A 38-year-old man with type 1 diabetes mellitus presents with two days of severe thigh pain. You are called to see him because of hypotension. On examination he is drowsy, BP 80/60 mmHg, HR 140/min and temperature of 40.2°C. There is gross swelling on the medial aspect of his right thigh with clear cellulitis and visible central necrosis.
Describe the management priorities in the first 24 hours and briefly justify your responses.
• High flow oxygen,
• Support BP with fluids +/- vasopressors
• Measure & fix BSL
• The presentation is that of necrotising fasciitis. T1DM a significant risk factor.
Group A streptococcus (type 2) or polymicrobial aerobic and anaerobic organisms (type1) are both possible. Initial cover should be broad and include an extended spectrum beta-lactam or meropenem, and clindamycin. Clindamycin suppresses toxin formation from GAS, has other favourable in-vitro effects (facilitating phagocytosis).
• Further survey: extent of cellulitis, perineal involvement.
3. Surgical Referral and post-operative management
• Requires urgent debridement, with removal of dead/infected tissue back to bleeding tissue
• Takes priority over other therapies including hyperbaric O2
• Expectation of major blood loss and massive transfusion
• Likely to be highly unstable post-operatively with major support requirement
• Routine ICU care of patient with severe sepsis
4. Specific Therapies
• In vitro neutralisation of streptococcal super-antigens and clostridial toxins
• Streptococcal toxic shock syndrome (with or without nec. fasc.) listed as “emerging”
indication for IVIG by ARCBS, and available for use
5. Hyperbaric O2
• Observational studies only
• Conflicting results with both reduction and increases in mortality seen cf. observational controls
• Possible reduction in need for debridement
• Usually bd to tds dives of 90 min at 3 atm.
• Severe organ failure may limit logistics
So, the college has presented us with a picture of a diabetic who clearly has a necrotising fasciitis.
A boringly algorithmic answer to this question would look something like this:
- 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%).
The key points to remember are:
- Source control
- IV immunoglobulin
- Hyperbaric oxygen
Hasham, Saiidy, et al. "Necrotising fasciitis." Bmj 330.7495 (2005): 830-833.
Mulla, Zuber D. "Treatment options in the management of necrotising fasciitis caused by Group A Streptococcus." Expert opinion on pharmacotherapy 5.8 (2004): 1695-1700.
Darenberg, Jessica, et al. "Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial." Clinical infectious diseases 37.3 (2003): 333-340.
Brown, D. Ross, et al. "A multicenter review of the treatment of major truncal necrotizing infections with and without hyperbaric oxygen therapy." The American journal of surgery 167.5 (1994): 485-489.
Soh, Chai R., et al. "Hyperbaric oxygen therapy in necrotising soft tissue infections: a study of patients in the United States Nationwide Inpatient Sample." Intensive care medicine 38.7 (2012): 1143-1151.