Necrotizing Fasciitis

Today we saw a case of necrotizing skin and soft tissue infection (not quite necrotizing fascitis) presenting in the groin area of a diabetic patient.

Patients who inject drugs or who have diabetes, obesity, or immunosuppression are at higher risk of these infections. Pain is an early presenting feature with later development of haemodynamic instability. Early changes resemble cellulitis; however, late changes include tense edema outside the area of compromised skin, pain disproportionate to appearance, skin discoloration, blisters/bullae and necrosis, and crepitus and/or subcutaneous gas.





Necrotizing fascitis (review) can be characterized based on the pathogens involved:

• Type I: Mixed aerobic and anaerobic infection. Often in diabetics. Includes Fornier's gangrene where the infection involves the fascial planes in the perineal area and in males can involve the scrotum and penis.
  
• Type II: Group A Streptococcus and MRSA
• Other organisms (below)
  

Treatment:

• Highly skilled surgical debridement and source control
• Appropriate antibiotics (in GAS penicillin G and clindamycin for Type I broad spectrum anaerobic and gram negative coverage -- i.e. piperacillin-tazobactam)
• IVIG -the case-control study on the use of IVIG in Invasive Group A Streptococcal disease is available here.
• Treatment of close contacts discussed here.
  

Endocarditis

We discussed endocarditis today. I will take this opportunity to 'show off' the search function of the blog and direct you here.

Duke Criteria:

Major Criteria

Microbiologic:

Positive blood cultures (>=2) with an organism that classically causes endocarditis (viridans group streptococci, staphylococcus aureus, enterococcus, HACEK organisms)
OR
Persistantly positive (>=3 or >=2 12h apart) for another organism

Echocardiologic:
Vegetation on valve not otherwise explainable or dehiscence of mechanical valve or abscess

OR

Clinical: *NEW* (not worsening) regurgitant murmur

Minor Criteria

• Predisposition -- known pre-existing valvular disease or IVDU
• Fever
• Evidence of vascular phenomenon -- septic emboli, mycotic aneurysm, Janeway lesions,
• Immunologic: glomerulonephritis (like this case), positive RF, roth spots, Osler nodes,
• Microbiologic: Blood culture not meeting major
• Echocardiographic not meeting major

Diagnosis: 2 Major, or 1 major 3 minor, or 5 minor

The ACC has updated guidelines on the management of valvular heart disease including endocarditis and endocarditis prophylaxis. These address the diagnostic algorithm and treatment in more detail.

Prosthetic Joint Infection

Today we discussed prosthetic joint infection (Recent review here)
UPDATE AUG 20 - NEJM Review Recently Published here.


Treatment options include:

• 2 stage revision -- removal of hardware, insertion of spacer with ~6weeks antibiotics before re-implantation. Highest chance for cure, significant morbidity
  
• 1 stage revision -- removal of hardware, debridement and re-implanataion with concomitant antibiotics. Less morbidiy, less chance of cure
  
• Debridement, Antibiotics and Retention -- chance of failure, little morbidity
  
• Palliation -- i.e. chronic suppressive antibiotics
  

We spent some time discussing debridement and retention (original JAMA article here, review here). In general this can be considered for MSSA, MRSA and CNST prosthetic joint infections provided:

• Relatively short duration of illness
• No loosening of the prosthesis
• Healthy overlying tissues
  
• Full OR debridement occurs
• The organism is susceptible to quinolones and rifampin (and the patient can tolerate both)

In general there is a two week induction with beta-lactam + rifampin or vancomycin + rifampin followed to ~ 3 months for THR and 6 months for TKR with levofloxacin or moxifloxacin with rifampin 450 PO BID. Treatment is continued past 3 (or 6) months if the CRP/ESR fails to normalize. Failure would be recurrent infection, intractable pain, loosening, drug intolerance.

Also -- here is a review of the use of combination rifampin with other antibiotics for the treatment of Staphyloccal infections.

