bone and joint infections

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BONE AND JOINT INFECTIONS. นพ. ยอดปิติ ตั้งตรงจิตร กลุ่มงานศัลยกรรมกระดูก โรงพยาบาลแพร่ 3 ตุลาคม 2555. SEPTIC ARTHRITIS. Septic Arthritis. Epidemiology ~2 to 10/100,000 in general population ~30-40/100,000 in RA ~40-68/100,000 in joint prostheses 2 age peaks : < 5 years , > 64 years. - PowerPoint PPT Presentation

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BONE AND JOINT INFECTIONS

นพนพ . . ยอดปิ�ติ ติ��งติรงจิติรยอดปิ�ติ ติ��งติรงจิติรกลุ่��มงานศั�ลุ่ยกรรมกระด�ก โรงกลุ่��มงานศั�ลุ่ยกรรมกระด�ก โรงพยาบาลุ่แพร�พยาบาลุ่แพร�

3 3 ติ�ลุ่าคม ติ�ลุ่าคม 255525551

SEPTIC ARTHRITISSEPTIC ARTHRITIS

2

Septic ArthritisSeptic Arthritis

• Epidemiology~2 to 10/100,000 in general population

~30-40/100,000 in RA

~40-68/100,000 in joint prostheses

• 2 age peaks : < 5 years , > 64 years

3

• knee 40-50%

• hip 20-25%

• Shoulders, ankles, elbows 10-15%

• wrist 10%

• in infants and very young children, hip is the most common joint infection.

4

Definition Definition • Acute - < 14days• Subacute – 2-6 wks• Chronic - > 6wks

• Monoarthritis – 1 joint• Oligoarthritis – 2-3 joints• Polyarhritis - > 4 joints

5

Acute MonoarthritisAcute Monoarthritis

Crystal-induced synovitis

Septic arthtitis

Acute traumatic and hemorrhagic arthritis

Acute presentation of systemic rheumatic diseases eg.RA, SNSA

Other rheumatic disorders – Adult still’s disease

6

MicroorganismsMicroorganisms

• Bacteria - the most important – Neisseria– Non-neisseria

• Viruses • Fungi • Parasites

7

Gram-Positive CocciGram-Positive Cocci

Streptococci• S. pyogenes (beta-hemolyticus group A) • S. pneumoniae • Group B and G hemolytic Streptococci.

Staphylococci • Staph. aureus • Staphylococcus epidermidis

8

Gram Negative OrganismGram Negative Organism

Neisseria

• Neisseria gonorrhoeae – septic or reactive forms of

arthritis,

• N. meningitidis,

9

Gram Negative OrganismGram Negative Organism

Non- Neisseria • Haemophilus influenzae • Gram-negative rods

– Enterobacteriaceae• E. coli • Shigella • Salmonella • Yersinia • Klebsiella pneumoniae.• Proteus mirabilis • Pasteurellaceae ( Pasteurella multocida)• Campylobacter jejuni

10

• Viruses– HIV – parvovirus B19 – herpes viruses – adenoviruses

• Anaerobes– Clostridium– Eubacterium – Propionibacterium – Bacteroides– Fusobacterium

Others • Mycobacterium • Nocardia. • Spirochetes• Borrelia burgdorferi

( Lyme disease)• Chlamydias• Mycoplasmas and

Ureaplasma. • Fungi, Parasites

11

Bacterial isolationBacterial isolation

Organism Percentage of cases Staphylococcus aureus 40–50

Staphylococcus edidermis 10–15

Streptococcal species 20

Gram-negative bacteria 15

S. pneumoniae 2

H. influenzae 2

Anaerobes 5 12

Microbiology

13

14

Clinical features

• Acute bacterial infection– Fever 60%-80% (< 39°c )– Monarticular : inv. 90%– Limited ROM– Swelling (seen synovial effusion)– Most common : knee > hip – Refusal walk ,limping, Irritability,

failure to thrive, asymmetry of limb position

15

Clinical FeaturesClinical Features

• Systemic symptoms - neonatal period– High fever – sepsis

• local signs – children, adult– Pain– Swelling – Erythema and warm – Limitation of movement

16

17

18

19

• Predisposing factors. 1) prosthetic joint. 2) age> 60 yrs. 3) present underlying jt. disease( RA, much less

for OA ). 4) co morbidity( malignancy, DM, alcoholism,

cirrhosis, hemophilia) 5) use of immunosuppressive drug. 6) skin infection.

