Cellulitis (see Cellulitis, [[Cellulitis]]): skin infection of deeper dermis and subcutaneous fat (resulting from bacterial breach of the skin) characterized by erythema, warmth, and edema without an underlying suppurative focus
Erysipelas (see Erysipelas, [[Erysipelas]]): skin infection of upper dermis and superficial lymphatics (resulting from bacterial breach of the skin) characterized by erythema, warmth, and edema without an underlying suppurative focus
Impetigo (see Impetigo, [[Impetigo]]): infection of superficial layers of the epidermis
Necrotizing Soft Tissue Infection: all of these are characterized by fulminant tissue destruction, systemic toxicity, and high mortality rates
Necrotizing Cellulitis
Meleney’s Synergistic Gangrene
Clostridial Anaerobic Necrotizing Cellulitis
Non-Clostridial Anaerobic Necrotizing Cellulitis
Necrotizing Fasciitis: deep-seated infection of subcutaneous tissue (involving fascia and fat), which may spare the skin
Clostridial Myonecrosis (Gas Gangrene) (see Clostridial Myonecrosis, [[Clostridial Myonecrosis]]): life-threatening muscle infection which develops either contiguously from a site of trauma or via hematogenous spread from the gastrointestinal tract to the muscle
Furuncle (Boil) (see Skin Abscess, [[Skin Abscess]]: infection of hair follicle where purulent material extends through the dermis into the subcutaneous tissue, forming a small abscess
Carbuncle (see Skin Abscess, [[Skin Abscess]]: coalescence of several inflamed follicles into a single inflammatory mass with purulent drainage from multiple follicles
Skin Abscess (see Skin Abscess, [[Skin Abscess]]): collection of pus within dermis and deeper skin tissues
History
Civil War: first description of necrotizing fasciitis by the Confederate Army surgeon, Joseph Jones
1883: Fournier described necrotizing fasciitis in the perineal and genital region
1952: Wilson first used the term “necrotizing fasciitis”
Diagnosis
Laboratory Risk Indicator for Necrotizing Soft Tissue Infection (LRINEC)
C-Reactive Protein (CRP) (mg/L)
CRP < 150 -> 0 points
CRP ≥ 150 -> 4 points
WBC
WBC < 15 -> 0 points
WBC 15-25 -> 1 point
WBC >25 -> 2 points
Hemoglobin (g/dL)
Hb >13.6 -> 0 points
Hb 11-13.5 -> 1 points
Hb < 10.9 -> 2 points
Sodium (mmol/L)
Na ≥ 135 -> 0 points
Na < 135 -> 2 points
Creatinine (mg/dL)
Cr ≤ 1.6 -> 0 points
Cr >1.6 -> 2 points
Glucose (mg/dL)
Glc ≤ 180 -> 0 points
Glc >180 -> 1 point
LRINEC Score -> Probability of Necrotizing Fasciitis
Low Risk: <5 points -> <50% probability of necrotizing fasciitis
Intermediate Risk: 6-7 points -> 50-75% probability of necrotizing fasciitis
High Risk: >8 points -> >75% probability of necrotizing fasciitis
May Reveal Gas in Soft Tissues: although these are of limited utility in cases where gas is unlikely to be found (ie: those due to Strep and MRSA) and may delay the necessary surgical management
CT
Useful to Image Soft Tissues
MRI
Useful to Differentiate Fasciitis from Cellulitis
Gas in deep tissues is more common with Clostridium and mixed aerobic-anerobic cases (but is unusual in Strep and MRSA-associated cases)
Ultrasound with Aspiration of Perifascial Fluid Collections
May Be Useful
“Dishwater” appearance of fluid
Finger Test
Procedure: 2 cm incision down to deep fascia (with local anesthesia)
Lack of bleeding from incision or “dishwater” fluid expressed -> suggest necrotizing fasciitis
