A Shock to the System – Morning Report November 9th

This week in Morning Report we discussed an approach to skin and soft tissue infections. We also reviewed features of necrotizing fasciitis and management, and discussed a case of streptococcal toxic shock syndrome and the diagnostic criteria, treatment, and prophylaxis. A summary is included below:

1. Approach to Skin and Soft Tissue Infections (SSTI)

An approach to skin and soft tissue infections is outlined below – diagram adapted from IDSA guidelines:

Adapted from the Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America (https://www.idsociety.org/practice-guideline/skin-and-soft-tissue-infections/)

Purulent infections include:

  • Folliculitis which is a superficial bacterial infection of the hair follicles
  • Carbuncle, a series of abscesses in subcutaneous tissue (drains via hair follicles)
  • Furuncle – well-circumscribed, painful, suppurative nodule that usually develops from folliculitis
  • Skin abscess – collection of pus within the dermis and deeper skin tissues, usually manifest as erythematous tender fluctuant painful nodules with a pustule and erythematous surround this

(From UpToDate)

As above, management for purulent infections involves incision and drainage, and in setting of moderate/severe antimicrobial therapy as well. Moderate purulent skin and soft tissue present with both purulent infection and systemic signs of infection. Severe infection is seen in patients who have failed I&D with oral therapy, or those with systemic signs of infection (T > 38, tachycardia > 90 BPM, tachypnea > 24 BPM), or abnormal WBC, or immunocompromised patients.

With nonpurulent SSTIs, mild infection is delineated by a typical cellulitis or erysipelas. Moderate infection involves systemic signs of infection, and severe includes patients who have failed oral treatment with antibiotics or systemic signs of infection, or clinical signs of deeper infection (bullae, skin sloughing, hypotension, or organ dysfunction).

When a specific pathogen is identified in a severe nonpurulent SSTI, therapy can be targeted.

2. Erysipelas versus Cellulitis

Below is a table and images to help differentiate between cellulitis and erysipelas:

Deeper dermis and subcutaneous fatUpper dermis and superficial lymphatics
With or without purulenceNonpurulent
Indolent course with development of localized symptoms over daysAcute onset of symptoms with systemic manifestations, including fever, chills, severe malaise, and headache; 
Less well-demarcated borderClear demarcation between involved and uninvolved tissue.There may be a raised, advancing border or erythema with central clearing.
Erysipelas of the leg
Example of erysipelas – Reference: https://ykhoa.org/d/image.htm?imageKey=ID/82542

3. Features and Types of Necrotizing Fasciitis (NF)

In terms of pathophysiology of necrotizing fasciitis, there is microbial invasion of the subcutaneous tissues which occurs through external trauma or from perforated viscous. Growth of bacteria in superficial fascia releases enzymes and toxins that allows for spread throughout the fascia. This results in poor microcirculation, ischemia, and cell death and necrosis.

In necrotizing fasciits, the infection starts at the level of subcutaneous fat and deep fascia and for this reason, the erythema and edema of skin are not apparent early on and the degree of infection isn’t obvious.

Features include at stage 1: Swelling, erythema, warmth, tenderness/edema beyond the erythema, pain out of proportion
Stage 2: Formation of blisters, bullae, skin fluctuance.
Stage 3: Manifests with haemorrhagic bullae, crepitus, skin necrosis, and gangrene

As the infection progresses, one can have tachycardia, tense  edema  outside  the  area  of compromised  skin,  pain  disproportionate to appearance, skin discoloration  (ecchymosis),  blisters/bullae  and  necrosis,  and crepitus  and/or  subcutaneous  gas. Systemic  findings  include fever,  tachycardia,  hypotension,  and  shock.

The diagnosis is clinic and goal standard is surgical exploration and biopsy of the issues. The diagnosis is made by presence of fascial necrosis and myonecrosis and loss of integrity of tissue planes in the fascia and evidence of muscle inovlement.

There is a scoring tool called the the LRINEC (Laboratory Risk Indicator for Necrotising Fasciitis) scoring system for assessing for NF.

Management involves PROMPT surgical consultation and intervention and broad-spectrum antibiotics as described above. When Group A streptococcus is the targeted organisms, antibiotics can be tailored to penicillin and clindamycin.

4. Invasive Group A Streptococcal (GAS) Infection

GAS releases exotoxins that act as superantigens and a few forms of invasive GAS have been listed below:

  • In the absence of toxic shock syndrome examples are:
    • Necrotizing soft tissue infection
    • Pregnancy-associated infection (peripartum)
    • Can cause pneumonia

5. Streptococcal Toxic Shock Syndrome (STSS)

STSS is a complication of invasive GAS which involves multi-organ failure.

In addition to isolation of GAS from a sterile body site, the presentation involves:

  • Hypotension (sBP < 90 mmHg)
  • PLUS 2 or more of the following 6: renal impairment, coagulopathy, liver involvement, acute respiratory distress syndrome, generalized erythematous macular rash that may desquamate, or soft-tissue necrosis

Management includes management of sepsis, surgical debridement if necrotizing SSTI, empirically therapy will involve Clindamycin+Vancomycin+ either carbapenem or piperacillin-tazobactam.

Tailored antimicrobials usually involve penicillin+clindamycin or ceftriaxone+clindamycin. (or alternatives if allergy to penicillin).

The use of intravenous immunoglobulin to boost antibody levels was reviewed in one meta-analysis of five studies in 2018 (one randomized and four non-randomized), this showed reduction in 30-day mortality in patients on clindamycin. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6186853/) However prior data has been inconclusive on this. As per CDC, severely ill patients early in the clinical course can receive IVIG, however evidence is require to determine efficacy.

Risk of infection is highest among those who live in the same household as index case and are age 65 or older and in the 30 days following exposure. Antibiotic chemoprophylaxis is considered for these patients – in adults, penicillin 250 mg orally four times daily for 10 days.


Please don’t hesitate to reach out if you have any questions or comments – cmr@wchospital.ca!

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