Oil Spill – Spreading and Destruction

Demolition is a part of construction

Daniel H. Wilson

We don’t want to waste time, let’s dive into it!

A 52 y/o female presents to the ER 36 hours after a minor bruise on the left lower leg during gardening at home. The triage classified it as a “minor case”.

Her past medical history includes NIDDM, HTN on oral medication, and smoking.

She is in pain (NRS 10/10), BP 107/76, HR 110, Sp0₂ 96%, Temp 37,7°C. On physical examination, her left lower leg is swollen, with diffuse erythema and small ecchymosis.

After a hour blood samples came back: WBC 13’800, Htc 50, Na 131, Glucose 348, Creatinine 2.05.

Painkillers with NSAID’s and amoxicillin IV were started.

The plain x-ray showed edema of the soft tissue and minor gas component.

After 3 hours, the pt is finally moved from the ER to the observation unit with the diagnosis of cellulitis. At that time, some skin blisters are recorded.

After 6 hours, the ER doctor is paged for altered mental status and hypotension. A fluid challenge is attempted with success.

After 8 hours, a second hypotensive episode occurred, and an ICU consult is done with the indication of transferring the pt to a high dependency unit.

After 12 hours MOF showed off, and in 24 hours the pt died.

Introduction

Necrotizing soft tissue infections (NSTIs) are life-threatening complications of the most common skin and soft tissue infections (SSTIs) with a reported mortality rate ranging from 20% to 80% due to tissue destruction that may lead to septic shock and multi-organ failure.

SSTIs are a heterogeneous group of pathological conditions. The WSES guidelines divide SSTIs into three main groups: surgical site infections (SSIs), non-necrotizing SSTIs (including erysipelas, impetigo, folliculitis, simple abscess, and complex abscesses which may be treated by antibiotics or drainage alone), and the most dangerous necrotizing SSTIs.

Speaking of NSTIs, what are these infections triggered by?

Bacterias start spreading in the soft tissue, growing and releasing toxins. Through these toxins, these so-called flesh-eating bacteria may cause vascular thrombosis leading to ischemic necrosis on a local level, and causing a systemic uncontrolled inflammatory response due to T-cells and macrophages stimulation. 

Authors have reported in literature numerous classifications based on features like the infection depth, the anatomical site, and the etiology of the infection. NSTIs may involve any of the layers of the soft tissues, from the dermis and the subcutaneous compartment (necrotizing cellulitis) to the fascial compartment (necrotizing fascitis) and the muscular compartment (necrotizing myositis).

NSTIs may affect any part of the body… The genital and/or perineum involvement is known as Fournier’s gangrene (FG) with a reported mortality rate of 20-50%. The site of origin of this infection is usually the anorectal or the genitourinary tract, and it may expand up to the thighs, the anterior abdominal wall, and the retroperitoneum.

We can classify NSTIs in three types by the bacteriological source:

• Type I – Polymicrobial infection due to aerobic and anaerobic bacteria (Staphylococcus spp, Enterococcus spp, Clostridium spp) is the most frequent type. It is usually seen in the elderly with comorbidities, such as type 2 diabetes or under chronic corticosteroid therapy. The most often involved anatomical location is the trunk, followed by the perineum. Typically report no history of previous trauma. A rare but severe type is represented by Clostridia, known as clostridial myonecrosis or gas gangrene.
• Type II – Monomicrobial pathogenesis due to gram-positive bacteria. Group A Streptococcus pyogenes (GAS) is the most common bacteria involved, followed by Methicillin-resistant Staphylococcus aureus (MRSA). Patients with type II NSTI, compared to type I, are typically younger, healthier, and they frequently report a history of previous trauma, surgery, or IV drug use. GAS toxins can cause toxic shock syndrome (TSS).
• Type III – Monomicrobial pathogenesis due to gram-positive or gram-negative bacteria such as Vibrio vulnificus, Clostridia, Eikenella, Aeromonas hydrophila. It can be linked with seafood ingestion or water contamination wounds.

Mycotic infection may be rarely seen in immunocompromised patients.

Diagnosis

The diagnosis is mainly clinical, looking for local and systemic signs.

• The most frequent local signs are:
  • Disproportionate pain;
  • Edema along with erythema;
  • Subcutaneous emphysema;
  • Reduced skin sensitivity;
  • Skin bullae or necrosis (at a later stage).
• The systemic signs are:
  • Fever;
  • Tachycardia;
  • Hypotension;
  • Shock.

