Septic Arthritis - © Arthritis Research Campaign

[Guest guest]

Septic Arthritis - © Arthritis Research Campaign

ARC Reports on Rheumatic Diseases: Series 3

May 1996 No. 7

Medical Editors:

Robin

Malcolm Jayson

McKenna

GI

GP Adviser:

Million

Production Editor:

Keir Windsor (ARC)

ISSN 1351-4873

WARNING:

THESE

PUBLICATIONS

ARE INTENDED

FOR MEDICAL

PRACTITIONERS.

SOME OF THEIR

CONTENTS MAY

BE DISTURBING

TO READERS

WITH ARTHRITIS

OR THEIR

CARERS.

SEPTIC ARTHRITIS

RA MRCP MD

Rheumatology Department

St 's Hospital

Guildford Road

Chertsey

Surrey

KT16 0PZ

--------------------------------------------------------------------------

DEFINITION

Septic arthritis is defined as joint inflammation caused by the presence

of live intra-articular micro-organisms. Septic arthritis may be associated with

osteomyelitis, infection of an adjacent bone, especially in childhood. Septic

arthritis arises as a result of infection with bacteria, viruses, fungi and,

more rarely, other esoteric micro-organisms such as protozoa. Septic arthritis

is uncommon but diagnosis must be made early and effective anti-microbial

treatment started without delay. Joint sepsis must be distinguished from

reactive arthritis in which synovitis is triggered by a primary infection at a

site distant from the joint. Although bacterial antigens may be found in the

joint in reactive arthritis, joint material is sterile on microbial culture and

antibiotic treatment is of unproven efficacy. In this report the main focus will

be on the investigation and treatment of bacterial septic arthritis.

CLINICAL PRESENTATION

Septic arthritis most commonly presents as an acute hot joint or joints

together with the cardinal signs of acute inflammation: swelling and joint

effusion, redness, pain and loss of function. The presence of an acutely painful

or swollen joint, especially in association with a joint prosthesis, underlying

inflammatory joint disease or in a patient with diabetes mellitus, should prompt

the suspicion of joint infection. However the presentation of septic arthritis

may be atypical in infants, when commonly the patient presents with systemic

malaise and fever, with few specific signs or symptoms of joint disease. In the

young child, sepsis may occur in the hip which is held immobile in flexion and

abduction. In the elderly, and in individuals with coexistent joint disease,

immunosuppression and in those on steroid treatment, the clinical signs of an

infected joint may be atypical with a minimum of evidence of inflammation. The

appearance of sinuses or fistula and tissue necrosis surrounding prosthetic

joints should suggest joint infection.

Extra-articular manifestations of infection may be more prominent than

joint signs in some cases of septic arthritis. Gonococcal septic arthritis may

be associated with urethritis, erythematous skin lesions with subsequent

necrosis and sometimes with prominent tenosynovitis. Joint infection can occur

by haematogenous spread in patients with bacterial endocarditis in whom heart

murmurs and splinter haemorrhages may be more prominent. Infection with

Staphylococcus aureus - a common joint pathogen - may present in children with

Scalded Skin syndrome and in adults with the clinical features of Toxic Shock

syndrome or erythema multiforme.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of septic arthritis is that of the acute hot

joint. Damaged, inflamed and prosthetic joints are more susceptible to

infection; this must not be forgotten as infection occurs more frequently in

abnormal joints and the two pathologies can co-exist. Crystal arthritis, acute

inflammatory arthritis, post-traumatic synovitis, extra-articular inflammation

(for example olecranon bursitis), and haemarthrosis can all mimic septic

arthritis. Septic arthritis is the most important of the differential diagnoses

of the acute hot joint since a misdiagnosis and failure to treat with

antibiotics can have devastating consequences for the joint and for the patient.

THE ROUTE OF INFECTION

Infection of the joint in septic arthritis can occur by one of five routes

(Figure 1). Most commonly, spread of the micro-organism is haematogenous, such

as seen following septicaemia; frequently septic arthritis arises from infective

foci in the skin such as wound infections and abscesses, sepsis in the mouth and

teeth or after dental procedures or in association with infection of the

respiratory or urogenital tract. Direct penetrating trauma to the joint with

sharp objects such as thorns or needles or during major traumatic injury can

lead to joint infection. Diagnostic and therapeutic techniques of joint

aspiration and injection and surgical procedures such as joint replacement can

result in joint infection. Osteomyelitis can spread to involve the joint

especially in young children. Finally, infection of the soft tissues adjacent to

the joint, such as inflamed bursae or tendon sheaths, can spread to involve the

joint space.

Spread of infection by the haematogenous route is still the most frequent

cause of joint sepsis. The incidence of septic complications following joint

replacement surgery has fallen as more elaborate peri-operative precautions are

taken to avoid infection, together with the widespread use of prophylactic

antibiotics and advances in surgical technique.

