Episode #6

Canine Necrotising Fasciitis – A Short Review of the Literature

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Episode Notes

What is Canine necrotising fasciitis?

Canine necrotising fasciitis (NF) is an uncommon, deep-seated destructive infection of the skin, subcutaneous, and superficial fascia. Rarely, the process also can occur in the muscle, when it is termed necrotising myositis (NM)1.

Both of these conditions can be associated with another syndrome called toxic shock syndrome (TSS1).

What causes it?

A number of different bacterial species have been isolated from dogs with NF, and include the following1,2,3:

  • Streptococci species
    • Most streptococcal species isolated from canine NF belong to a group of commensal streptococci belonging to the group G streptococci, which includes the species Streptococci canis
    • Streptococcus canis has been isolated from dogs in the following infections
      • Urinary tract infection
      • Mastitis 
      • Metritis
      • Skin infections
      • Septic bacteraemia
  • Pseudomonas aeruginosa
  • Escherichia coli
  • Clostridia species
  • Pasteurella species
  • Staphylococcus pseudointermedius

What are the risk factors?

  • Fluoroquinolone antibiotic administration1
    • Fluoroquinolone antibiotics induce expression of a bacteriophage-encoded streptococcal super-antigen
  • Potential risk factors1,2
    • Immune-suppression
    • Corticosteroid administration
    • Radiation therapy4
  • Trauma1
    • Note that pre-existing traumatic injury or trauma is not always evident or necessary for NF or NM to occur
    • Pre-existing trauma can be major (e.g. bite wounds; surgery) or very minor. Case reports in veterinary literature have cited injection sites for subcutaneous fluid administration, and small wounds as potential points of entry for causative organisms. Surgical sites may be recent, or may be many years old e.g. cruciate surgery etc.)
    • Where no wound is found, it is assumed bacteria gain entry to tissues from haematogenous routes

Pathophysiology

The following is a brief description of the progression of infection to overt disease1-3:

  1. Bacteria gain entry from wound, or haematogenous spread and localise in fascia/muscle
  2. Bacteria produce endotoxins and proteases that cause local tissue damage, creating a nidus for bacterial proliferation
  3. Infection spreads along fascial planes
  4. Toxin-induced thrombosis and vasoconstriction in infected tissue, and surrounding skin and muscle results in decreased tissue viability and increased spread of infection.
  5. Toxic shock syndrome may ensue as a result of tissue destruction and haematogenous spread of endotoxins and inflammatory mediators
  6. Steatitis may occur without skin destruction in some cases.

Progression is extremely rapid, with clinical signs of swelling over an affected area to discoloration and progressing to septic shock taking minutes to hours without treatment.

 

infectious-disease-course-2020-IMG

 

Diagnosis

Early diagnosis is crucial in reducing the severity of disease as failure to diagnose NF or NM early during illness is thought to play a major role in the high mortality rates – which can approach 100%.

The following list outlines clinical features of the disease:

  • No age or sex predilection
  • The patient is usually normal up to a few hours prior to presentation
  • Acute pain – with or without noticeable swelling or injury
  • Intense pain – often disproportionate to an injury, wound, old surgery site or swelling. In some cases, no injury is found
  • Swelling at the site of pain. Occasionally, spasm and rigidity is seen about affected tissue
  • Visual characteristics:
    • Usually, there is no discoloration or demarcation on the skin initially. However, it usually develops over several hours
    • Infections by Pseudomonas are characterised by early erythema and rapid discoloration
  • Pyrexia may develop within 24 hrs. of presentation
  • Clinical signs of septic shock
    • Hypotension
    • Tachycardia or bradycardia
    • Hyperaemic/red mucous membranes
    • Collapse

Diagnostic evaluation should include the following:

  1. Careful evaluation for evidence of wounds (bite wounds, old scars etc.)
  2. Diagnostic imaging1,5
    • Radiography – may reveal gas pocketing within soft tissues
    • Ultrasonography – may reveal fluid accumulations in tissues, that may be aspirated for cytology, gram stain and culture
  3. Fluid analysis
    • Fluid characteristics
      • Streptococcus Canis: cream/gray-coloured, purulent material with no odour (dish-water pus)
      • Clostridia spp: cream-coloured malodourous pus
    • Cytology
      • Streptococcus canis: chains of cocci
      • E. coli: gram negative rods
      • Clostridia: plump, gram positive rods
      • Pasteurella multocida: bipolar gram-negative rods
    • Gram stain
    • Antimicrobial culture and sensitivity

Treatment

Patients with NF or NM, with or without toxic shock, require urgent and intensive therapy. Treatment falls broadly into two categories: stabilisation and supportive care; and fasciitis/myositis management.