20

Predisposing FactorsPredisposing Factors

Abnormal joint RA Crystal induced

synovitis Prosthetic joint Severe OA Severe Charcot’s joint Severe hemarthrosis Intrarticular injection

Abnormal host Chronic systemic

disease - DM ,SLE, CRF, liver disease

HIV IVDU Chronic steroid therapy Malignancy Old age New born

21

Risk factors for the development of joint sepsis

• rheumatoid arthritis (RA) or osteoarthritis• prosthetic joints• low socioeconomic status• intravenous drug abuse• alcoholism• diabetes• previous intra-articular corticosteroid injection• cutaneous ulcers

22

Differential diagnosis

23

PathogenesisPathogenesis

• Mechanism– Hematogenous route.

• Skin, oral cavity, respiratory tract, urinary or intestinal tract infections, or endocarditis.

– Dissemination from metaphysis or epiphysis. – Vicinity of the joint – Iatrogenic or penetrating trauma

24

Source of infection

25

Hematogenous spreadSystemic bacteremia

Invade synovial cartilaginous junction

Synovial infected

Increase inflammatory cell

Destruction of the articular cartilage

Joint dislocation, subluxation, osteomyelitis 26

1. Hematogenous route. 2,3 Dissemination from bone

4. Vicinity of the joint 5. Iatrogenic or penetrating trauma 27

SynoviumBacteria

Inflammation

Pannus

Leukocytes migration Synovial cell proliferation

Blood flow Exudation Enzymes

Erythema Swelling DestructionTenderness

Irreversible destruction 28

InvestigationsInvestigations

• CBC,ESR,CRP • Blood culture• Synovium fluid• Plain radiographs ( 2-3 weeks or more) • Scintigraphy

– 99mTc phosphate (three-phase bone scan) – 99mTc nanocolloid scanning – Indium 111-labeled leukocytes

• Computed tomography (CT) • Magnetic resonance imaging (MRI)

29

Laboratory

• CBC

- often normal.

- predominance of segmented neutrophil.

• ESR ( erytrocyte sedimentation rate)

- elevation, but not specific for infections.

- present for less than 48 hr, return to normal ~3 weeks.

30

time

level

24 48 72

CRP

ESRxx

Subside

3-5days

31

Laboratory• CRP ( C- reactive protein).

- elevation.

- inc. within 6 hr, return to normal 1 week after treatment began.

- better way to follow the response to ATB.

• Blood culture

- positive~ 50%-70%.

32

Laboratory

• Synovial fluid analysis

- should be aspirated immidiately if there is suspicious.

- recommended: crystals examination.

33

DiagnosisJoint aspiration

disease WBC % PMN

normal <200 <25

traumatic <5,000+rbc <25

Toxic synovitis 5,000-15,000 <25

Acute rheumatic 10,000-15,000 50

JRA 15,000-80,000 75

Septic arthritis >80,000 >7534

Synovial fluidSynovial fluid

Method Percent

Gram positive

Gram negative

N. gonorrhea

Gram strain 80 50 25

Synovial C/S 80-90 60-70 40

35

36

Streptococci37

Neisseria gonorrhoeae38

Radiologic EvaluationRadiologic Evaluation

Initial plain x-ray baseline assessment exclude osteomyelitis

Definitive changes usually take a number of weeks

Rapidity depends on virulence of organism

39

Radiologic EvaluationRadiologic Evaluation

Earliest : joint effusion with displacement of fat padDuring first week

– periarticular osteoporosis Within 7-14 days

- joint space narrowing & erosions

>20days: bone destruction40

41

Radiologic EvaluationRadiologic Evaluation

periarticular osteoporosis 42

Radiologic EvaluationRadiologic Evaluation

joint space narrowing & erosions 43

Radiologic EvaluationRadiologic EvaluationCT / MRIDifficulty to evaluate clinically Complex anatomical structure

