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A Rheumatology & Infectious Joint Conference
by
Gresaneth Claire Lumasag, MD
Jennifer Cabanilla, M.D
20 September 2017
West Visayas State University MedicalCenter
Department of Internal Medicine
I.
1. Present a case of a 75 y.o with left knee pain
2. Discuss approach to monoarthritis, specifically
on infection related arthritis as to
 Diagnosis
 Pathophysiology
 Etiologic agents
 Management
 Prognosis
 Prevention
objectives
II.
a. Complications
b. Ethical, Moral Decision-making
• 75/ F
• Tubungan, Iloilo
• Roman Catholic
Left Knee pain
for 4 days
following a simple
gardening chores
CASE
4 days PTC Day of Consult
✓Pain of left
knee,
aggravated by
movement,
VAS 5/10
✓Swelling and
warm to
touch
✓Increasing
severity of
left knee pain,
with
limitation of
ROM, VAS 8-
9/10
✓Fever
A
D
M
I
S
S
I
O
N
(+) S/P STROKE WITH RESIDUAL LEFT SIDED
WEAKNESS 4/5
MAINTENANCE:
ASA 80MG/TAB 1 TAB OD
LOSARTAN 50MG/TAB 1 TAB OD
(-) PREVIOUS SURGERY OR ADMISSION
(-) TRAUMA
Past medical history
(+) Hypertension-
mother
(-) DM
(-) BA
(-) CA
Family history
• Housekeeper
• 10 pack-year smoker
• Non-alcoholic
drinker
• Single parent
Personal & Social History
At the emergency room
 wheelchair-borne
 Grimacing in pain
 Not in pulmonary
distress
• VITAL SIGNS
• BP 100/60 MMHG
• CR 106 BP M
• RR 18 CPM
• O2 SAT 98% AT ROOM AIR
• BMI 20
Skin:
Fair skin, (+) brownish hyperpigmentation on extremities
HEENT:
Anicteric sclerae, pinkish conjunctiva, pupils 2-3mm equally reactive to light and
accommodation, no cervical lymphadenopathies
Chest and Lungs:
Symmetrical Chest expansion, equal vocal and tactile fremiti, clear breath sounds
Heart:
Adynamic precordium, PMI at 5th left intercostal space MCL, normal cardiac rate and
regular rhythm, no murmurs
Abdomen:
Flat, no striations noted, hypoactive bowel sound, soft abdomen,
(-) organomegaly, (-) ascitic fluid wave, (-) direct tenderness
(-) rebound tenderness
Physical examination
Extremities:
•LKJ (+) swelling grade 3
• (+) redness
• (+) warm to touch,
• (+) limitation of
• movement
Physical examination
Admitting Impression
ACUTE MONOARTHRITIS, PROBABLY
SEPTIC
HOWto APPROACH APATIENT presenting WITH acute
monoarthritis?
History and physical examination
Is it articularTrauma/fracture
Soft tissue rheumatism
no
> 6 weeks
yes
Chronic
yes
Acute
Infectious arthritris
Crystal induced
Reactive arthritis
No
Signs of inflammation
Chronic
noninflamatory
arthritis
DIP, CMC1,Hip
,Knee joint
osteoarthritis
yes
Osteonecrosis
Charcots joint
no
yesChronic
inflammatory
arthritis
Joints involved
1-3
Psoriatic symmetrical
>3
Psoriatic
Reactive
no
yes
PCP,MCP/MT
P
yes
Rheumatoid
no
SLE/Scleroderma
no
Differential Diagnosis:
Infectious (Septic Arthritis)- a direct invasion of joint
space by various microorganisms, most commonly caused
by bacteria.
Crystal induced- an intensely painful type of arthritis
that occurs mainly in the joints of the big toe. It can also
attack the top of the foot and ankle.
Reactive (Infection-related arthritis)- an infection in
another party of the body – usually the intestines,
genitals or urinary tract – triggers an inflammatory
response in the joints.
Arthrocentesis!