Figure 1. Routes of access to the joint in bacterial septic

arthritis

THE PATHOGENESIS OF JOINT DESTRUCTION IN SEPTIC ARTHRITIS

The presence of live micro-organisms in the joint stimulates the

activation of immunological defence mechanisms. Neutrophils aggregate in the

joint space and synovium in order to phagocytose invading micro-organisms whilst

recruitment of lymphocytes and activation of the complement cascade result in

accentuation of the acute inflammatory response. Increase in vascular

permeability causes joint effusion and intra-articular pressure increases,

which, in itself, can compromise the integrity of cartilage. The release of

cytokines and degradative enzymes such as elastase and collagenase, and the

generation of free radicals in the joint result in rapid and irreversible

destruction of joint tissue and adjacent bone and atrophy of surrounding

muscles. Sepsis can also stimulate pannus formation which persists long after

micro-organisms have been eliminated. Rapid treatment of joint sepsis is

paramount if joint damage is to be limited.

MICRO-ORGANISMS IN SEPTIC ARTHRITIS

The likely microbial aetiology of joint sepsis will vary with the age of

the patient, the coexistence of underlying disease, the route of spread of

infection and the distribution of affected joints (Table 1). It is important to

know the likely pathogens in particular clinical situations as antibiotic

treatment is usually started before results of culture and sensitivity are fully

available. In all ages and clinical situations the most common micro-organism to

cause joint sepsis is Staphylococcus aureus. In neonatal septic arthritis,

Escherichia coli and Haemophilus influenzae must be considered as candidate

pathogens, whilst in children from age 1 month to 5 years Haemophilus influenzae

is the most common cause of haematogenous joint sepsis. Gram-negative intestinal

bacterial are more common in patients who are elderly and incontinent and in

patients with diabetes mellitus or prosthetic joints. In cases of penetrating

injury, and in intravenous drug abusers, infection with Pseudomonas aeroginosum

or Staphylococcus epidermidis may be found. Septic arthritis is uncommon in fit

young adults and should prompt a search for Neisseria gonorrhoeae or

meningococcal infection. Chronic low grade septic arthritis, especially in the

spine, can be the result of infection with micro-organisms such as Mycobacteria

or Brucella abortus and biopsy may be necessary to establish diagnosis. As HIV

infection becomes more widespread so the range of joint pathogens becomes more

diverse. Immunosuppression and low CD4 T lymphocyte counts have been associated

with an increase in cases of atypical mycobacterial and fungal joint infections.

Table 1. Micro-organisms causing bacterial septic arthritis

Gram positive Staphylococcus aureus (80% cases)

Streptococcus pyogenes/pneumoniae

Gram negative Haemophilus influenzae

Neisseria gonorrhoeae/meningitidis

Pseudomonas aeroginosa

Coliforms

Bacteroides fragilis

Brucella species

Salmonella species

Fusiform bacteria

Acid-fast bacilli Mycobacterium tuberculosis

Atypical mycobacteria

Spirochaetes Leptospira icterohaemorrhagica

INVESTIGATION AND DIAGNOSIS

A history should be obtained to include evidence of prior or current

infection elsewhere in the body, especially the genito-urinary tract in the

adult. Any risk of HIV infection should be identified and counselling for HIV

testing considered. A history of prior exposure to antibiotics should be

obtained as recent oral treatment can mask ongoing joint infection and the joint

may appear to be sterile.

Where joint sepsis is suspected joint aspiration must be performed and

referral to hospital for in-patient investigation considered. Joint aspiration

should be carried out under aseptic conditions and any joint aspirate despatched

in a sterile container for immediate Gram stain, special stain for acid-fast

bacilli and subsequent culture. Where immunosuppression is suspected, the

microbiologist should be alerted to culture for unusual micro-organisms.

Synovial fluid should be sent for a cell count as high neutrophil and total

white cell counts raise the probability of infection. Synovial fluid should also

be examined under polarised light to search for crystals. Blood should be taken

into blood culture bottles and the ears and throat should be examined and

swabbed especially in children. If gonococcal infection is suspected in the

adult, genital, throat and anal swabs should be taken into appropriate media and

sent immediately to the laboratory. In suspected cases where no microbiological

proof of infection can be established synovial biopsy may be necessary.

TREATMENT OF JOINT SEPSIS

All patients with proven septic arthritis should be admitted to hospital

for treatment with intravenous antibiotics and rest of the affected joint. The

duration of treatment will depend on severity and clinical response.

Treatment should only be started after samples have been taken for

microbiological identification of the relevant micro-organism. An initial

regimen of antibiotic treatment is suggested for use prior to the availability

of culture and sensitivity results (Table 2). The prevalence of antibiotic

resistance is changing. An increasing number of Haemophilus strains are

resistant to penicillin (approximately 15% of isolates at the present time)

prompting the choice of a cephalosporin in the young. As more strains of

multiple-resistant Staphylococcus aureus (MRSA) emerge so the choice of

antibiotics may become more difficult. Treatment should always include adequate

analgesia by an appropriate route as this condition can be very painful.

