Download Septic Bacterial Arthritis

Clinical Approach to Acute
Monoarthritis
Mohammad Hasan Jokar
Acute Arthritis
• The sudden onset of inflammation of the
joint, causing severe pain, swelling, and
redness.
• Structural changes in the joint itself may
result from persistence of this condition.
Signs of Inflammation
• Swelling
• Warmth
• Erythema
• Tenderness
• Loss of function
Key Points
• Distinguish arthritis from soft tissue non articular
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syndromes (discrepancy between “active” and
“passive” ROM suggests periarticular/soft tissue)
If the problem is articular distinguish single joint
from multiple joint involvement
Inflammatory or non-inflammatory disease
Always consider septic arthritis!
Articular Vs. Periarticular
Clinical feature
Anatomic
structure
Painful site
Pain on
movement
Swelling
Articular
Synovium,
cartilage,
capsule
Diffuse, deep
Active/passive,
all planes
Common
Periarticular
Tendon, bursa,
ligament,
muscle, bone
Focal “point”
Active, in few
planes
Uncommon
Inflammatory Vs.
Noninflammatory
Feature
Inflammatory
Noninflammatory
Pain (when?)
Swelling
Erythema
Warmth
AM stiffness
Systemic features
î ESR, CRP
Synovial fluid WBC
Examples
Yes (AM)
Soft tissue
Sometimes
Sometimes
Prominent
Sometimes
Frequent
WBC >2000
Septic, RA, SLE, Gout
Yes (PM)
Bony
Absent
Absent
Minor (< 30 ‘)
Absent
Uncommon
WBC < 2000
OA, AVN
Acute Monoarthritis
• Inflammation (swelling, tenderness,
warmth) in one joint
• Occasionally polyarticular diseases
can present with monoarticular onset:
(RA, JRA,Reactive and enteropathic arthritis, Sarcoid
arthritis, Viral arthritis, Psoriatic arthritis)
Acute Monoarthritis - Etiology
• THE MOST CRITICAL DIAGNOSIS TO
CONSIDER: INFECTION !
• Septic
• Crystal deposition (gout, pseudogout)
• Traumatic (fracture, internal
derangement)
• Other (hemarthrosis, osteonecrosis,
presentation of polyarticular disorders)
Questions to Ask – History
Helps in DD
• Pain come suddenly, minutes? – fracture.
• 0ver several hours or 1-2 days? –infectious,
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crystals, inflammatory arthropathy.
History of IV drug abuse or a recent infection? –
septic joint.
Previous similar attacks? – crystals or
inflammatory arthritis.
Prolonged courses of steroids? – infection or
osteonecrosis of the bone.
Acute Monoarthritis
Indications for Arthrocentesis
• The single most useful diagnostic study in
initial evaluation of monoarthritis:
SYNOVIAL FLUID ANALYSIS
• 1. Suspicion of infection
• 2. Suspicion of crystal-induced arthritis
• 3. Suspicion of hemarthrosis
• 4. Differentiating inflammatory from
noninflammatory arthritis
Tests to Perform on Synovial
Fluid
• Total leukocyte count/differential:
inflammatory vs. non-inflammatory.
• Polarized microscopy to look for crystals.
• Gram stain and cultures
• Not necessary routinely: Chemistry
(glucose, total protein, LDH) unlikely to
yield helpful information beyond the
previous tests.
Case 1
• 52 yo wm presents to the Emergency
Department with a 2 day history of
excrutiating pain, with swelling, of the left
knee. He denies a history of trauma. He
reports fever of 39 degrees and chills.
Physical Exam:
T= 39.5 BP=150/92 P=105 RR=18
The physical exam is notable only for the
musculoskeletal exam which reveals:
Left knee with erythema, warmth, and
swelling. There is exquisite tenderness
and pain with any motion. There is
reduced range of motion due to pain.
Other joints are normal.