Synovial Fluid Result
Amount 5 cc
Color Yellow with blood tinge
Transparency purulent
Cell count 80448
RBC count 380
Segmenters 82%
Lymphocytes 8%
Gram stain
Many pus cells. Occasional
gram negative bacilli and
gram positive cocci in singles
and in pairs
On Admission Result Normal
Hemoglobin 139 g/L 120-160
Hematocrit 0.41 L/L 0.37-0.47
WBC 27.11 4.5-11
Segmenters 0.93 0.50-0.70
Lymphocytes 0.03 0.20-0.40
Platelet 266 150-450
ESR 125 0- 10
A.L.
Infectious arthritis,
- direct invasion of joint space by various
microorganisms (bacteria, viruses, mycobacteria
& fungi)
Rheumatologic emergency as joint destruction
occurs rapidly and can lead to significant
morbidity and mortality.
Septic arthritis
Infectious Arthritis
Septic
Arthritis
Acute
Monoarticular Polyarticular
Chronic
Monoarticular Polyarticular
Etiologic Agents of infectious Arthritis
• Acute
– Monoarticular
• Staphylococcus aureus
• Streptococcus pneumoiae
• Β-Hemolytic streptococci
• Gram Negative bacilli
• Neisseria gonorrhoeae
• Candida spp
– Polyarticular
• Immunologic reaction
(endocarditis, rheumatic fever,
dessiminated nesserial
infection, acute hepatitis B)
• Chronic
– Mycobacterium tuberculosis
– Non tuberculous mycobacteria
– Borrelia burgdoferi
– Treponema pallidum
– Candida spp
– Sporothrix schenckii
– Coccioides immitis
– Blastomyces dermatitidis
– Aspergillus spp
– Cryptococcus neoformans
– Nocardia spp
– Brucella spp
Infectious arthritis,
- direct invasion of joint space by various
microorganisms (bacteria, viruses, mycobacteria
& fungi)
Rheumatologic emergency as joint destruction
occurs rapidly and can lead to significant
morbidity and mortality.
Septic arthritis
Treatment
Antibiotics + Drainage with Culture
IV VancomycinIV 3rd Gen Cephalosporin MRSA ?
yes
Oxacillin or Nafcillin
Definitive therapy is based on Isolated organism and antibiotic susceptibility
no
Treatment
• Staphylococcal – oxacillin, nafcillin, vancomycin (4 weeks)
• Pneumococcal and Streptococcal
– penicillin-susceptible– Penicillin G (2 weeks)
– Penicillin-resistant- Cefotaxime /Ceftriaxone (2 weeks)
• Gram Negative – 2nd or 3rd gen Cephalosporin IV or IV
Flouroquinolone (3-4 weeks)
• Pseudomonas – combination aminoglycoside+ extended
spectrum penicillin or antipseudomonal cephalosporin (4
weeks)
• Gonococcal –IV/IM Ceftriaxone q24H
❖Elderly >60 years
❖Diabetes mellitus
❖Rheumatoid arthritis
❖Prosthetic joint
❖Recent joint surgery
❖Skin infection, cutaneous ulcers
❖IV drug abuse, alcoholism
❖Previous intra-articular injection
PREDISPOSING FACTORS
RISK FACTORS
 Age > 60 y.o
 female
 Recent Bacteremia
 Degenerative joint disease
 Rheumatoid Arthritis
 Corticosteroid therapy
 Co-morbidities (DM, Cirrhosis,
Renal Disease)
 Immunocompromised State
(eg. HIV)
Hematogenous
Spread
Direct
Introduction
Extension from
Contiguous site
Of infection
Recent Trauma/
Injury
Bacterial Seeding within the space
Bacterial Adherence and
Colonization
• Blood- WBC, CRP, ESR- low specificity;
suggestive but not diagnostic
• WBC>10 000
• ESR>30
• CRP>100
DIAGNOSTICS: What to Request?
DIAGNOSIS
• Synovial fluid
usually purulent with increased count (50,000 to
150,000 cells/mm3)
The synovial fluid glucose is often depressed and
lactic acid concentration is elevated.
DIAGNOSIS
OTHER DIAGNOSTIC
MODALITIES
• X-ray, CT, MRI: less helpful in diagnosis
The earliest findings are soft tissue swelling
around the joint and a widened joint space
from joint effusion.
