Lecture 4: Fasciitis, Myonecrosis, Osteomyelitis

Necrosis

pathologic death of most or all cells in an organ or tissue due to irreversible damage (disease, injury, or failure of the blood supply)

Gangrene

necrosis due to obstruction, loss, or diminution of blood supply

Necrotizing Fasciitis

Infection spreads rapidly along muscle/deep fascia (poor blood supply)

Overlying tissue initially unaffected; then 2° infection of overlying skin, soft tissues, & muscles

Initially pain out of proportion to clinical presentation → anesthesia → skin necrosis

Type I Necrotizing Fasciitis

Polymicrobic disease – facultative & obligate anaerobic bacteria

≥1 anaerobe + Enterobacteriaceae + ≥1 facultative anaerobic streptococci other than GAS

Older adults &/or individuals with underlying comorbidities

Diabetes, especially with peripheral vascular disease

Perineum (Fournier gangrene) – breach in integrity of GI or urethral mucosa → Abrupt onset w/ pain; may spread rapidly to anterior abdominal wall & gluteal muscles

Men >>>> women; scrotum, penis, labia

Necrotizing infection of the head and neck - anaerobes from mouth (Fusobacterium):

Breach in oropharynx mucous membrane following surgery or instrumentation or odontogenic infection

Lemierre's Syndrome – Anerobic Infections

Type II Necrotizing Fasciitis

Streptococcus pyogenes (GAS) + Staphylococcus aureus

Hematogenous spread of GAS from throat (pharyngitis) to site of blunt trauma/muscle strain

M protein

Types 1 & 3 associated with streptococcal toxic shock syndrome

Streptococcal pyrogenic exotoxins (SpeA) = superantigens

Aeromonas hydrophila – traumatic freshwater injury

Vibrio vulnificus – traumatic saltwater injury

Risk factors – cirrhosis; ingestion of contaminated oysters

Necrotizing Fasciitis Clinical Manifestations

Most commonly involve extremities – lower>>upper

Presents acutely (hours) or subacutely (days)

Rapid progression to extensive destruction

Leads to systemic toxicity; limb loss, &/or death

Erythema + edema that extends beyond erythema

Severe pain – may be out of proportion to exam findings

Fever – 102 F to 105 F

As disease progresses - skin bullae, necrosis, or ecchymosis

Systemic toxicity with tachycardia

Crepitus if Type I

Hypotension & confusion

Malaise; myalgias, diarrhea, and anorexia (toxin dissemination)

Subcutaneous tissue – firm & indurated

Changes in skin color – red-purple to blue-gray within 3-5 days of onset

Skin breakdown w/ bullae to cutaneous gangrene

Gas bubbles if Type I

Necrotizing Fasciitis Treatment

Empiric

IV delivery:

Carbapenem OR Piperacillin-tazobactam (β-lactam - β-lactamase inhibitor)

PLUS

Agent activity against MRSA – vancomycin or daptomycin

PLUS

Clindamycin – staph & strep

Clostridial Myonecrosis

Clostridium perfringens

Clostridium septicum

Endospore-forming ANAEROBIC bacilli

Traumatic – C. perfringens- obligate anaerobe

DNases, hyaluronidases and proteases

Spontaneous – C. septicum-aerotolerant; devitalized tissue

Short doubling

Alpha toxin

Clostridium perfringens

Traumatic Myonecrosis

Lecithinase - cytotoxic and destructive to membranes

Primarily responsible for clostridial myonecrosis symptoms

Phospholipase C:

Lyses RBCs, myocytes, fibroblasts, platelets, leukocytes

Decrease cardiac inotropy (force of contraction)

Triggers histamine release, platelet aggregation, and thrombus formation

Theta toxin

Clostridium perfringens

Traumatic Myonecrosis

Causes direct vascular injury, cytolysis, hemolysis

Leukocyte degeneration and PMN destruction

Poor host inflammatory response

Absence of inflammatory cells in biopsies

Kappa Toxin

Clostridium perfringens

Traumatic Myonecrosis

Collagenase

Rapid spread of necrosis through muscle tissue

Traumatic Myonecrosis

Gas Production

Make insoluble H2 gas - fermentation

Bubbles coalesce

Gather along fascial planes + separate tissues

Damage allows:

Nutrients – access to fresh tissue

Ischemia - collapse - blood vessels (ischemia) - keeps regions anaerobic

Spontaneous (non-traumatic) gas gangrene

Hematogenous spread from GI tract

Often associated underlying disease- Carcinoma of bowel, diabetes mellitus, hematologic malignancies, neutropenia, peripheral vascular disease, alcoholism or drug abuse

C. septicum

Aerotolerant – capable of initiating infection w/out obvious tissue damage

Traumatic Myonecrosis Clinical Manifestation

Acute onset with severe pain at disease site

Pain – toxin-mediated ischemia – even before other findings

Typical incubation <24 hr

Skin overlaying injury:

Pale - bronze – purple/red – finally blackish green

Becomes tensely edematous & exquisitely tender

Bullae – clear, red, blue, purple

Rapid development of system toxicity

Tachycardia & fever – may be out of proportion – hi bpm::low temp

Shock with multiple organ dysfunction syndrome

Thin hemorrhagic exudate with no odor to “Sweet mousy” smell - C perfringens

Crepitus in soft tissue

Damaged and infected muscle tissue does not bleed + contract; Grossly edematous; Reddish-blue to black discoloration

Degenerating muscle bundles

Large gram-variable bacilli - injury site

Gram-positive in culture

ABSENCE inflammatory cells

C. perfringens has double zone of hemolysis

Beta-hemolysis of theta-toxin

Incomplete hemolysis alpha-hemolysis of alpha-toxin

Acute Hematogenous Osteomyelitis

Occurs more commonly in children, boys, (4-6 yrs; <17 yrs. of age)

Common site of infection – metaphysis

Major blood vessels penetrates midshaft; splits to both ends

Forms metaphyseal loops (near epiphyseal plate)

Blood (bacteremia) slows for loop

Bacterial from distant sources – skin, teeth, nose, etc.

Phagocytes migrate to area & surround infection

Produce inflammatory exudates = metaphyseal abscess

Acute Hematogenous Osteomyelitis Clinical Manifestations

Gradual onset of symptoms over several days

Dull pain at involved site

Local findings – HEET – easily seen proximal tibia & distal fibula

Systemic symptoms – fever, rigors, vomiting, ill-looking

Inability to bear weight on infected lower extremity

May also present as Septic Arthritis

Leukocytosis

Elevated ESR or ‘sed rate” – slow decline

Elevated C-reactive protein – most responsive

MRI – most sensitive method to diagnose

Becomes positive very early in disease process

Unlike radiography – 10-14 days

Can show subperiosteal abscess

Will show nearby joint affections

Septic Arthritis

Spreading of infection from metaphysis

Breaks through cortex within capsular reflection of joint

Secondary infection

Joints – long bone metaphysis within joint capsule reflections

Knee, hip, & shoulder

Newborns – long bone structure can lead quickly to septic arthritis

Infection spreads from metaphysis to adjacent joints via transphyseal vessels

Vessels no longer present older children

Acute Hematogenous Osteomyelitis Treatment

Clindamycin

Vancomycin

Indications for Surgical intervention in Acute Hematogenous Osteomyelitis

Subperiosteal abscess

No response to medical treatment after 36 hr.

Septic arthritis - extension to nearby joint