It seems easy, doesn´t it? Unfortunately, the diagnosis is tricky because the infection spreads with little overlying skin change… So, do not forget that the extent of infection is larger than that suggested by skin findings. The suspicion of necrotizing infection should be high, taking into account the above signs and the patient’s history together.

Two sets of blood cultures should be obtained as soon as possible when NSTI is suspected (see our posts on sepsis management – part 1 & part 2).

During the last decades, many scores were described to evaluate NSTIs. The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score is one of the most used to differentiate between necrotizing and non-necrotizing forms of soft tissue infections, and it is based on six independent variables:

A LRINEC score > 6 has a positive predictive value of 92% and a negative predictive value of 96%. A score of eight or higher reflects a 75% risk of necrotizing infection. On the other hand, many studies about LRINEC show conflicting results; therefore, the diagnostic process cannot be based on this score alone. In fact, the physician needs to always rely on a high clinical suspicion.

Imaging may provide useful information for the diagnosis of NSTIs, but should not delay surgical intervention. So…what about radiologic imaging?

• A plain X-ray is not really suitable. Gas in tissues is typically one of the latest signs. It can be useful to identify findings contributing to infection, such as foreign bodies.
• Ultrasound can be easily performed at the bedside. Diffuse thickening of the subcutaneous tissue accompanied by a layer of fluid accumulation more than 4 millimeters in depth along the deep fascial layer (compared to the contralateral healthy tissue).
• Computed tomography (CT) has almost 100% of sensitivity to identify NSTI and 81% of specificity. Typical findings are fat stranding, fluid, and gas collections.
• Magnetic resonance imaging (MRI) is difficult to perform in an emergency setting. On T2-weighted images, necrotizing infection signs usually are fluid collection with thickness and abnormal signal intensity of the deep fascia (> 3 mm), involvement of three or more compartments in one extremity, low intensity, and extensive involvement of the deep fascia.

Let’s take a closer look at the CT findings… In 2011, a CT-based scoring system for soft-tissue infections was developed to discriminate between non-NSTIs and NSTIs. A score >6 points is 86.3% sensitive and 91.5% specific for diagnosis of NSTIs (positive predictive value 63.3%, negative predictive value 85.5%).

A clinical trick is the “Finger test”! Let’s perform a 2-cm incision down to the deep fascia under local anesthesia and gently probe the tissues with your gloved finger. A positive “Finger test” includes all the three following signs:

1. Lack or minimal tissue resistance to finger dissection;
2. Dishwater fluid;
3. Absence of bleeding in subcutaneous tissue.

The “Finger test” is a readily available diagnostic tool at the bedside, but it’s liable to the surgeon’s clinical judgment. An objective and definitive diagnosis can be obtained through an early frozen section of the fascia, but it needs experience and time.

A simple algorithm for the diagnosis of necrotizing infections:

What to Do First?

NSTIs require prompt surgical intervention with drainage of infected fluids, irrigation, and debridement of necrotic tissues. Intraoperative specimens should be always sent for Gram stain and cultures.  The recommended intravenous empiric therapy for adults should be broad-spectrum until culture-specific results:

1. Daptomycin 6 mg/kg q24h OR Linezolid 600 mg q12h for the treatment of Gram-positive bacteria, including MRSA;
2. Piperacillin-Tazobactam according to creatinine for the treatment of Gram-negative bacteria in the setting without a high prevalence of ESBL-producing Enterobacteriaceae OR  Carbapenems (Meropenem, Imipenem-Cilastatin, Doripenem) in the setting with a high prevalence of ESBL.
3. Clindamycin 600-900 mg q8h for anaerobic bacteria and Group A Streptococci.

The therapy will be changed according to the bacteriological findings.

Hemodynamic support with fluids and vasopressors is frequently required. Patients with NSTIs may show multi-organ dysfunction and may need intensive care management.

Patients with NSTI in the setting of streptococcal TSS may benefit from the administration of intravenous immunoglobulin (IVIG). The use of IVIG is described to be associated with a 30-day reduction in mortality (from 33.7% to 15.7%).

Persisting Management

A single surgical debridement is rarely sufficient to fully assess tissue perfusion and viability. It’s recommended to leave the wound open with negative pressure wound therapy (NPWT) and to repeat explorations until no more debridement is necessary (i.e. when no necrotic tissue is found). The whole necrotic tissue should be removed. A big deal is to plan the first re-exploration. Many authors in literature focused less on this aspect and more on the patient’s clinical condition, which plays a central role. Just remember… Delaying re-exploration for more than 24-48 hours is associated with an increased mortality rate.