• The presentation of monoarticular arthritis
*****Aspiration of the joint*****
Lab tests
• CBC
• Joint fluid study
• Blood culture
• Synovial fluid
WBC 92,000
97 % PMNs
Gram Stain
Septic Arthritis
• Key Features:
– Monoarticular (almost always)
– Dolor, rubor, calor
– Swelling
– Exquisite pain
– Synovial fluid >50K WBCs and >95% PMNs
– Aggressive disease warranting aggressive
management
Septic Arthritis
• Management of the patient with septic
arthritis
– Arthrocentesis
– Hospital admission
– Orthopedic consult
– IV antibiotics
• Broad spectrum antibiotics until culture and
sensitivity available
Septic arthritis
******Drainage of the pus******
******IV antibiotics are essential******
Septic Arthritis
• Staphylococcus aureus - most aggressive
– Rapid evolution to joint destruction
– Importance of rapid diagnostic studies
– Rapid initiation of therapy
• Surgical drainage
• Intravenous antibiotics
Epidemiology
• 1:1 M:F
• Mean Age=55
• 85%=Monoarticular
• Patients with Damaged Joints are at
Increased Risk
• Most are hematogenously spread
• Fever present in only 60% of non-GC
septic arthritis
• Crystalline arthritis is 4x as common as
septic arthritis; fevers/rigors non-specific
Specific Infectious Agents
• Causative agents identified in 2/3 of patients in
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whom suspected
50% have known portal of entry
25% are iatrogenic
75% have extra-articular source: Look for skin,
respiratory, or GU sources
Groups at risk for septic arthritis
• Rheumatoid Arthritis: Account for up to 50% of cases
• Immunosuppressed Host, especially Organ
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Transplant Patients
Advanced Age: Greater than 60, especially with
Prosthetic Joints: May result in Osteomyelitis
Diabetes
Neoplasm
IV Drug Use: Repetitive transitory Bacteremia:
Staphylococci (MRSA)>Enterobacter, Serratia, and
Pseudomonas
Hemodialysis: Recurrent Vascular Infections,
especially Staphylococci
Right wrist destruction by
Staphylococcus aureus
Antibiotics and Supportive Therapy
• Guided by local antibiotic sensitivity patterns
• Intra-articular antibiotics are not required and
may cause a chemical synovitis
• Usually administered for 4 to 6 weeks
• NSAID’s avoided until the diagnosis is secure
• Joint Immobilization for 1 to 3 days
• ROM as soon as possible
Case 2
• 22 yo wf presents to the Emergency
Department with c/o left wrist pain of 2
days’ duration. She reports 2 weeks ago,
the onset of left ankle pain and swelling
which subsequently resolved in 3 days.
She then developed 3 days of swelling and
pain in the left knee, followed by 3 days of
swelling and pain in the right knee.
Physical Exam
– Temp 39
– Normal examination of HEENT, Lungs, CV,
and Abdomen
– Skin: Pustular lesions right 3rd and 4th fingers
– Musculoskeletal: Left wrist warm, swollen
(arthritis) with erythema extending along the
extensor tendons of the hand (tenosynovitis)
Gonorrhea: rash, vesicle, and
pustule
Gonorrhea: rash, pustule, and
bulla
Gonorrhea: pustule
Gonococcal Arthritis
• Key Features
– Migratory arthritis (immune mediated or
reactive)
– Tenosynovitis
– Rash
– Sexually active patient (though this may not
be disclosed on history)
Gonococcal Arthritis
• Evaluation
– Aspiration of affected joint
• Inflammatory joint fluid (>2000 WBC’s)
• Rarely WBC count in the “septic” range (>50,000
WBC’s)
• Cultures usually negative
– Culture
• Oropharynx, anus, cervix/urethra, skin lesions
Gonococcal Arthritis
• Migratory
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Polyarthralgias/Polyarthritis/Tenosynovitis = 66%;
Knee>hand>wrist
Dermatitis=sparse peripheral necrotic pustules in
40%
83%=female, mean age=23, GU involvement in
63%, often asymptomatic
Check VDRL and HIV and Co-treat Chlamydia
DGI-like arthritis-dermatitis can also occur with H.
influenzae, N. meningitidis, and S. moniliformis
Management
• Antibiotics
– Ceftriaxone
– Doxycycline added (to cover likely
concomittant Chlamydia infection)
– Surgical drainage of the joint rarely necessary
Case3
• 32 y/o WM admitted to the hospital with 2 days
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of acute onset of arthritis in his right knee that
progressed to the left knee. The day previous to
the admission, he was evaluated in the ER, and
an arthrocenthesis was attempted. The patient
was discharged on ceohalexin 500 mg QID.
ROS: 3 weeks previous to admission he had an
episode of diarrhea that lasted for 10 days and
improved after treatment with Cipro.
Family History: Sister with recurrent uveitis.
Physical Examination
• PE: fever 38.5. Otherwise within normal limits.
• Joint exam: tenderness, redness and effusions in both
knees.
• Labs: ESR 60, Synovial fluid showed no crystals and
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Gram stain revealed no organisms. HLA B-27 positive.
Patient was started on indomethacin 50 mg PO QID with
significant improvement of his symptoms.
Reactive Arthritis
• “Reactive Arthritis (ReA) is an infectious induced
systemic illness characterized by an aseptic inflammatory
joint involvement occurring in a genetically predisposed
patient with a bacterial infection localized in a distant
organ/system”.
Reactive Arthritis
• Epidemiology
• ReA is an acute and insidious polyarthritis after an
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enteric and urogenital infections.
Incidence varies widely (1% to 20%).