( hip, shoulder, SC jt, SI jt ) Early bony erosions, soft tissue extension

Bone scanAxial joints infectionssensitivityCannot differentiate septic from aseptic Jt. 44

Laboratory

• CT scan– good definition of contiguous bone lesions

and ability to guide needle aspiration

• MRI– better defines soft tissue (distended joint

space and extension to periarticular structures)

45

Laboratory• Radionuclide

- physiologic picture.

- reflect inflammatory change/ reaction of bone to infection.

- 3 most common use

1) Technitium 99m phosphate.

2) gallium 67 citrate.

3) indium 111-labled leukocytes.46

Bone scan

47

Polyarticular Septic ArthritisPolyarticular Septic Arthritis

15% 50% RA

systemic illness/IVDU Most common

S.aureusGroup G streptococcusH.influenza S. Pneumoniae Polymicrobial

30% died!!49

TreatmentPrinciple in the management of acute septic arthritic

(Nade )

1. Joint must be adequately drained

2. Antibiotic must be given to diminish the systemic effects of sepsis

3. Joint must be rested in a stable position

50

Treatment.1. synovial analysis and blood cultures before IV a

ntibiotic treatment2. rapid administration of IV antibiotics IV oxacillin in combination with IV ceftriaxone, cefotaxime, or ceftizoxime. 3. drainage of the septic joint4. evaluation5. Arthroscopic drainage or arthrotomy

51

Treatment & OutcomeTreatment & Outcome

ATB should be started as soon as

ATB selected on the basis of gram

stain and clinical picture

Adjust ATB on the basis of sensitivity,

toxicity and cost

Most iv ATB at least 2 weeks ,followed

by 1-2 weeks of oral ATB52

53

Organism ATB of choice Alternative

S. Aureus

MRSA

Cloxacillin

Vancomycin

Cefazilin,clindamycin

Streptococcus

Group A

non group A

pneumococci

Penicillin

PG + aminoglycoside

Penicillin

Cefazolin

Cefazolin + aminoglycoside

vancomycin

N. Gonorrhea 3rd cephalosporin Ciplofloxacin, olfloxacin

H. Influenza Amox. + calvulanate 3rd cephalosporin, Ciplofloxacin

Enterobacteria 3rd cephalosporin Imipenem

Ps. Aeruginosa Antipseudomonas Imipenem

Anaerobe Metronidazole, doxycycline

Clindamycin

54

Treatment• Recommendation for arthrotomy/ arthroscope

1) Hip joint.

2) Immunocompromised host

3) Joint that are difficult to access: sacroiliac, sternoclavicular jt.

4) Difficult to completely drain: shoulder, wrist.

5) Close needle aspiration> 7 days.

6) P.aeruginosa or gram negative bacteria.

55

Treatment• Recommendation for arthrotomy/ arthroscope

7) Sepsis

8) Extension into soft tissue or secondary

osteomyelytis

9) Fungal infection

10) Prosthetic or FB

11) Unresponse to ATB

12) Superimpose on joint disease - RA

56

Closed needle aspiration should be the initial Rx of choice

Serial synovial fluid c/s & wbc count

Acute,suppurative phase : sling/splint/cast should be used to maintain

the joint in optimal position

: muscle-tightening exercises

57

Poor prognosis factors– Immunodeficiency– RA – prematurity – osteomyelitis, – hip – prosthetic infections– + blood cultures,– symptoms >1 week,– >4 joints,– + cultures after aspiration after 7 days of abx tx