Anti-pyretics and anti-inflammatories can be useful.

Table 2. Recommended initial regimen for antibiotic therapy in

septic arthritis

Patients Antibiotics Doses

Neonates and children under 5 years

. Cefotaxime 50mg/kg BD

Flucloxacillin 25mg/kg 4 hourly

Adults Benzyl penicillin 1.2g 4 hourly

. Flucloxacillin 500mg-1g QDS

Following the availability of results of culture and sensitivity, and

dependent on clinical response, the regimen can be altered subsequently.

Intravenous antibiotics are normally continued for up to 14 days followed by

oral antibiotics for up to four weeks depending on clinical response. In cases

of prosthetic joint infection antibiotics may need to be continued long-term.

There is no need for intra-articular injections of antibiotics in the treatment

of septic arthritis.

The role of repeated aspiration and of surgery in the treatment of septic

arthritis is still uncertain. No well-designed randomised clinical trials have

been carried out that address this issue. In joints that are difficult to

aspirate due to loculation of fluid and presence of fibrin, an initial joint

arthroscopy should be considered. Repeated needle aspiration of infected joints

is sometimes performed but there is little evidence to support this practice.

Orthopaedic treatment of joint sepsis will usually involve invasive joint

washout and subsequent irrigation of the joint although, in uncomplicated cases,

there is no clinical evidence that this is better than intravenous antibiotic

treatment alone. In a young child with an infected hip, joint washout is often

performed and arthroscopy appears to be as beneficial as open arthrotomy.

Caution should be exercised when any invasive joint manoeuvre is

considered as new pathogens may be introduced into the joint. Invasive

procedures should be avoided where possible. Immobilisation of the infected

joint in the early days of treatment can be aided by the use of a plaster back

slab or splint. Surgery, with removal of the joint prosthesis and all associated

foreign material, is often necessary when joint replacements become infected.

Enthusiastic rehabilitation must follow antibiotic treatment with involvement of

physiotherapy for muscle building and mobilisation.

GUIDELINES FROM THE RCP AND BSR WORKING PARTIES

In an attempt to ensure the early identification and correct treatment of

septic arthritis a working party from the British Society for Rheumatology and

the Royal College of Physicians produced guidelines in 1992 for the management

of the acute hot joint (Table 3).

An audit of the adherence to these guidelines has shown them to be

practical in both hospital and general practice. The audit revealed that

casualty department staff relied too heavily on x-rays in the assessment of the

acute hot joint and that over-confidence in clinical diagnosis of septic

arthritis in hospitial meant that aspiration was not always performed before

treatment was started. The suggested outcome measures were unhelpful and require

further modification. The greatest delay before diagnosis of septic arthritis

was made and treatment started was the result of initial hesitation by patients

themselves before seeking advice.

Table 3. BSR and RCP guidelines for the management of the acute hot

joint (see references)

Prompt assessment by an experienced clinician

Investigations

Microscopy including polarised microscopy of synovial fluid

Gram stain and culture of synovial fluid

Blood culture

Full blood count

Measures of acute phase response (ESR and/or C reactive protein)

Joint x-rays

Treatment

Appropriate to diagnosis

Outcome measures

Death

Joint destruction

Dissemination of infection

Length of hospital stay

REFERENCES FOR FURTHER READING

1. Hedstrom SA, Lidgren L. Practical Rheumatology Eds Klippel JH, Dieppe

PA. 1995 Mosby pps 277-288.

2. Currey HLF. Acute Monarthritis - Differential Diagnosis, and

Management. Practical Problems, ARC Reports on Rheumatic Diseases (Series 2)

September 1988 No 10.

3. Frederiksen B, Christiansen P, Knudsen FU. Acute osteomyelitis and

septic arthritis in the neonate, risk factors and outcome. European J Pediatrics

1993; 152: 577-580.

4. Lambert HP, O'Grady FW. Antibiotic and Chemotherapy 1992, Churchill

Livingstone, London.

5. Report of a joint working group of the Brititsh Society for

Rheumatology and the Research Unit of the Royal College of Physicians.

Guidelines and a proposed audit protocol for the initial management of an acute

hot joint. J R Coll Physicians Lond 1992; 26: 83-85.

6. DJ, Young I, Hassey GA, AMM. The acute hot joint in

medical practice. J R Coll Physicians Lond 1995; 29: 101-104.

© Arthritis Research Campaign 1996 3-PP7

This publication has been produced because of voluntary donations

given to the Arthritis Research Campaign. Printed copies can be ordered on this

web site or by writing to ARC Publications, PO Box 31, Newark NG24 2BS, United

Kingdom.