Frequency varies from 0 to 15% after infection with
Salmonella, Shigella, Campylobacter or Yersinia.
• HLA-B27 can be present in 72% to 84% of the cases.
• Incidence after Chlamydia trachomatis is not well known.
Reactive Arthritis
• ReA can occurs in the absence of HLAB27, this play a very important role.
Reactive Arthritis
• Causative organisms
• Frequent association:
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Chlamydial trachomatis
Ureaplasma urealyticum
Salmonella enteritidis
Salmonella typhimurium
Shigella flexneri
Shigella dysenteriae
Campylobacter jejuni
Yersinia enterocolitica
Streptococcus SP
Reactive Arthritis
• Less common association:
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Chlamydia pneumoniae
Neisseria meningitidis serogroup B
Bacillus cereus
Pseudomonas
Clostridium difficile
Borrelia burgdorferi
Escherichia coli
Helicobacter pillory
Lactobacillus
Brucella abortus
Hafnia alvei
Reactive Arthritis
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Clinical Manifestations:
Postenteric ReA is described equally in men an women.
Postchlamydial is most common in men.
In patients with postenteric ReA, the episode of diarrhea
is usually prolonged.
• Arthritis presents usually 2 to 3 weeks after the episode
of diarrhea.
• Arthritis usually resolves within 6 months, but a few
patients had recurrences an a minority develops a
chronic arthritis.
Reactive Arthritis
• In patients with postchlamydial disease, urethritis is
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usually mild, painless and nonpurulent.
Conjunctivitis is usually observed very early, before the
onset of arthritis, uveitis is less common but occurs in
15% of patients with chronic persistent disease.
Skin manifestations include: Keratoderma blenorrhagica,
Circinate balanitis and oral ulcers.
Less common patients can develop valvulitis, rhythm
disturbances.
Reactive Arthritis
• Treatment:
• NSAIDS are the first line of treatment.
• In patient with frequent recurrences or chronic arthritis
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benefit from DMARDS such us sulfasalazine or
methotrexate.
If there is axial involvement they will benefit from TNFalpha blockers.
Topical steroids are indicated in conjunctivitis and
uveitis.
In monoarthritis steroid injections could be beneficial.
Case 4
– 24 yo wm treated for gonococcal urethritis 2
weeks prior to presentation has complaint of
low back pain, left ankle and right knee pain
and swelling. He has noted “pink eye” in his
left eye.
Physical exam
– Afebrile
– HEENT- Left eye with conjunctival injection
– Musculoskeletal- Tender right SI joint
Effusion with warmth and tenderness of left
ankle and right knee
Evaluation
– CBC, CMP- normal
– ESR- 62
– U/A- neg protein, 2 WBCs, 5 RBCs
• Culture and sensitivity negative
– Xrays- SI joints, knees, ankles- normal
Reiter’s Syndrome
(Reactive Arthritis)
• Triad: Conjunctivitis, urethritis, arthritis
• Other features: Sausage digits, oral
erosions, keratoderma blenorrhagicum,
circinate balanitis
• Triggered by a recent GI/GU(STD)
infection
Keratoderma Blennorrhagicum
Reiter’s Syndrome
• Key Features:
– Preceding GI/GU infection
• The GU infection may have been asymptomatic
(especially in women), or not yet detected
– Triad: Conjunctivitis, urethritis, arthritis
(lower extremity>upper, asymmetric,
oligoarticular)
– Usually self-limited (3-12 month course)
– 15% develop chronic, destructive arthritis
Reiter’s Syndrome
• Radiographic features
• Xrays may be normal acutely, however
changes develop over time
– Periostitis
– Sacroiliitis
• Unilateral
Reiter’s Syndrome
• Management
– Detection of underlying infection
– Treatment of underlying infection
– NSAID’s
– DMARD’s- mixed results
– Best evidence supports use of sulfasalazine
Case 5
• 45 yo m presents to the Emergency
Department with a 12 h history of
excrutiating pain, with swelling, of the left
foot
Physical Exam:
T= 39 BP=150/92 P=105 RR=18
The physical exam is notable only for the
musculoskeletal exam which reveals:
Left foot with erythema, warmth, and
swelling. There is exquisite tenderness
and pain with any motion. There is
reduced range of motion due to pain.
Other joints are normal.