If the tissues at level of the deep fascia dissect with minimal resistance, the finger test is positive -> suggests necrotizing fasciitis
Tissue Biopsy with Rapid Frozen Section Analysis
May Demonstrate Obliterative Vasculitis of Subcutaneous Vessels, Acute Inflammation, and Subcutaneous Tissue Necrosis
Clinical Pattern-Necrotizing Cellulitis
Meleney’s Synergistic Gangrene
Epidemiology
Rare
Occurs in Postoperative Patients
Microbiology
Combined Staphylococcus Aureus + Microaerophilic Streptococci (see Staphylococcus Aureus, [[Staphylococcus Aureus]] and Streptococcus, [[Streptococcus]]): involves a synergistic interaction between these organisms
Physiology
Confined to the Superficial Fascia
Clinical
Slowly Expanding Indolent Ulceration Confined to Superficial Fascia
Clostridial Anaerobic Necrotizing Cellulitis
Epidemiology
XXXX
Microbiology
Clostridium Perfringens (see Clostridium Perfringens, [[Clostridium Perfringens]]): most common etiology
Clostridium Septicum (see Clostridium Septicum, [[Clostridium Septicum]]): less frequent etiology
Physiology
Portal of Entry
Spread of Infection from Bowel to Perineum/Abdominal Wall/Lower Extremities
Surgical Contamination
Trauma
Clinical
Gradual Onset with Subsequent Rapid Spread
Pain/Swelling/Systemic Toxicity are Not Prominent Features
Milder Clinical Illness Distinguishes this from True Gas Gangrene
Thin, Dark, Foul-Smelling Wound Drainage: may contain fat globules
Tissue Gas Formation (see Skin Crepitus, [[Skin Crepitus]])
Sparing of Fascia and Deep Muscle
Treatment
Surgical Exploration/Debridement is Required to Distinguish Anaerobic Cellulitis from Fasciitis and Myonecrosis
Non-Clostridial Anaerobic Necrotizing Cellulitis
Epidemiology
Risk Factors
Diabetes Mellitus (DM) (see Diabetes Mellitus, [[Diabetes Mellitus]])
Breach in Gastrointestinal/Genitourinary Tract or Labia: by diverticulum, malignancy, hemorrhoid, anal fissure/perianal abscess, Bartholin abscess, episiotomy, , vulvovaginal infection, decubitus ulcer, or urethral tear
Once Infection Reaches the Deep Fascia of Perineum, Rapid Spread Along Fascial Planes, Through Venous Channels and Lymphatics to Involve the Anterior Abdominal Wall/Gluteal Muscles/Scrotum/Penis
Brawny Edema: may extend beyond the area of erythema
Subcutaneous tissues may feel wooden/hardened with loss of feeling of fascial planes and muscle groups
Vesicular Skin Lesions: may occur
Crepitus (see Skin Crepitus, [[Skin Crepitus]]): may occur
Later Findings
Dark Red Induration of Skin
Bullae Filled with Blue/Purple Fluid
Late Findings
Friable Bluish/Maroon/Black Skin (due to extensive thrombosis of blood vessels in dermal papillae)
Brownish/Gray Skin (due to extension into the deep fascia)
Septic Shock/Multiorgan Failure (see Sepsis, [[Sepsis]])
Streptococcal Gangrene
Epidemiology
Age: can occur in any age group
Most Cases are Community-Acquired
Most Cases Occur in Patients without Co-Morbid Conditions (in Contrast to Type I Necrotizing Fasciitis Cases)
Of the 3.5 Million Cases of Invasive Streptococcus Pyogenes Cases Per Year in th US, Necrotizing Fasciitis Accounts for Approximately 6% of These Cases
Non-Steroidal Anti-Inflammatory Drugs (NSAID’s) (see Non-Steroidal Anti-Inflammatory Drug, [[Non-Steroidal Anti-Inflammatory Drug]]): possible predisposing factor
Peripheral Arterial Disease (PAD) (see Varicella-Zoster Virus, [[Varicella-Zoster Virus]])