Can demonstrate: joint effusion
Synovial thickening
Perisynovial edema
Cartilage destruction
Bone destruction
Bursitis, tenosynovitis
DIAGNOSIS
 Blood cultures are
positive in about 50
percent of cases.
Blood culture: NO GROWTH
TREATMENT
The first priority is to aspirate
the joint and the fluid. Treatment
is then started without further
delay!
TREATMENT
• Principle:
Antibiotics
Joint drainage
Joint rest.
Duration of Treatment
• No controlled trials
• Usually IV antibiotics at least 2 weeks in
duration followed by at least two weeks oral
therapy
• May need longer for particular organisms- P.
aeruginosa, Enterobacter spp. or S. Aureus
with septicaemia
TREATMENT
• Principle:
Antibiotics
Joint drainage
Joint rest.
Joint Drainage
• Aim to remove pus from joint space- i.e. drain
abscess
– Surgical: arthroscopy or arthrotomy
– Closed needle aspiration
Indication of Surgical Drainage
1. Joints that do not respond to antimicrobial
therapy and daily arthrocentesis
2. Any joint with limited accessibility, including the
sternoclavicular joint or the hip joint
3. Patients with underlying disease, including DM,
RA, immunosuppression, or other systemic
symptoms, should be treated aggressively with
earlier surgical intervention
2nd Hospital Day
(+) abdominal pain
(+) vomiting
(+) cold clammy extremities
Rpt ECG: ST elevation high lateral wall
Trop I: 27
• ECG:
• Assessment: Acute Coronary Syndrome- ST
Elevation MI- lateral wall
Arthrotomy: risks and benefits
TREATMENT
• Principle:
Antibiotics
Joint drainage
Joint rest
JOINT REST
General support:
analgesics, antipyretics and joint splintage
for first few days.
GUIDELINES
Are intra-articular antibiotics preferred
over systemic antibiotics?
Intra-articular antibiotics are not
recommended because effective parenteral
or oral therapy produces adequate levels of
antimicrobial agents in joint fluid.
In addition, direct instillation of antibiotics
into a joint may cause an inflammatory
response
How can the risk of septic arthritis be decreased
in hospitalized patients?
• 1. Prompt treatment of local skin infections
• 2. Prompt identification and control of bacteremia.
• 3. Removal of intravenous catheters as soon as
possible, and only placing such catheters when
needed.
• 4. Exercising discretion regarding the use of intra-
articular corticosteroid injections and invasive
orthopedic procedures in patients at high risk for septic
arthritis.
What can be done to alter morbidity and
mortality associated with septic arthritis?
• 1. Joint aspiration for a synovial fluid sample before
initiation of antibiotics.
• 2. Initiation of empiric antibiotic therapy as soon as
possible
• 3. Adjustment of antibiotic therapy as soon as synovial
fluid culture and susceptibility results are available.
4. Prompt drainage of the infected joint
5. Monitoring response to therapy with serial
synovial fluid analyses with or without serum
inflammatory markers (ESR, CRP).
6. Treatment with antibiotics for at least 3 to 4
weeks, with initial parental therapy.
COMPLICATIONS
Partial or complete destruction of
epiphysis.
Retarded growth
Ankylosis
Osteomyelitis
Sepsis
PATHOPHYSIOLOGY
PROGNOSIS
Poor outcome predictors:
Age older than 60 years
Infection of hip or shoulder
Underlying RA
Persistent positive findings.
Delay in therapy.
PROGNOSIS
Irreversible loss of joint function in 25-
50%
Mortality ranges from 5-15%6.
KEYPOINTS
• Acute monoarthritis – EMERGENCY!
• Untreated septic arthritis  rapid joint
destruction
• Consider septic arthritis in patients with
underlying inflammatory arthritis if one joint
is more acutely inflamed than the others
• Aspiration of the involved joint is critical to
identifying the organism
KEYPOINTS
• Thank you

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Infectious arthritis

  • 1. A Rheumatology & Infectious Joint Conference by Gresaneth Claire Lumasag, MD Jennifer Cabanilla, M.D 20 September 2017 West Visayas State University MedicalCenter Department of Internal Medicine
  • 2.