  1. Stabilisation and supportive care involves support of respiratory and cardiovascular systems as dictated by patient clinical status1,3.
    • Stabilisation
      • Oxygen supplementation
      • Provision of ventilation support may be required in patients with acute respiratory distress due to septic shock and acute respiratory distress syndrome (ARDS)
      • Intravenous fluid therapy should be applied to treat shock, provide for correction of hydration deficits, and electrolyte disorders.
      • Blood pressure should be monitored, and maintained within normal limits using intravenous fluid therapy, positive inotropes (dobutamine) and cautious use of vasopressors (noradrenaline) to achieve desired end-points (SAP >100 mm Hg; MAP > 70 mm Hg)
      • Urine output should be monitored and maintained at or above 1 ml/kg/hr
      • Coagulation abnormalities should be managed with fresh frozen plasma prior to surgical intervention and debridement of the areas of fasciitis (see below)
    • Supportive care
      • Analgesia should be provided using a multi-modal approach. Typically, an opioid infusion, such as fentanyl, combined with ketamine continuous infusion is recommended. Addition of intravenous lidocaine +/- local nerve block with lidocaine/bupivacaine will improve the quality of analgesia. Epidural analgesia should generally be avoided in septic patients.
      • Antimicrobial therapy should commence immediately following sample collection for antimicrobial culture and sensitivity. 
  • Initial antibiotic choice is based on cytological appearance and gram stain
        • Gram positive cocci in chains (Streptococci): clindamycin 10 mg/kg q 12 hrs.; amoxycillin/clavulanate 10-20 mg/kg q 12 hrs.
        • Gram negative rods (Pseudomonas, E. coli) – enrofloxacin or ciprofloxacin
        • Gram positive rods (clostridia): metronidazole 10 mg/kg q 12 hrs.
        • Pasteurella: cefazolin 20 mg/kg q 8-12 hrs.
        • NOTE: fluoroquinolones SHOULD NOT be administered to patients with gram positive infections
  1. Surgical Management involves debridement of affected tissues, and should be performed as early as possible to reduce bacterial load and necrotic tissue1,2.
    • Remove all necrotic tissue until bleeding is observed from all remaining tissues (muscle, subcutaneous tissues). Fat resection in affected areas must be meticulous, as adipose tissue has a relatively poor blood supply.
    • Copious wound lavage with lactated Ringers’ solution or 0.9% NaCl is recommended
    • Closure
      • Where debridement is required: manage as an open wound using debridement dressings, with manuka honey or sugar. Delayed primary closure may be attempted only when it is clear infection no longer remains (granulation tissue will begin to appear at this stage)
      • Where debridement is not required, primary closure may be applied
      • Vacuum-assisted wound closure has been applied and may reduce wound healing time and improve wound contracture2,6.

Conclusion

Patients exhibiting pain in a localised area, especially when accompanied by fever, must have necrotising fasciitis placed on their differential diagnosis list. In these cases, it is important to avoid specific therapies mentioned above, such as routine use of fluoroquinolones etc., and to intensively monitor the patients, intervening with appropriate surgical and medical therapy early in the disease.

Necrotising fasciitis is a serious and potentially fatal infectious condition that requires a high index of suspicion to be applied, along with early, aggressive intervention in order to achieve optimal outcome.

References  

  1. Mathews KA, Singh A. Necrotizing Fasciitis. Small Animal Surgical Emergencies. 2015 Dec 3:465.
  2. Csiszer AB, Towle HA, Daly CM. Successful treatment of necrotizing fasciitis in the hind limb of a great dane. Journal of the American Animal Hospital Association. 2010 Nov;46(6):433-8.
  3. Sharma B, Kumar Srivastava M, Srivastava A, Singh R. Canine Streptococcal Toxic Shock Syndrome associated with Necrotizing Fasciitis: An Overview. Veterinary World. 2012 May 1;5(5).
  4. Mayer MN, Rubin JE. Necrotizing fasciitis caused by methicillin-resistant Staphylococcus pseudointermedius at a previously irradiated site in a dog. The Canadian Veterinary Journal. 2012 Nov;53(11):1207.
  5. Bowlt KL, Pivetta M, Kussy F, Rossanese M, Stabile F, Dennis R, Holloway A. Imaging diagnosis and minimally invasive management of necrotizing fasciitis in a dog. Veterinary and Comparative Orthopaedics and Traumatology. 2013;26(04):323-7.
  6. Abma E, Kitshoff A, Vandenabeele S, Bosmans T, Stock E, De Rooster H. Treatment of necrotizing fasciitis using negative pressure wound therapy in a puppy. Vlaams Diergeneeskundig Tijdschrift. 2015;84(3):147-53.

Host:

Dr. Philip Judge

Dr. Philip Judge

BVSc MVS PG Cert Vet Stud MACVSc (VECC; Medicine of Dogs)

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