Osteomyelitis, Myositis, Pyomyositis, Myonecrosis Flashcards

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1
Q

What is osteomyelitis?

A

infection localized to bone characterized by bone destruction, formation of sequestra (dead bone) caused by production of local inflammatory mediators that promote necrosis

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2
Q

What is the most common cause of OM? Why?

A

Staph aureus because it expresses high-affinity adhesions to components of bone matrix that express fibronectin, laminin, and collagen

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3
Q

How does OM present?

A

can get vague symptoms including non-sepecific pain around the involved site with absence of systemic signs (i.e. fever/chills, local swelling, erythema around site UNCOMMON but can be seen)

-draining sinus tracts can present

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4
Q

How is OM diagnosed? Standard of care for diagnosis?

A

in a radiograph, you might be able to see abnormalities 10-14 days after infection onset. However, MRIs (below) and CT are considered SOC (expensive, but very sensitive)- will show inflammation and bone destruction

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5
Q
A

Sequestrum: dead bone

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6
Q

Why are sequestra formed?

A

infection in the bone leads to an increase in intramedullary pressure due to inflammatory exudates, vascular thrombosis ensues and bone necrosis follows due to lack of blood supply= sequestra are formed

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7
Q

Diagnosis rules for OM

A

IDing the organism is important to help optimize medical therapy (best accomplished by surgical sampling or needle aspiration using radiologic guide to obtain tissue for pathology and culture)

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8
Q

Common causes of OM?

A
  • common (S. aurues, Coag neg staph (S. epi))
  • some (Streptococci, Enterococci, MTB, anaerboes)
  • rare (dimorphic fungi)
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9
Q

OM caused by someone stepping on a nail is most likely _____

A

Pseudomonas

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10
Q

Treatment of OM?

A

Remove hardware, drain/debride and start ABX

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11
Q

ABX DOC for OM?

A

-B-lactams (Cephalosporins and penicillinase-resistant penicillin commonly used due to low toxicity profile and spectrum of activity) and Vanc common

most given 4-6 weeks of IV therapy

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12
Q

Other options for OM ABX?

A
  • Linezolid for strep, staph, and VRE
  • Dapto against gram+
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13
Q

AE of Linezolid?

A

Prolonged use has been associated with significant pancytopenia (esp thrombocytopenia), peripheral neuropathy, optic neuritis, and lactic acidosis.

Use has been limited to patients with VRE or patients who are intolerant of Vanc.

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14
Q

How can vertebral osteomyelitis and spondylodiskitis occur?

A

these infections of intervertbral disks and adjacent vertebrae can arise from skin/soft tissue infection, GU tract infection, infective endocarditis, or post-operatively

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15
Q

How do vertebral osteomyelitis and spondylodiskitis present?

A

localized insidious pain/tenderness in spine area in 90% of patients, with fever sometimes, and nerve root compression/motor deficiencies common in only about 15% of patients

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16
Q

Most common causes of VO and spondylodiskitis?

A

S. aureus and Coag-neg staph

and MTB and Brucella in endemic regions

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17
Q

Diagnosis of VO or spondylodiskitis?

A

MRI is very useful in establishing diagnosis

Image-guided percutaneous biopsy sometimes helpful

If an epidural abscess (abscess enclosed within confines of spinal column, picture next slide) is present, it should be drained if possible

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18
Q

Osteopathies are common in DM and are commonly the result of vascular insufficiency. Why?

A

Neuropathy, vascular insufficiency and hyperglycemia lead to variety of consequences that lead to development of skin ulcer and osteomyelitis

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19
Q

What factors increase the risk of foot ulcers in DMs?

A

DM for 10+ years, poor glucose control, CV disease, retinal or renal complications, peripheral neuropathy, evidence of increased local pressure (callus), PVD

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20
Q

Treatment of ulcers in DM?

A
  • debride, revasculization
  • Broad-spectrum ABX required (zosyn, entrapenem, cephalosporins, quinolones)
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21
Q

Acute hematogenous osteomyelitis in children most commonly occurs where?

A

•Involves mostly metaphyses (due to its weird anatomy) of long bones with tibia or femur affected in most cases.

–Half of cases of neonatal OM also have involvement of adjacent joint with septic arthritis

22
Q

What causes acute hematogenous osteomyelitis in children?

A

Capillary ends of the nutient artery make sharp loops under the growth plate and feed into large venous sinusoids where blood flow becomes slow and turbulent. Obstruction of these capillaries (due to any minor trauma) can lead to areas of avascular necrosis and allow the entry of bacteria

23
Q

Most common causes of acute hematogenous OM in children?

A

S. aureus and S. pneumoniae

and GBS and E. Coli in neonates

24
Q

How is AHOM in children treated?

A

mostly cases with 3 weeks of ABX with switching to PO only when the patient becomes afebrile

25
Q

What are the common causes of OM in SCD?

A

Salmonella and S. aureus are the most common

MOST patients are children

26
Q

Why does OM occur in SCD?

A

–Capillary occlusion secondary to intravascular sickling may devitalize and infarct the gut, permitting Salmonella invasion. Reduced function of the liver and spleen suppresses clearing of these organisms from the blood stream

–Bone is also devitalized and serves as a nidus of infection

27
Q

OM in IVDU is common BUT the sites impacted are abnormal and thus good clues. What are some sites commonly affected by IVDU and not typical OM?

A

sternoclavicular, sternochondral joint, pubic symphysis

28
Q

Most common pathogens of OM in IVDU?

