Septic arthritis
Septic arthritis: Excerpt from Handbook of Diseases
A medical emergency, septic (infectious) arthritis is caused by bacterial invasion of a joint, resulting in inflammation of the synovial lining. If the organisms enter the joint cavity, effusion and pyogenesis follow, with eventual destruction of bone and cartilage.
Septic arthritis can lead to ankylosis and even fatal septicemia. However, prompt antibiotic therapy and joint aspiration or drainage cures most patients.
Causes
In most cases of septic arthritis, bacteria spread from a primary site of infection, usually in adjacent bone or soft tissue, through the bloodstream to the joint.
Common infecting organisms include four strains of gram-positive cocci — Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Streptococcus viridans — and two strains of gram-negative cocci — Neisseria gonorrhoeae and Haemophilus influenzae. Various gram-negative bacilli — Escherichia coli, Salmonella, and Pseudomonas, for example — also cause infection.
Anaerobic organisms such as gram-positive cocci usually infect adults and children older than age 2. H. influenzae most often infects children younger than age 2.
Risk factors
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as cancer, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, alcoholics and elderly people run a higher risk of developing septic arthritis.
Of course, susceptibility increases with diseases that depress the autoimmune system or with prior immunosuppressant therapy. I.V. drug abuse (by heroin addicts, for example) can also cause septic arthritis.
Other predisposing factors include recent articular trauma, joint surgery, intra-articular injections, and local joint abnormalities.
Signs and symptoms
Acute septic arthritis begins abruptly, causing intense pain, inflammation, and swelling of the affected joint, with low-grade fever. Although it usually affects a single, large joint, it can affect any joint, including the spine and small peripheral joints.
CLINICAL TIP: Systemic signs of inflammation may not appear in some patients. Migratory polyarthritis sometimes precedes localization of the infection. If the bacteria invade the hip, pain may occur in the groin, upper thigh, or buttock, or may be referred to the knee.
UNDER STUDY: The tumor necrosis factor (TNF) 2 allele has been associated with higher septic shock susceptibility and mortality. Investigation of polymorphisms within the TNF alpha cluster will be important in understanding the role of TNF alpha regulation in specific diseases.
Treatment
The goals of treatment are to provide oxygen and to treat respiratory distress, if present; to monitor and reverse shock through volume expansion; to treat underlying infections with antibiotic therapy; and to support poorly functioning organs.
Treatment begins with the administration of I.V. fluids and the insertion of a pulmonary artery catheter to check pulmonary circulation and PAWP. Administration of whole blood or plasma may be necessary to help raise the PAWP to a satisfactory level of 14 to 18 mm Hg. A urinary catheter allows accurate measurement of hourly urine output.
The patient may require endotracheal intubation and placement on a ventilator to overcome hypoxia. Adjustments are necessary to promote adequate cellular oxygenation and support hyperdynamic needs.
Antibiotic therapy
Treatment also requires immediate administration of I.V. antibiotics to control the infection. Depending on the organism, an antibiotic combination may be necessary.
Appropriate anti-infectives for causes of septic shock depend on the suspected organism. Other measures to combat infections include surgery to drain and excise abscesses and debridement.
Other drug therapy
If shock persists after fluid infusion, treatment with a vasopressor, such as dopamine, maintains adequate blood perfusion to vital organs. Other treatment includes correction of acidosis and, possibly, I.V. corticosteroids.
Special considerations
❑ Determine which of your patients are at high risk for developing septic shock. Know the signs of impending septic shock, but don’t rely solely on technical aids to judge the patient’s status. Consider any change in mental status and urine output as significant as a change in CVP.
❑ Maintain pulmonary, cardiac, and renal function. Carefully monitor hemodynamic parameters. Check ABG values for adequate oxygenation or gas exchange, watching for any changes.
❑ Keep accurate intake and output records. Maintain adequate urine output (0.5 to 1 ml/kg/hour) and systolic pressure. Be careful to avoid fluid overload.
❑ Monitor the serum antibiotic level as indicated.
❑ Watch closely for complications of septic shock: DIC (abnormal bleeding), renal failure (oliguria, increased specific gravity), heart failure (dys-pnea, edema, tachycardia, neck vein distention), adult respiratory distress syndrome (tachypnea, tachycardia, poor oxygenation), GI ulcers (hematemesis, melena), and hepatic abnormalities (jaundice, hypoprothrombinemia, and hypoalbuminemia).
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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