  • 3. I. 1. Present a case of a 75 y.o with left knee pain 2. Discuss approach to monoarthritis, specifically on infection related arthritis as to  Diagnosis  Pathophysiology  Etiologic agents  Management  Prognosis  Prevention objectives II. a. Complications b. Ethical, Moral Decision-making
  • 4. • 75/ F • Tubungan, Iloilo • Roman Catholic
  • 5. Left Knee pain for 4 days following a simple gardening chores
  • 6. CASE 4 days PTC Day of Consult ✓Pain of left knee, aggravated by movement, VAS 5/10 ✓Swelling and warm to touch ✓Increasing severity of left knee pain, with limitation of ROM, VAS 8- 9/10 ✓Fever A D M I S S I O N
  • 7. (+) S/P STROKE WITH RESIDUAL LEFT SIDED WEAKNESS 4/5 MAINTENANCE: ASA 80MG/TAB 1 TAB OD LOSARTAN 50MG/TAB 1 TAB OD (-) PREVIOUS SURGERY OR ADMISSION (-) TRAUMA Past medical history
  • 8. (+) Hypertension- mother (-) DM (-) BA (-) CA Family history
  • 9. • Housekeeper • 10 pack-year smoker • Non-alcoholic drinker • Single parent Personal & Social History
  • 10. At the emergency room  wheelchair-borne  Grimacing in pain  Not in pulmonary distress • VITAL SIGNS • BP 100/60 MMHG • CR 106 BP M • RR 18 CPM • O2 SAT 98% AT ROOM AIR • BMI 20
  • 11. Skin: Fair skin, (+) brownish hyperpigmentation on extremities HEENT: Anicteric sclerae, pinkish conjunctiva, pupils 2-3mm equally reactive to light and accommodation, no cervical lymphadenopathies Chest and Lungs: Symmetrical Chest expansion, equal vocal and tactile fremiti, clear breath sounds Heart: Adynamic precordium, PMI at 5th left intercostal space MCL, normal cardiac rate and regular rhythm, no murmurs Abdomen: Flat, no striations noted, hypoactive bowel sound, soft abdomen, (-) organomegaly, (-) ascitic fluid wave, (-) direct tenderness (-) rebound tenderness Physical examination
  • 12. Extremities: •LKJ (+) swelling grade 3 • (+) redness • (+) warm to touch, • (+) limitation of • movement Physical examination
  • 14. HOWto APPROACH APATIENT presenting WITH acute monoarthritis?
  • 15. History and physical examination Is it articularTrauma/fracture Soft tissue rheumatism no > 6 weeks yes Chronic yes Acute Infectious arthritris Crystal induced Reactive arthritis No Signs of inflammation Chronic noninflamatory arthritis DIP, CMC1,Hip ,Knee joint osteoarthritis yes Osteonecrosis Charcots joint no yesChronic inflammatory arthritis Joints involved 1-3 Psoriatic symmetrical >3 Psoriatic Reactive no yes PCP,MCP/MT P yes Rheumatoid no SLE/Scleroderma no
  • 16. Differential Diagnosis: Infectious (Septic Arthritis)- a direct invasion of joint space by various microorganisms, most commonly caused by bacteria. Crystal induced- an intensely painful type of arthritis that occurs mainly in the joints of the big toe. It can also attack the top of the foot and ankle. Reactive (Infection-related arthritis)- an infection in another party of the body – usually the intestines, genitals or urinary tract – triggers an inflammatory response in the joints.
  • 18.
  • 19. Synovial Fluid Result Amount 5 cc Color Yellow with blood tinge Transparency purulent Cell count 80448 RBC count 380 Segmenters 82% Lymphocytes 8% Gram stain Many pus cells. Occasional gram negative bacilli and gram positive cocci in singles and in pairs
  • 20. On Admission Result Normal Hemoglobin 139 g/L 120-160 Hematocrit 0.41 L/L 0.37-0.47 WBC 27.11 4.5-11 Segmenters 0.93 0.50-0.70 Lymphocytes 0.03 0.20-0.40 Platelet 266 150-450 ESR 125 0- 10 A.L.