A

S. aureus, Pseudomonas, and Candida

Eikenella corrodens, normal oral flora bacterium, can cause OM in IVDU who lick the needle tip or skin before infection (“needle licker osteomyelitis”)

29
Q

MTB OM usually affects where?

A

•MTB osteomyelitis often affects the spine and most cases are the result of hematogenous spread from a pulmonary source

30
Q

How does MTB OM present?

A
  • Clinical: Pain and swelling with abscess and sinus formation
  • Vertebral osteo (Pott’s disease): among most common osteoarticular manifestations of TB.

–Systemic symptoms often absent. Back pain/stiffness commonly only symptom

31
Q

Diagnosis of MTB OM? How commonly does this happen in MTB infection?

A

Occurs in 1-5% of cases of TB.

Significant overlap in imaging appearances between TB OM and other forms of OM exists. Diagnosis should rely on presence of MTB in culture or stain. CXR abnormal in less than 50% of patients with MSK TB but should always be obtained.

50% of patients: MRI shows paravertebral soft tissues abscess in addition to bone lesion.

32
Q

What is this?

A

Pott’s Disease

33
Q

What is myositis?

A

general term for inflammation of the muscles (uncommon in skeletal muscle) that can be caused by any type of microbe (bacteria, virus, fungi, etc.)

34
Q

How can myositis occur?

A

Bacteria invade muscle from either contiguous sites of infection (skin/subcu abscesses, penetrating wounds, decubitus ulcers, osteomyelitis) or by hematogenous spread from a distant focus

35
Q

How does bacterial pyomyositis present?

A

–Most commonly caused by S. aureus

–Pus accumulates within muscles initially

–Clinically characterized by fever, localized muscle pain and stiffness/swelling/tenderness

36
Q

Most cases of pyomyositis occur where globally?

A

Most cases occur in the tropics; in more temperate areas it is very uncommon

37
Q

Note about pyomyositis

A

Bacteremic spread of infection to skeletal muscle extremely uncommon. Among fatal cases of staph sepsis, abscesses in skeletal muscle are found in less than 1% of patients.

infection is not usually due to primary infection of adjacent skin, soft tissue and bone (i.e. this infection occurs in the absence of a predisposing site of infection)

38
Q

What is the pathogenesis of pyomyositis?

A

–Previous bacteremia, commonly asymptomatic and transient along with (likely) some minor muscle trauma or injury

39
Q

How does pyomyositis present?

A

Fever, distinct muscle tenderness and swelling with warm overlying skin; pus can be aspirated. If patient is not diagnosed, sepsis can develop along with striking erythema, exquisite tenderness and fluctuance.

40
Q

What are the risk factors for pyromyositis?

A

HIV, IVDU, DM, alcoholic liver disease, corticosteroid therapy, hematologic malignancies (leukemia, lymphoma, multiple myeloma)

Postpartum, postabortion and postop states are rare predisposing risk factors

HIV/AIDS: repeatedly reported and usually due to S. aureus. Predisposition relates to granulocyte dysfunction, progressive cell-mediated immunodeficiency, and possible muscle injury (HIV myopathy, HAART side effects, myositis from parasitic disease)

41
Q

What the most common sites for pyomyositis?

A

large muscle of LEs and trunk muscles including the shoulder

42
Q

Most common causes of pyomyositis?

A

–S. aureus causes 60-70% of cases in temperate areas

–Group A Strep 1-5%

43
Q

How is pyomyositis diagnosed?

A
  • X rays may show presence of swelling or gas in soft tissue
  • Ultrasound may show focal abscess formation
  • MRI the best: identifies focal muscle edema, localizes presence of focal abscesses
44
Q

Treatment of pyomyositis?

A

–Drain the abscesses

–Initial antibiotic therapy should include Vancomycin

45
Q

What causes gas gangrene?

A

Clostridium perfringens (can also cause food poisoning)

46
Q

What is the structure of CP?

A

Alpha toxin is a hemolytic toxin

Anaerobic gram positive rod

47
Q

How is CP found? How does transmission occur?

A

–Clostridial spores are located in the soil; vegetative cells are members of the normal flora of the colon and vagina. Transmission through wound contamin.

48
Q

What happens once CP enters deep tissue DIRECTLY from soil after trauma?

A

–Organisms grow in traumatized tissue (especially muscle) and produce variety of toxins, most importantly alpha toxin (lecithinase) – damages cell membranes, including erythrocytes which results in hemolysis. Enzymes produce gas in tissues.

Trauma introduces organisms (vegetative or spore forms) directly into deep tissue. If trauma compromises the blood supply, an anaerobic environment forms with low oxidation-reduction potential and acidic pH, which is optimal for growth of clostridial organisms. Necrosis progresses within 24 to 36 hours of the traumatic injury.

49
Q

How does gas gangrene present?

A
  • Pain, edema, cellulitis and gangrene (necrosis) are present.
  • Crepitus indicates presence of gas in tissues.
  • Hemolysis common.
  • Shock and death occur; high mortality.
50
Q

How is gas gangrene diagnosed?

A
  • Smears of tissue and exudate show large GPRs. Spores not usually seen.
  • Organisms cultured anaerobically and then identified by sugar fermentation reactions and acid production
  • Exhibit double zone of hemolysis on blood agar.
51
Q

Treatment of gas gangrene?

A

Pencillin G

52
Q
A

Clostridium perfrigens