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44. Necrotizing Fasciitis: Flesh Eating Follies
Keywords
Streptococcus pyogenesPolymicrobial infectionNecrotizing fasciitisHemorrhagic bullaeHyperbaric oxygenGas-forming organismsCase
Rapidly Progressing Cellulitis
Pertinent History
A patient presented to the emergency department (ED) at midnight with pain in the posterior aspect of her left calf and shin area with associated redness and warmth. The pain began at 9 PM, 3 hours prior to arrival. She denies any specific trauma and has been well up until last evening. She does have chronic lower extremity edema. She also has rheumatoid arthritis for which she takes immunosuppressant medications.
PMH
Rheumatoid arthritis
Meds: Anakrina, prednisone, denosumab and others
SH
Nonsmoker, no drug use
Pertinent Physical Exam
BP 152/103, Pulse 120, Temp 98.1 °F (36.7 °C), RR 17, SpO2 97%
Except as noted below, the findings of a complete physical exam are within normal limits.
Cardiovascular:
Tachycardia with regular rhythm, normal heart sounds, and intact distal pulses. Exam reveals no gallop and no friction rub or murmur heard.
Extremity:
She has 3+ pitting edema of the bilateral lower extremities, but on the left side there is spreading erythema and warmth on the anterior and posterior aspect. She also has associated tenderness generally in that area. The knee itself is not tender.
Pertinent Diagnostic Testing
Test | Results | Results | Results | Units | Normals |
|---|---|---|---|---|---|
02:03 | 08:24 | 10:54 | |||
WBC | 6.06 | 10.67 | 11.12 | K/uL | 3.8–11.0 × 103/mm3 |
Hgb | 10.9 | 9.2 | 9.4 | g/dL | Male: 14–18 g/dL Female: 11–16 g/dL |
Na | 139 | 139 | 141 | mEq/L | 135–148 mEq/L |
pH | 7.33 | 7.40 | – | – | 7.35–7.45 |
Lactate | 1.8 | 3.9 | 4.8 | mmol/L | < 2.0 |
CRP | 5.7 | 24.5 | – | Mg/L | < 8 mg/L |
Cr | 0.79 | 0.72 | 0.73 | mg/dL | 0.6–1.5 mg/dL |
Glucose | 149 | 115 | 120 | mg/dL | 65–99 mg/dL |
Computed Tomography (CT)
CT findings are suggestive of lower leg cellulitis without any evidence of subcutaneous air or organized fluid collections. Findings, however, do not exclude a necrotizing infection.
Emergency Department Course
The initial plan was to treat for cellulitis. A CT of the tibia/fibula (tib/fib) was obtained and did not show gas or fluid collections. The patient was started on piperacillin–tazobactam. Plan was for admission.
Update 1: (0300)
Patient’s cellulitis progressed rapidly and she continued to have pain out of proportion on examination. Vancomycin and clindamycin were added to her antibiotic regimen. She continued to be tachycardic and had minimal decrease in pain after getting hydromorphone. There became a mounting concern for necrotizing fasciitis as she was on chronic immunosuppressant drugs. The general surgery service was consulted and the resident who saw the patient believed this was not necrotizing fasciitis (NF). They would continue to follow. However, the ED team continued to keep NF on the differential and treat accordingly.
Update 2: (0730)
As per recheck around 07:30, patient’s area of cellulitis progressed rapidly, her pain is still out of proportion and she is still tachycardic. A phone call placed to the general surgery attending regarding our pressing concern for necrotizing fasciitis as the leading diagnosis.
As of this moment, she has received IV vancomycin, piperacillin/tazobactam, and clindamycin.
The general surgery attending came to re-evaluate the patient. The patient was scheduled to go to the operating room.
Central line placed.
Update 3: (0845)
Patient to OR
Learning Points: Necrotizing Soft Tissue Infections
Priming Questions
- 1.
In terms of pathophysiology, what sets Necrotizing Fasciitis apart from other soft tissue infections?
- 2.
How is this diagnosis made, and what roles do laboratory and imaging studies play?
- 3.
What is the definitive treatment of Necrotizing Fasciitis and what treatment should be initiated in the Emergency Department?
Introduction/Background
- 1.
Although uncommon, Necrotizing Fasciitis (NF) produces a life-threatening infection with a mortality rate from 25% to 35%, despite maximal therapy [1]. NF has been reported to occur in around 500–1500 patients annually in the United States [2, 3].
- 2.
NF is soft tissue infection that rapidly progresses to cause necrosis of muscle fascia and subcutaneous tissues via endotoxins, exotoxins, and protease enzymes. They produce an expanding local tissue injury while also causing severe systemic toxicity [4].
The infection has been reported to spread at the rate of 1 inch (2.54 cm) per hour without manifesting overlying skin changes until the infection is in its advanced state.
Those who survive the initial infection frequently undergo multiple surgical debridements and sometimes amputations.
This is usually followed by surgical reconstruction of the original infection sites, leading to significant ongoing morbidity.
Physiology/Pathophysiology
- 1.
NF tends to occur in two different but occasionally overlapping patterns. Some acknowledge it as Type III infection. Each one is characterized by different organisms and typically affects different populations of patients.
Type I NF (the most common form) is a polymicrobial infection and tends to develop in older and sicker patients who have a history of chronic systemic disease such as peripheral vascular disease, immunosuppression, or diabetes. Although the inciting factor can include various forms of skin trauma such as decubitus ulcers, postoperative wounds, animal or insect bites, or insulin injection sites, often there is no obvious source of injury and the cause is unclear.
The bacteria present in Type I NF include aerobic and anaerobic bacteria. Wound cultures frequently grow S. aureus, E. coli, B. fragilis, and various species of Enterococci, Peptostreptococcus, Prevotella, and Porphyromonas. Clostridium perfringens, the same organism that usually causes “gas gangrene” is often reported in Type I NF, though it is less frequently isolated [5–7]. Group A, Beta-Hemolytic Strep (Strep pyogenes) is usually also present.
Fournier’s gangrene, a form of NF that attacks the perineal region and abdominal wall, is also polymicrobial but enteric organisms predominate.
Type II NF accounts for about 15–20% of cases [8–10].
It is the monomicrobial form and until recently, was caused almost exclusively by Group A Streptococcus (Streptococcus pyogenes). Recently, however, community-associated methicillin-resistant S aureus (MRSA) has been increasingly reported as the sole organism [11, 12].
Type II NF can develop spontaneously in apparently healthy people who have no known causative factor or portal of entry for bacteria [13]. In most patients, however, predisposing factors, such as minor skin trauma and blunt injury, can be identified. IV drug use has emerged as another significant cause of Type II NF [14].
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