Microbiology
Streptococcus Pyogenes (Group A Strep) (see Streptococcus Pyogenes, [[Streptococcus Pyogenes]]): most common Streptococcus species associated with necrotizing fasciitis
Concomitant Streptococcus Pyogenes and Staphylococcus Infection May Occur in Some Cases
Streptococcus Agalactiae (Group B Strep) (see Streptococcus Agalactiae, [[Streptococcus Agalactiae]]): reported cases
Physiology
Cases with Defined Portal of Entry: 50% of cases
Infection Usually Enters Through Penetrating Trauma or Cutaneous Site of Infection
Early Findings: signs of superficial skin infection
Later Findings: purple (violaceous) bullae, skin sloughing, etc
Once Infection Reaches the Deep Fascia, it Rapidly Spreads Along Fascial Planes, Through Venous Channels and Lymphatics
Cases with No Defined Portal of Entry: 50% of cases
Asymptomatic/Symptomatic Pharyngitis Likely Results in Subsequent Hematogenous Dissemination to a Site of Non-Penetrating Minor Trauma (Such as a Bruise or Muscle Strain)
Early Findings: severe pain, fever (without signs of superficial skin infection)
Later Findings: purple (violaceous) bullae, skin sloughing, etc
Clinical
Approximately 66% of Cases Occur in the Lower Extremities
Early Findings
Severe Pain Over Skin and Underlying Muscle: sensitive, early finding that may precede development of fever and other constitutional symptoms [MEDLINE]
Crepitus (see Skin Crepitus, [[Skin Crepitus]]): may occur
Fever: may be absent early
Brawny Edema: may extend beyond the area of erythema
Subcutaneous tissues may feel wooden/hardened with loss of feeling of fascial planes and muscle groups
Vesicular Skin Lesions: may occur
Later Findings
Dark Red Induration of Skin
Bullae Filled with Blue/Purple Fluid
Late Findings
Friable Bluish/Maroon/Black Skin (due to extensive thrombosis of blood vessels in dermal papillae)
Brownish/Gray Skin (due to extension into the deep fascia)
Septic Shock/Multiorgan Failure (see Sepsis, [[Sepsis]])
Anaerobic Streptococcus (Peptostreptococcus) (see Peptostreptococcus, [[Peptostreptococcus]])
Epidemiology
XXXX
Aeromonas Hydrophila-Associated Necrotizing Fasciitis (see Aeromonas Hydrophila, [[Aeromonas Hydrophila]])
Epidemiology
Necrotizing Soft Tissue Infection is Associated with Traumatic Injuries in Freshwater
Clinical
XXXX
Clostridium Novyii-Associated Necrotizing Fasciitis (see Clostridium Novyii, [[Clostridium Novyii]])
Epidemiology
XXXX
Risk Factor
Intravenous Drug Abuse (IVDA) with Subcutaneous Injection of Black Tar Heroin (see Intravenous Drug Abuse, [[Intravenous Drug Abuse]])
Portal of Entry
Breach of Skin/Mucosa
Clinical
Gas Gangrene
Clostridium Sordellii-Associated Necrotizing Fasciitis (see Clostridium Sordellii, [[Clostridium Sordellii]]
Epidemiology
XXXX
Risk Factor
Intravenous Drug Abuse (IVDA) with Subcutaneous Injection of Black Tar Heroin (see Intravenous Drug Abuse, [[Intravenous Drug Abuse]])
Portal of Entry
Breach of Skin/Mucosa
Clinical
Necrotizing Fasciitis
Vibrio Vulnificus-Associated Necrotizing Fasciitis (see Vibrio Vulnificus, [[Vibrio Vulnificus]])
Epidemiology
Necrotizing Soft Tissue Infection is Associated with Traumatic Injuries in Seawater
Necrotizing Soft Tissue Infection in Patients with Cirrhosis is Associated with Ingestion of Contaminated Oysters
Portal of Entry
Breach of Skin/Mucosa
Clinical
XXXX
Synergistic Necrotizing Cellulitis
Epidemiology
Risk Factors