  • 21. Infectious arthritis, - direct invasion of joint space by various microorganisms (bacteria, viruses, mycobacteria & fungi) Rheumatologic emergency as joint destruction occurs rapidly and can lead to significant morbidity and mortality. Septic arthritis
  • 23. Etiologic Agents of infectious Arthritis • Acute – Monoarticular • Staphylococcus aureus • Streptococcus pneumoiae • Β-Hemolytic streptococci • Gram Negative bacilli • Neisseria gonorrhoeae • Candida spp – Polyarticular • Immunologic reaction (endocarditis, rheumatic fever, dessiminated nesserial infection, acute hepatitis B) • Chronic – Mycobacterium tuberculosis – Non tuberculous mycobacteria – Borrelia burgdoferi – Treponema pallidum – Candida spp – Sporothrix schenckii – Coccioides immitis – Blastomyces dermatitidis – Aspergillus spp – Cryptococcus neoformans – Nocardia spp – Brucella spp
  • 24. Infectious arthritis, - direct invasion of joint space by various microorganisms (bacteria, viruses, mycobacteria & fungi) Rheumatologic emergency as joint destruction occurs rapidly and can lead to significant morbidity and mortality. Septic arthritis
  • 25.
  • 26.
  • 27. Treatment Antibiotics + Drainage with Culture IV VancomycinIV 3rd Gen Cephalosporin MRSA ? yes Oxacillin or Nafcillin Definitive therapy is based on Isolated organism and antibiotic susceptibility no
  • 28. Treatment • Staphylococcal – oxacillin, nafcillin, vancomycin (4 weeks) • Pneumococcal and Streptococcal – penicillin-susceptible– Penicillin G (2 weeks) – Penicillin-resistant- Cefotaxime /Ceftriaxone (2 weeks) • Gram Negative – 2nd or 3rd gen Cephalosporin IV or IV Flouroquinolone (3-4 weeks) • Pseudomonas – combination aminoglycoside+ extended spectrum penicillin or antipseudomonal cephalosporin (4 weeks) • Gonococcal –IV/IM Ceftriaxone q24H
  • 29. ❖Elderly >60 years ❖Diabetes mellitus ❖Rheumatoid arthritis ❖Prosthetic joint ❖Recent joint surgery ❖Skin infection, cutaneous ulcers ❖IV drug abuse, alcoholism ❖Previous intra-articular injection PREDISPOSING FACTORS
  • 30. RISK FACTORS  Age > 60 y.o  female  Recent Bacteremia  Degenerative joint disease  Rheumatoid Arthritis  Corticosteroid therapy  Co-morbidities (DM, Cirrhosis, Renal Disease)  Immunocompromised State (eg. HIV) Hematogenous Spread Direct Introduction Extension from Contiguous site Of infection Recent Trauma/ Injury Bacterial Seeding within the space Bacterial Adherence and Colonization
  • 31. • Blood- WBC, CRP, ESR- low specificity; suggestive but not diagnostic • WBC>10 000 • ESR>30 • CRP>100 DIAGNOSTICS: What to Request?
  • 32. DIAGNOSIS • Synovial fluid usually purulent with increased count (50,000 to 150,000 cells/mm3) The synovial fluid glucose is often depressed and lactic acid concentration is elevated.
  • 34. OTHER DIAGNOSTIC MODALITIES • X-ray, CT, MRI: less helpful in diagnosis The earliest findings are soft tissue swelling around the joint and a widened joint space from joint effusion. Can demonstrate: joint effusion Synovial thickening Perisynovial edema Cartilage destruction Bone destruction Bursitis, tenosynovitis
  • 35. DIAGNOSIS  Blood cultures are positive in about 50 percent of cases. Blood culture: NO GROWTH
  • 36. TREATMENT The first priority is to aspirate the joint and the fluid. Treatment is then started without further delay!
  • 38.