Consider diverting colostomy for NSTIs involving the perineal/perianal region.

Severe NSTIs may require limb amputation and/or disarticulation, which should be considered in case of diabetic foot infection and/or non-functioning limb.

Post-surgery hyperbaric oxygen (HBO) can be used, even though there is neither sufficient nor definitive evidence supporting its benefits. HBO therapy uses delivery of 100% oxygen at a pressure of 2-3 absolute atmospheres, improving neutrophils action and inhibition of aerobic growth. If available, HBO should be considered for synergistic infections, particularly involving Clostridium spp.

Take-Home Messages

Necrotizing infections evolve rapidly so… timely diagnosis and treatment are essential!!!

Clinical signs and direct exploration are key points for the diagnosis.

The source control of NSTIs needs three combined aspects: early surgical incision, broad-spectrum antimicrobial therapy, and supportive management. When a patient is successfully treated with antibiotics alone, NSTIs can be excluded.

Now let’s see how things could have been done better for our lady patient:
From the beginning, the doubt of a wide subcutaneous infection should have been raised, even more considering the blood test results and the subcutaneous emphysema seen on the X-Ray. A surgical consult could have been asked and a second level test should have been performed (e.g. CT scan or the “Finger test”). Last but not least, proper antibiotic treatment was needed along with a first emergency debridement done rapidly…

Who knows, her life could have been saved… 

Let’s try one more time… maybe…

It’s 3 am and your phone rings, waking you up. It’s Ana from the ICU and she wants you to see the CT scan of a patient admitted to her department the day before.

The patient is a 67-year-old female who came to the A&E department the day before at 6 am with symptoms of a shock (i.e. hypotension and tachycardia; for more read our previous post) and a stroke (she couldn’t speak properly). The stroke protocol was activated, and a contrast-enhanced CT scan of the brain was done showing an ischemic area on the left temporal lobe due to arterial occlusion. An arterial stent was placed right after.

Due to an unclear history of recurrent urinary infections and a persistent shock status, the ICU colleagues asked for an abdominal CT scan… and here is where you come into play…

After having seen those images, you run (after waking up a bit) to the ICU. The patient is obese, in shock (70/40 mmHg, 115 bpm, intubated and sedated, lactates are high in a picture of metabolic acidosis), and with a 3 cm-wide blister in the suprapubic area. The abdominal examination is negative with no tenderness.

What would you do?

After this short recap, you should know… right?

You call for help, take the patient to the theater, and debride as much as you can…

A transverse incision of the abdomen was done just to find the colliquative collection in the subcutaneous tissue with a wide area of necrosis. Luckily the peritoneum doesn’t seem to be affected by the infectious process. At the end of the debridement, the team decide to dress the wound with a VAC system to help with the fight.

The patient is then brought back to the ICU with a wide spectrum antibiotic hoping for her to recover…

References

1. Sartelli M, et al. 2018 WSES/SIS-E consensus conference: recommendations for the management of skin and soft-tissue infections. World J Emerg Surg 2018;13:58.
2. Morgan MS. Diagnosis and management of necrotising fasciitis: a multiparametric approach. Journal of Hospital Infection 2010;75:249-57.
3. Andreasen TJ, et al. Massive infectious soft-tissue injury: diagnosis and management of necrotizing fasciitis and purpura fulminans. Plast Reconstr Surg 2001;107:1025-35.
4. Wong CH, et al. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med 2004;32:1535-41.
5. Yen ZS, et al. Ultrasonographic screening of clinically-suspected necrotizing fasciitis. Acad Emerg Med 2002;9:1448-51.
6. McGillicuddy EA, et al. Development of computed tomography-based scoring system for necrotizing soft-tissuei infections. J Trauma 2011;70:894-9.
7. Paz Maya S, et al. Necrotizing fasciitis: an urgent diagnosis. Skeletal Radiol 2014;43:577-89. 
8. Parks T, et al. Polyspecific intravenous immunoglobulin in clindamycin-treated patients with streptococcal toxic shock syndrome: a systematic review and meta-analysis. Clin Infect Dis 2018;67:1434-36.

How to Cite This Post

Benuzzi L, Sammartano F, Bellio G, Marrano E. Oil Spill – Spreading and Destruction. Surgical Pizza. Published on January 10, 2022. Accessed on May 16, 2025. Available at [https://surgicalpizza.org/emergency-surgery/oil-spill-spreading-and-destruction/].