the 2 primary categories of acute osteomyelitis: hematogenous osteomyelitis and direct or contiguous inoculation osteomyelitis.

Hematogenous osteomyelitis is an infection caused by bacterial seeding from the blood. Acute hematogenous osteomyelitis is characterized by an acute infection of the bone caused by the seeding of the bacteria within the bone from a remote source. This condition occurs primarily in children. The most common site is the rapidly growing and highly vascular metaphysis of growing bones. The apparent slowing or sludging of blood flow as the vessels make sharp angles at the distal metaphysis predisposes the vessels to thrombosis and the bone itself to localized necrosis and bacterial seeding. Acute hematogenous osteomyelitis, despite its name, may have a slow clinical development and insidious onset.

Direct or contiguous inoculation osteomyelitis is caused by direct contact of the tissue and bacteria during trauma or surgery. Direct inoculation (contiguous-focus) osteomyelitis is an infection in the bone secondary to the inoculation of organisms from direct trauma, spread from a contiguous focus of infection, or sepsis after a surgical procedure. Clinical manifestations of direct inoculation osteomyelitis are more localized than those of hematogenous osteomyelitis and tend to involve multiple organisms.

Additional categories include chronic osteomyelitis and osteomyelitis secondary to peripheral vascular disease. Chronic osteomyelitis persists or recurs, regardless of its initial cause and/or mechanism and despite aggressive intervention. Although listed as an etiology, peripheral vascular disease is actually a predisposing factor rather than a true cause of infection.

Disease states known to predispose patients to osteomyelitis include diabetes mellitus, sickle cell disease, acquired immune deficiency syndrome (AIDS), IV drug abuse, alcoholism, chronic steroid use, immunosuppression, and chronic joint disease. In addition, the presence of a prosthetic orthopedic device is an independent risk factor as is any recent orthopedic surgery or open fracture.

For the radiologic perspective, see Osteomyelitis, Acute Pyogenic and Osteomyelitis, Chronic.

Frequency

United States

The overall prevalence is 1 per 5,000 children. Neonatal prevalence is approximately 1 per 1,000. The annual incidence in sickle cell patients is approximately 0.36%. The prevalence of osteomyelitis after foot puncture may be as high as 16% (30-40% in patients with diabetes).

International

The overall incidence is higher in developing countries.

Mortality/Morbidity

  • Morbidity can be significant and can include localized spread of infection to associated soft tissues or joints; evolution to chronic infection, with pain and disability; amputation of the involved extremity; generalized infection; or sepsis. Up to 10-15% of patients with vertebral osteomyelitis will develop neurologic findings or frank spinal-cord compression. Up to 30% of pediatric patients with long-bone osteomyelitis may develop deep venous thrombosis (DVT). The development of DVT may also be a marker for disseminated infection.1
  • Mortality rates are low, unless associated sepsis or an underlying serious medical condition is present.

Race

There is no increased incidence of osteomyelitis based on race.

Sex

Male-to-female ratio is approximately 2:1.

Age

In general, osteomyelitis has a bimodal age distribution.

  • Acute hematogenous osteomyelitis is primarily a disease in children.
  • Direct trauma and contiguous focus osteomyelitis are more common among adults and adolescents than in children.
  • Spinal osteomyelitis is more common in persons older than 45 years.

Clinical

History

Hematogenous osteomyelitis usually presents with a slow insidious progression of symptoms. Direct osteomyelitis generally is more localized, with prominent signs and symptoms. General symptoms of osteomyelitis include the following:

  • Hematogenous long-bone osteomyelitis
    • Abrupt onset of high fever (fever is present in only 50% of neonates with osteomyelitis)
    • Fatigue
    • Irritability
    • Malaise
    • Restriction of movement (pseudoparalysis of limb in neonates)
    • Local edema, erythema, and tenderness
  • Hematogenous vertebral osteomyelitis
    • Insidious onset
    • History of an acute bacteremic episode
    • May be associated with contiguous vascular insufficiency
    • Local edema, erythema, and tenderness
    • Failure of a young child to sit up normally2
  • Chronic osteomyelitis
    • Nonhealing ulcer
    • Sinus tract drainage
    • Chronic fatigue
    • Malaise

Physical

Findings at physical examination may include the following:

  • Fever (present in only 50% of neonates)
  • Edema
  • Warmth
  • Fluctuance
  • Tenderness to palpation
  • Reduction in the use of the extremity (eg, reluctance to ambulate, if the lower extremity is involved or pseudoparalysis of limb in neonates)
  • Failure of a young child to sit up normally
  • Sinus tract drainage (usually a late finding or one that occurs with chronic infection)

Causes

Note that responsible pathogens may be isolated in only 35% to 40% of infections.

Bacterial causes of acute and direct osteomyelitis include the following:

  • Acute hematogenous osteomyelitis
    • Newborns (younger than 4 mo): S aureus, Enterobacter species, and group A and B Streptococcus species
    • Children (aged 4 mo to 4 y): S aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species
    • Children, adolescents (aged 4 y to adult): S aureus (80%), group A Streptococcus species, H influenzae, and Enterobacter species
    • Adult - S aureus and occasionally Enterobacter or Streptococcus species
    • Note increasing reports of other pathogens in bone and joint infections including community-associated methicillin-resistant Staphylococcus aureus (MRSA), Kingella kingae,3 and others.
  • Direct osteomyelitis
    • Generally - S aureus, Enterobacter species, and Pseudomonas species
    • Puncture wound through an athletic shoe - S aureus and Pseudomonas species
    • Sickle cell disease -S aureus and Salmonellae species

Also see Medscape's Infectious Diseases Resource Center.

More on Osteomyelitis

Overview: Osteomyelitis
Differential Diagnoses & Workup: Osteomyelitis
Treatment & Medication: Osteomyelitis
Follow-up: Osteomyelitis
Multimedia: Osteomyelitis
References
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References

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Further Reading

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Keywords

osteomyelitis, bone infection, central osteitis, hematogenous osteomyelitis, direct inoculation osteomyelitis, chronic osteomyelitis, osteomyelitis secondary to peripheral vascular disease, contiguous inoculation osteomyelitis, vertebral osteomyelitis, spinal-cord compression, spinal osteomyelitis, Staphylococcus aureus, Enterobacter species, Haemophilus influenzae, Streptococcus species, Pseudomonas species, Salmonellae species, diabetes mellitus, sickle cell disease, acquired immune deficiency syndrome, AIDS, IV drug abuse, alcoholism, chronic steroid use, immunosuppression, chronic joint disease, MRSA, methicillin-resistant Staphylococcus aureus, community-associated methicillin-resistant Staphylococcus aureus, Kingella kingae

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Contributor Information and Disclosures

Author

Randall W King, MD, Assistant Clinical Professor of Emergency Medicine, Medical College of Ohio; Program Director, Associate Chair, Department of Emergency Medicine, St Vincent Mercy Medical Center
Randall W King, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, National Association of EMS Physicians, Ohio State Medical Association, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Challenger corporation None Other

Coauthor(s)

David Johnson, MD, Assistant Clinical Professor, Department of Surgery, Medical University of Ohio; Associate Chair, Department of Emergency Services, Director, Lucas County Emergency, St Vincent's Mercy Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Dana A Stearns, MD, Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital
Dana A Stearns, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Eric L Weiss, MD, DTM&H, Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine
Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society
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

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting

 
 
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