Lab tests
• CBC: WBC 13000 PMN 85%
• Creatinine:1
• Uric acid :6.5
• Synovial fluid :40000 90% PMNs
Management of gouty arthritis
• Asymptomatic hyperuricemia
• Acute gouty arthritis
• Chronic or tophaceous gout
Purine nucleotides
hypoxanthine
Xanthine
oxidase
xanthine
Uric acid
Urinary
excretion
Alimentary
excretion
Tissue deposition
in excess
Urate crystal
Phagocytosis
with acute
inflammation
and arthritis
microtophi
Management of gouty arthritis
• Asymptomatic hyperuricemia
• Acute gouty arthritis
• Chronic or tophaceous gout
Management of gouty arthritis
Treatment of asymptomatic
hyperuricemia usually in not necessary
Preventive measures
• Avoiding excess weight gain
• Reducing risks for hypertension
• Avoiding diuretic therapy
• Control alcohol intake
Management of gouty arthritis
• Asymptomatic hyperuricemia
• Acute gouty arthritis
• Chronic or tophaceous gout
Purine nucleotides
hypoxanthine
Xanthine
oxidase
xanthine
Uric acid
Urinary
excretion
Alimentary
excretion
colchicine
Tissue deposition
in excess
Urate crystal
microtophi
Phagocytosis
with acute
inflammation
and arthritis
NSAID
Management of acute gout
Do not attempt to modify plasma urate
concentrations
• NSAID
• Colchicine
• steroids
Management of acute gout
• NSAID
Shorter half life
– Indomethacin (50mg qid-50mg tid-25mg tid)
– Ibuprofen 800mg q6h
Contraindications
– Renal insufficiency, peptic ulcer, warfarin
therapy, liver disease, chronic heart failure
Management of acute gout
Colchicine
Effective within the 24 hours of an attack
Mechanism of colchicine
• Inhibit phagocytosis (microtubular system)
• Affect chemotaxis
• Affect motility and adhesion of neutrophil
• Reduce release PGE2 and LTB4
Management of acute gout
Colchicine
• Side effect
– GI disturbance, blood dyscrasias,
myoneuropathy
• Contraindications
– Renal dysfunction, liver disease, sepsis, bone
marrow dysfunction
Management of acute gout
Corticosteroids
•
NSAID and colchicine are contraindicated
Prednisone
20-50mg
oral
3-20days
• Intra-articular steroids
Prophylactic therapy
• Indications
– Recurrent attacks
– Tophi
– Renal disease
– Uric acid urolithiasis
– Inherited metabolic disorders
– Degree of hyperuricemia (11.8 mg/dl)
Prophylactic therapy
• Colchicine
• NSAID
• Urate-lowering therapy
– Allopurinol
– Uricosuric agents
Induce a flare up
Concurrent colchicine prophylaxis
Purine nucleotides
hypoxanthine
allopurinol
Xanthine
oxidase
xanthine
Uric acid
Urinary
excretion
Alimentary
excretion
Tissue deposition
in excess
Urate crystal
microtophi
Phagocytosis
with acute
inflammation
and arthritis
NSAID
uricosurics
colchicine
Prophylactic therapy
• Dietary restriction of purines rarely causes
a fall in the plasma urate concentration
more than 1.0 gm/dl
• Flares occure during a fall in serum urate
level
Purine nucleotides
hypoxanthine
allopurinol
Xanthine
oxidase
xanthine
Uric acid
Urinary
excretion
Alimentary
excretion
Tissue deposition
in excess
Urate crystal
Phagocytosis
with acute
inflammation
and arthritis
microtophi
Prophylactic therapy
• Allopurinol
Xanthine oxidase inhibitor
Indications
– Renal insufficiency
– Nephrolithiasis
– Tophi
– Tumor lysis syndrome
– Primary metabolic defects
Prophylactic therapy
• Allopurinol
– 300mg-900mg
– Side effect (<2%)
• Potentiating imuran marrow suppressive effect
• Hypersensitivity syndrome
• Hepatitis
• Interstitial nephritis
Purine nucleotides
hypoxanthine
Xanthine
oxidase
xanthine
Uric acid
Urinary
excretion
Alimentary
excretion
Tissue deposition
in excess
Urate crystal
uricosurics
Phagocytosis
with acute
inflammation
and arthritis
microtophi
Prophylactic therapy
• Uricosuric agents
– Probenecid
– Sulphinpyrazone
– Benzbromarone
Mechanism
– Inhibit renal tubular reabsorption
Prophylactic therapy
• Uricosuric agents
Side effects
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Uric acid crystalluria
GI disturbance
Allergy
Hepatic impairment
Contraindications
– Renal insufficiency
– nephrolithiasis
Prophylactic therapy
• When instituting uricosuric therapy
– Concurrent colchicine prophylaxis
– Initial low dose, increase dose gradually
– Maintain alkaline diuresis
– Not use in urine volume less than 1400ml/24
hours
Purine nucleotides
hypoxanthine
allopurinol
Xanthine
oxidase
xanthine
Uric acid
Urinary
excretion
Alimentary
excretion
Tissue deposition
in excess
Urate crystal
microtophi
Phagocytosis
with acute
inflammation
and arthritis
NSAID
uricosurics
colchicine