  • 39. Duration of Treatment • No controlled trials • Usually IV antibiotics at least 2 weeks in duration followed by at least two weeks oral therapy • May need longer for particular organisms- P. aeruginosa, Enterobacter spp. or S. Aureus with septicaemia
  • 41. Joint Drainage • Aim to remove pus from joint space- i.e. drain abscess – Surgical: arthroscopy or arthrotomy – Closed needle aspiration
  • 42. Indication of Surgical Drainage 1. Joints that do not respond to antimicrobial therapy and daily arthrocentesis 2. Any joint with limited accessibility, including the sternoclavicular joint or the hip joint 3. Patients with underlying disease, including DM, RA, immunosuppression, or other systemic symptoms, should be treated aggressively with earlier surgical intervention
  • 43. 2nd Hospital Day (+) abdominal pain (+) vomiting (+) cold clammy extremities Rpt ECG: ST elevation high lateral wall Trop I: 27
  • 44. • ECG: • Assessment: Acute Coronary Syndrome- ST Elevation MI- lateral wall
  • 47. JOINT REST General support: analgesics, antipyretics and joint splintage for first few days.
  • 49. Are intra-articular antibiotics preferred over systemic antibiotics? Intra-articular antibiotics are not recommended because effective parenteral or oral therapy produces adequate levels of antimicrobial agents in joint fluid. In addition, direct instillation of antibiotics into a joint may cause an inflammatory response
  • 50. How can the risk of septic arthritis be decreased in hospitalized patients? • 1. Prompt treatment of local skin infections • 2. Prompt identification and control of bacteremia. • 3. Removal of intravenous catheters as soon as possible, and only placing such catheters when needed. • 4. Exercising discretion regarding the use of intra- articular corticosteroid injections and invasive orthopedic procedures in patients at high risk for septic arthritis.
  • 51. What can be done to alter morbidity and mortality associated with septic arthritis? • 1. Joint aspiration for a synovial fluid sample before initiation of antibiotics. • 2. Initiation of empiric antibiotic therapy as soon as possible • 3. Adjustment of antibiotic therapy as soon as synovial fluid culture and susceptibility results are available.
  • 52. 4. Prompt drainage of the infected joint 5. Monitoring response to therapy with serial synovial fluid analyses with or without serum inflammatory markers (ESR, CRP). 6. Treatment with antibiotics for at least 3 to 4 weeks, with initial parental therapy.
  • 53. COMPLICATIONS Partial or complete destruction of epiphysis. Retarded growth Ankylosis Osteomyelitis Sepsis
  • 55. PROGNOSIS Poor outcome predictors: Age older than 60 years Infection of hip or shoulder Underlying RA Persistent positive findings. Delay in therapy.
  • 56. PROGNOSIS Irreversible loss of joint function in 25- 50% Mortality ranges from 5-15%6.
  • 57. KEYPOINTS • Acute monoarthritis – EMERGENCY! • Untreated septic arthritis  rapid joint destruction
  • 58. • Consider septic arthritis in patients with underlying inflammatory arthritis if one joint is more acutely inflamed than the others • Aspiration of the involved joint is critical to identifying the organism KEYPOINTS

Editor's Notes

  1. When to do arthrotomy When to start anticoagulant
  2. Psoriatic arthritis is a form of arthritis that affects some people who have psoriasis — a condition that features red patches of skin topped with silvery scales. Most people develop psoriasis first and are later diagnosed with psoriatic arthritis, but the joint problems can sometimes begin before skin lesions appear. Reactive arthritis, formerly referred to as Reiter's syndrome, is a form of arthritis that affects the joints, eyes, urethra (the tube that carries urine from the bladder to the outside of the body), and skin. Reactive arthritis primarily affects sexually active males between the ages of 20 and 40. Those with HIV (human immunodeficiency virus) are at a particularly high risk. n sexually active males, most cases of reactive arthritis follow infection with Chlamydia trachomatis or Ureaplasma urealyticum, both sexually transmitted diseases. Rheumatoid arthritis is a destructive joint disease that is caused by inflammation in the tissue that normally produces lubrication fluid for joints. When this tissue remains inflamed, it leads to deformity by loosening joint ligaments and to joint destruction by eroding away cartilage and bone. Osteoarthritis is a noninflammatory joint disease whereby the cartilage of the joint thins, typically asymmetrically -- so only one knee or hand may be