58

Complication

– arthritis stiffness

– Dislocation or subluxation

– AVN

– local growth distrubance

– Osteomyelitis

– postinfection synovitis

59

Postinfectious arthritis

recurrent inflammatory when begin

ambulate, but sterile effusion

DDx - incompletely treated infection

NSAIDs

60

Results of Rx 10-15% mortality 25-50% chronic joint damage & disability

Poor outcome Persist/ Recurrent infection Marked decrease ROM/ankylosis Persistent pain

Outcome Outcome

61

Factors associated to poor outcome Duration of infection

Virulense of bacteria

The infected joints

Host defences

Age of patient

Comorbidity

Effective therapy

62

OSTEOMYELIS

63

Osteomyelitis

• Inflammation of the bone by organism.

– single portion.

– surrounding regions ; marrow , cortex & periosteum

64

Classification

1. Acute , subacute , chronic

2. Exogenous , hematogenous

3. Pyogenic , nonpyogenic

4. Neonate , children , adult

65

Source of infection •Blood circulation :

– infection in Oral, Throat, Ear, Gastrointestinal tract, Urinary tract, Skin and soft tissue

•Trauma (30-50%)– หกล้�ม กระแทก– Minor traumaCaution : in infant < 18 month ม�กเก ด

septic arthritis ร�วมก�บ Osteomyelitis 66

Acute Hematogenous Osteomyelitis

• Most common usually seen in children.

• Infection involve the metaphyses of rapidly growing long bones

67

Natural history and Pathogenesis of Acute hematogenous osteomyelitis

•Almost at “metaphysis”– lower extremities > upper

extremities 5 เท�า โดยเฉพาะท�� di st al f e mur แล้ะ proximal tibia

– met aphysi s ( no phagocytosis cell) ≠ diaphysis (diaphysis = reticuloendot

hel i al t i ssue +phagocyt osi s cel ls)

68

Why organism seeding the metaphyses ?

• nutrient capillaries form sharp loops to establishment of infection

• metaphysis has relatively fewer phagocytetic cell than the physis or diaphysis.

69

Pathogenesis

Source of Infection

Metaphysis

Bacterial colonization

Blood stream

Venous stasis

70

Inflammation: acute osteomyelitis • First 24 hours

• Vascular congestion• Polymorphonuclear leukocyte

infiltration• Exudation

71

• 2-3 day No treat with antibiotic

Intraosseus pressure intense pain

intravascular thrombosis ischemia

เด�กจิะร�องปิวดมาก

Inflammation: acute osteomyelitis

72

Suppuration 4-5 days Pus formation Subperiosteal abscess

via Volkmann canals Pus spreading

epiphysis joint medullary cavity soft tissue

73

Necrosis

• Bone death by the end of a week

• Bone destruction ← toxin ← ischemia

• Epiphyseal plate injury• Sequestrum formation

– small removed by macrophage,osteoclast.

– large remained74

New bone formation• By the end of 2nd week

(10 – 14 days)

• Involucrum (new bone formation from deep layer of periosteum ) surround infected tissue.

• If infection persist- pus discharge through sinus to skin surface Chronic osteomyelitis 75

PrimaryPrimary osteomyelitisosteomyelitis76

PrimaryPrimary osteomyelitisosteomyelitis

77

• Children < 2 yr. blood vessel cross the physis & spread infection into epiphysis.

• Children > 2 yr. , the physis effectively barrier to spread.

78

• In adult , after the physes closed , acute osteomyelitis is less common ; ; infection extend directly metaphysis to epiphysis to joint & hematogenous seeding in compromised host

79

• Spread to joint in children < 2 yr. , most commonly is hip joint . ( proximal humerous , radius neck , distal fibular are intraarticular , can lead to septic arthritis. )

80

Diagnosis

• History , Physical exam.

• Clinical : fever , malaise , fatigue , irritability , pain , local tenderness , swelling , restriction of movement

81

82

• Investigation : X- Ray , WBC , ESR , CRP , Bone scan , MRI , Blood culture , Bone aspiration for gram strain , culture & sensitivities.