Diabetes Mellitus (DM) (see Diabetes Mellitus, [[Diabetes Mellitus]])
Clinical
Variant of Necrotizing Fasciitis Which Involves the Skin/Muscle/Fat/Fascia
Usually Involves the Lower Extremities or Perineum
Example of Streptococcus Pyogenes Necrotizing Cellulitis
62 y/o Female with Left Forearm Cellulitis After Superficial Wound
Example of Type I Necrotizing Fasciitis
36 y/o Diabetic Caucasian Male (with HbA1C 13%) Who Presented with Ulcerating Left Foot Skin Lesions
Patient Underwent Immediate Surgical Incision and Drainage of the Left Foot/Distal Left Leg and Left Great Toe Amputation
12 hrs Later, He Developed Progressive Gangrene Adjacent to the Surgical Field (Picture Below), Requiring Repeat Surgical Debridement with Left Below the Knee Amputation
Blood Cultures were Positive for Streptococcus Agalactiae (Group B Streptococcus)
Wound Cultures were Positive for Escherchia Coli + Streptococcus Agalactiae (Group B Streptococcus)*
Unlike penicillin, the efficacy of clindamycin is not affected by the inoculum size or stage of bacterial growth
Clindamycin suppresses bacterial toxin synthesis
Subinhibitory concentrations of clindamycin facilitate Strep Pyogenes phagocytosis
Clindamycin decreases the synthesis of penicillin-binding protein, which, in addition to being a target for penicillin, is also an enzyme involved in cell wall synthesis and degradation
Clindamycin has a longer postantibiotic effect than β-lactams (such as penicillin)
Clindamycin suppresses LPS-induced mononuclear synthesis of tumor necrosis factor-α
Vancomycin (see Vancomycin, [[Vancomycin]]): or comparable agent, to cover for possible MRSA
Reported in the Treatment of Streptococcal Toxic Shock Syndrome (see Streptococcal Toxic Shock Syndrome, [[Streptococcal Toxic Shock Syndrome]]): may have a role in Streptococcus-associated necrotizing faasciitis cases (although this is not an FDA-approved indication)
Prompt Surgical Debridement Down to Fascia with Wide Excision
Early surgical intervention has been demonstrated to improve mortality and decrease tissue loss (amputation, etc).
Delayed surgical intervention is associated with increased risk of death [MEDLINE]
Average latency from admission to surgery in survivors: 25 hrs
Average latency from admission to surgery in non-survivors: 90 hrs
Hyperbaric Oxygen (HBO) (see Hyperbaric Oxygen, [[Hyperbaric Oxygen]])
Unclear Benefit in Necrotizing Fasciitis
Treatment of Septic Shock (see Sepsis, [[Sepsis]])
Standard Measures
Prognosis
Death: may occur if necrotizing fasciitis is not promptly recognized and treated
References
Determinants of mortality for necrotizing soft-tissue infections. Ann Surg. May 1995;221(5):558-63 [MEDLINE]
The changing spectrum. Dermatol Clin. Apr 1997;15(2):213-20 [MEDLINE]
Group B streptococcal necrotizing fasciitis and streptococcal toxic shock-like syndrome in adults. Arch Intern Med. 1998 Aug 10-24;158(15):1704-8 [MEDLINE]
A 46-year-old man with excruciating shoulder pain. Chest. Mar 2005;127(3):1039-44 [MEDLINE]
Group B streptococcal necrotizing fasciitis from a decubitus ulcer. Int J Emerg Med. 2010 Dec; 3(4): 519–520 [MEDLINE]
Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2014 Jul 15;59(2):e10-52. doi: 10.1093/cid/ciu444 [MEDLINE]
Necrotising soft tissue infection in a UK metropolitan population. Ann R Coll Surg Engl. 2015 Jan;97(1):46-51. doi: 10.1308/003588414X14055925058553 [MEDLINE]
