Outline the diagnostic clinical features, appropriate investigations and early management of necrotising fasciitis associated with Group A Streptococcal (GAS) infection.
This question is basically the same as Question 2 from the second paper of 2016, except it asks for "diagnostic clinical features, appropriate investigations and early management" instead of just "diagnosis and early management".
Features of history
- Rapidly develping symptoms
- Reasonably young patients
- Previously healthy
- History of minor trauma, eg. scratch, bruise
- Initial injury is frequently trivial and blunt rather than penetrating
- Intense pain and tenderness over the involved skin and underlying muscle
- Pain is out of proportion to physical findings
- Risk factors may be apparent: diabetes, alcoholism, obesity, steroid use.
Features of physical examination
- At the earliest stages, necrotising facsiitis is indistinguishable from severe cellulitis.
- Severe pain on palpation is an early feature
- The affected tissue is oedematous and has a "wooden, hardened feel"
- Erythema is present early.
- Skin "blebs", i.e. bullae with clear fluid develop as skin ischaemia progresses, and these become haemorrhagic in a late presentation
- Crepitus on palpation is another late sign
- Decreased sensation of the overlying skin develops late in the course, and the skin may appear clearly gangrenous
- Acute renal failure
- Coagulopathy; DIC
- Raised inflammatory markers (WCC, CRP)
- Metabolic (lactic) acidosis
- Rapid antigen detection test for Group A Strep: this is mainly for pharyngitis (Gerber et al, 2004), but has been used to achieve a rapid diagnosis of lifethreatening GAS soft tissue infection (Ault et al, 1996)
- "Streptozyme" tests; which, according to a 2009 book chapter by Gould and Reeves are "generally not helpful except as paired acute and convalescent titres", which means the patient will be long dead if you wait for these to become diagnostic of necrotising fasciitis. Oh well, here'es a list of theem anyway, directly from Question 2 from the second paper of 2016
- Anti-streptolysin (ASO)
- Anti-hyaluronidase (AHase)
- Anti-streptokinase (ASKase)
- Anti-nicotinamide-adenine dinucleotidase (anti-NAD)
- Anti-DNAse B antibodies
- CT findings:
- Deep fascial thickening
- Contrast enhancement
- Fluid and gas in the soft tissue planes in and around the superficial fascia
- Ultrasound findings:
- Thickening and distortion of the deep fascia
- Fluid collections along the deep fascia
- MRI findings
- Deep fascial thickening
- Deep fascial fluid collections
- Hyperintense T2W signal within the muscles
- The presence of grayish necrotic fascia
- A lack of resistance to blunt dissection: i.e. the normally firmly adherent superficial fascia just sort of falls apart under gentle traction your hands.
- Lack of bleeding of the fascia during dissection
- The presence of foul smelling ‘dishwater’ pus.
- The histologic criteria for diagnosis as described by Stamenkovic and Lew (1984) were as follows:
- Necrosis of the superficial fascia
- Polymorphonuclear infiltration of the dermis and fascia
- Fibrinous thrombi of arteries and veins coursing through the fascia
- Angiitis with fibrinoid necrosis of arterial and venous walls
- Presence of microorganisms within the destroyed fascia and dermis
- An absence of muscle involvement.
- S.pyogenes is frequently the organism found on tissue culture
- Blood cultures are also frequently positive
As for the management: the key points to remember are:
- Source control
- IV immunoglobulin
- Hyperbaric oxygen
That's the specific management. The supportive management is boring and algorithmic. The suitably boring and algorithmic answer to Question 25 from the first paper of 2016 is reproduced below. The candidates were offered a necrotising fasciitis in a diabetic leg, and were invited to "describe the management priorities in the first 24 hours".
- Attention to the ABCS, with management of life-threatening problems simultanous with a rapid focused examination and a brief history.
- Assess the need for intubation in the context of a potentially decreased level of consciousness
- Assess efficacy of spontaneous breathing, and the need for mechanical ventilation.
- Administer supplemental oxygen at a high flow- it may not be particularly helpful at atmospheric pressure, but hyperoxia does seem to retard the growth of anaerobic organisms.
- Circulatory support
- Administer a 20-30ml/kg fluid bolus
- Secure central venous access and commence vasopressors- start with noradrenaline
- Aim for a MAP over 65mmHg
- Specific investigations
- A full panel of blood tests including blood cultures, CK and an ABG
- A CT scan of the lower limbs and pelvis, as a prelude to surgical intervention
- Supportive management
- Continue fluid resuscitation and vasopressors in pursuit of haemodynamic goals
- Ensure normoglycaemia and normoxia
- Correct acid base balance
- Attend to organ system failure - consider early dialysis if there is rhabdomyolysis
- Admit to ICU
- Commence continuous blood pressure monitoring via arterial line
- Assess for ketosis/ketoacidosis - this is a Type 1 diabetic, and this is exactly the sort of trigger that would produce a DKA.
- Specific management
- Commence broad spectrum antibiotics. In this case, the choice is clindamycin plus anycillin or anypenem. The addition of clindamycin is well supported - particularly with Group A streptococci, where it inhibits the bacterial synthesis of endotoxin.
- Immediately contact surgical services for source control - debridement is the single most useful management strategy; everything else is fairly cosmetic in terms of decreasing mortality.
- Consider IV immunoglobulin (i.e. if this is a streptococcal toxic shock syndrome - which manifests as massive cardiovascular collapse and organ system failure very early in the infective process). The use of IVIG in this setting has been well studied, and though those European investigators didn't reach statistical significance in their primary endpoit (mortality), they did note a significant decrease in organ failure scores in the IVIG group.
- Consider an early referral to a specialist centre where hyperbaric oxygen therapy can be carried out. This management strategy historically did not seem to reduce either mortality or the number of debridements. However, recent data suggests that they were doing it wrong in the 1990s, and modern hyperbaric oxygen therapy seems to be associated with a 50% reduction in mortality (from 9.4% to 4.5%).