83

X-ray soft tissue swelling , periosteal reaction , bony destruction , 10–12 day after onset.

WBC often normalESR elevatedCRP elevated

84

• Bone scan can confirm diagnosis 24-48 hr. after onset.

• MRI show early inflamation changes in bone marrow and soft tissue

85

Treatment acute osteomyelitis

• Sequestered abscesses drainage.

• Simple inflammation without abscess ; antibiotic based on Gram strain

• Gram strain not found ; empirical antibiotics for most likely organism.

• CRP every 2-3 days

86

Two main indications for surgery

• abscess requiring drainage.

• failure iv antibiotic treatment. ( no clinical response 24-48 hr. )

87

Nade proposed five principles for treatment

1. appropriate antibiotic will be effective before pus formation.

2. avascular tissues or abscesss require surgical remove.

3. if such removal is effective , antibiotics should prevent their reformation & primary wound closure should be safe.

88

4. surgery should not further damage already ischemic bone & soft tissue.

5. antibiotics should be continuous after surgery.

89

Organism

Patient Type Propable Organism

NeonateGrp. B Strep , S. aureus , Gram-neg. rod (H. influenza)

Infants & children S. aureus

Sickle cell disease S. aureus , Sallmonella

90

Antibiotic

• Appropriate ; infection type , organisms , sensitivity , host , antibiotic

• Iv 4 – 6 wk. , switch iv 1 wk. + oral 6 wk.

91

Subacute osteomyelitis

• insidious onset & lacks the severity of symptom

• diagnosis delayed for more than 2 wks.

• systemic signs & symptoms are minimal.

• WBC normal

• ESR elevation ( 50% )

• blood culture ; usually negative.

92

• bone aspirate or biopsy ; 60% pathogen identified

• x-ray & bone scan ; positive.

• course ; increased host resistance , decreased bacterial virulence ,

antibiotic before the onset of symptom.

• differentiation lesion from a primary bone tumor.

93

Classification of subacute osteomyelitis

94

DifferentialType

I Langerhans’cell histiocytosis , Brodie abscess

II Eosinophilic granuloma , Osteogenic sarcoma

III Osteoid osteoma

IV Ewing sarcoma

V Chondroblastoma

VI Tuberculosis ; osteogenic sarcoma

95

Treatment subacute osteomyelitis

• Ross & Cole recommended biopsy & currettage aggressive lesions and antibiotics.

• biopsy not recommended in simple abscess lesion

96

Chronic osteomyelitis• Systemic symptom subside ; bone

contain purulant material , infection tissue

• Intermittant acute exacerbation ; respond antibiotic & rest

• Multiple organism ; culture & biopsy

97

98

Cierny & Mader Staging System for Chronic Osteomyelitis

Anatomical type

I Medullary

II Superficial

III Localized

IV Diffuse

Physiological class

A host Normal

B host Compromised

C host Prohibitive99

100

Diagnosis

• Gold standard ; biopsy , microbiological

• PE. skin , soft tissue , neurovascular

• ESR & CRP ; elevation

• WBC ; normal

• X-ray ; cortical destruction , periosteal reaction

• Bone scan

• MRI

101

Treatment

• Sequestrectomy , resection scar & infection bone

• Antibiotics 6 wk. ( 1 wk. for iv , 6 wk. for oral form)

• Reconstruction of bone & soft tissue ( bone graft , bone transfer , myoplasty , flap )

102

103

Fracture management

•Active infection ; sequestrectomy , debridement , antibiotics ( > 6 m.) & immobilization

•Active infection without involucrum ; debridement , bone graft , antibiotics & immobilization

•Inactive infection & no involucrum ; immobilization & bone graft.

104

Amputation for osteomyelitis

• malignant change

• arterial insufficiency , major nerve paralysis , joint stiffness

105

106

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