affected. Lupus is systemic, meaning that it affects a wide part of the body, including the joints, kidneys, skin, blood, brain and other organs. Nearly all joints can be affected by SLE, but hand and knee involvement are the most typical. Periarticular structures can be inflamed leading to tendonitis, tenosynovitis and tendon rupture. Avascular necrosis (AVN) also occurs causing joint pain and disability, typically in larger joints such as the hip and knee. Scleroderma often begins with Raynaud’s phenomenon (see below) – the fingers and sometimes the toes lose circulation and turn white upon exposure to cold. Raynaud’s phenomenon usually (but not always) precedes skin changes by several months with diffuse scleroderma and often precedes skin changes by several years with limited scleroderma. Other early symptoms may be painful joints, morning stiffness, red swollen hands, fatigue, and/or weight loss. Charcot joint or neuropathic joint, Charcot arthropathy is a progressive condition of the musculoskeletal system that is characterized by joint dislocations, pathologic fractures, and debilitating deformities Charcot neuropathy is a progressive deterioration of weight-bearing joints, usually in the foot or ankle
  3. Unlike septic arthritis, however, the infection itself is not present in the joint. Reactive arthritis- a sterile inflammatory process that may result from an extra-articular infectious process.
  4. source
  5. source
  6. Can be bacterial, fungal, mycobacterial or viral Bacterial divided into gonococcal and nongonococcal Gonococcal more common but less morbidity and mortality Staphylococcus Streptococcus
  7. Direct inoculation occurs through trauma, joint surgery, or bite wounds
  8. The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility. Ultrasonography is the most reliable method for revealing a joint effusion in early cases. Both hips should be examined for comparison. Widening of the space between capsule and bone of more than 2 mm s indicative of an effusion, which may be echo-free (perhaps a transient synovitis) or positively echogenic (more likely septic arthritis).
  9. The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility. Ultrasonography is the most reliable method for revealing a joint effusion in early cases. Both hips should be examined for comparison. Widening of the space between capsule and bone of more than 2 mm s indicative of an effusion, which may be echo-free (perhaps a transient synovitis) or positively echogenic (more likely septic arthritis).
  10. The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
  11. The synovial fluid glucose is often depressed and lactic acid concentration is elevated; however, these tests are not sufficiently sensitive to be of widespread diagnostic utility.
  12. Prompt treatment of local skin infections (including cellulitis and cutaneous ulcers), especially those that overlie joint surfaces. CLINICAL GUIDELINES BSR1, BHPR2, BOA3, RCGP4, and BSAC5 guidelines for management of the hot swollen joint in adults. Rheumatology 2006;45:1039–41. Infectious Diseases Society of America. Diagnosis and management of prosthetic joint infection: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2013;56:e1–25. 1 British Society for Rheumatology. 2 British Health Professionals in Rheumatology. 3 British Orthopaedic Association. 4 Royal College of General Practitioners. 5 British Society for Antimicrobial Chemotherapy.
  13. 2. Initiation of empiric antibiotic therapy as soon as possible, guided by the most likely infecting organisms and the result of the synovial fluid Gram stain.
  14. Bacteria entering the joint initially deposit in the synovial membrane and produce an acute inflammatory cell response. Because synovial tissue has no limiting basement plate, bacterial organisms may quickly gain access to the synovial fluid, characteristically creating acute-onset, purulent joint inflammation. there is marked hyperplasia of the lining cells in the synovial membrane within seven days. In addition, inflammatory cells release cytokines and proteases that cause cartilage degradation and inhibit cartilage synthesis. Pressure necrosis from large synovial effusions may result in further cartilage and bone loss.
  15. Positive findings on synovial fluid cultures after 7 days of appropriate therapy Delay of 7 days or longer in instituting therapy
  16. Acute monoarthritis should be evaluated emergently to rule out possibility of septic arthritis. Untreated septic arthritis can lead to rapid joint space destruction and systemic sepsis, so early diagnosis is imperative