Severe Falciparum Malaria

We discussed a case of a patient with 3% parasitemia but who had CNS symptoms compatible with cerebral malaria and mild renal failure.

In general, severe malaria is defined as a parasitemia of greater than 5% or disease associated with end-organ dysfuction (see NEJM article and table below)






















We also discussed the use of artesunate in the treatment of malaria. This Cochrane review suggests that as compared with IV quinine, artesunate reduced the risk of death (RR 0.62), cleared parasitemia faster, and had a lower risk of hypoglycemia. Consequently, it is likely currently the therapy of choice for severe malaria in non-pregnant adults.

Dosing is 2.4mg/kg given as an IV push at time 0, 12h, 24h and 48h. It is given in combination with a longer acting antimalarial such as doxycycline 100mg PO BID x 7days.

Generally fewer side effects than quinine or quinadine. Side effects include:

• GI symptoms (relatively common)
• Allergy ~1:3000
• Possible neurotoxicity manifesting as oto/vestibular toxicity (rare)

Candidemia

Today we discussed candidemia. The 2009 IDSA guidelines are available here.

In general:

• If the patient is critically ill, has recently been exposed to azoles, or the local prevalence of azole resistant candida is high initial therapy should be an echinocandin. Otherwise an azole like fluconazole would be appropriate.
  
• Line foci *must* be removed
• You should look for metastatic spread including the eyes or heart valves. Other investigations to look for osteomyelitis or septic thrombophlebitis should be based on history and clinical suspicion.
• Treatment duration varies depending on complication. In general, if there is no evidence of metastatic spread of infection treatment duration is 2 weeks after the last negative culture. There should be some clinical and microbiological follow-up to document relapse.
  

Prevention of Surgical Site Infections

Today we had a case of a post-sternotomy sternal wound infection. This led to a discussion on the prevention of surgical site infections (SSI) -- nosocomial, potentially preventable infections that lead to increased morbidity and mortality, cost, and length of stay.

Keys to prevention of SSI (SHEA guidelines here):

• Encourage smoking cessation
  
• Existing infections, distant from the surgical site should ideally be treated first
• Patient should be freshly showered either before the OR or the night before, often using chlorhexadine body wash (conflicting evidence on utility, see review here)
  
• Hair removal, if absolutely required, should be done with clippers
  
• Surgical site antimicrobial prophylaxis (SSP) should be chosen based on the local epidemiology and the type of surgery
• SSP should be administered within 1 hour of the first incision, ideally before the incision. Repeat doses should be administered based on the half life of the agents involved and the length of the case. Total duration should be less than 24 hours
  
• Maximal attention to sterile technique and the donning of sterile gloves, gowns, masks, and hats
• Avoidance of severe (more than 11.0) hyperglycemia peri-operatively
• Avoidance of intraoperative hypothermia (less evidence)
  

The article I was discussing regarding pre-operative chlorhexadine decolonization was actually older than I thought -- 2006 JAMA, available here. NNT was 16 to prevent nosocomial infection. Relatively high quality study.

Pre-operative mupirocin has not been shown to be beneficial for SSI (Canadian study here, larger study here) but may reduce nosocomial staph aureus infections.

No study has rigorously evaluated full pre-operative staph aureus decolonization with this protocol, which is used in Toronto for MRSA. I would probably choose to do this for elective surgeries for patients with known MRSA if there were no contraindications.

Infection of Cysts in Polycystic Kidney Disease

Today we were challenged by a case of a patient with PKD who had a urinary tract infection with a resistant E. Coli complicated by a presumed infected cyst.

In PKD, renal cyst infections are usually caused by E. Coli or other urinary organisms. They can be difficult to diagnose but often present with fever, abdominal pain, and elevated inflammatory markers. Cysts may enlarge or show evidence of complex septation or debris -- however, imaging is often not helpful in making the diagnosis.

Urine culture is positive in 40%, Blood in 25%, and cyst aspirates in another 12%. Medical therapy includes a relatively prolonged (3+ weeks) course of antibiotics. Usually fluoroquinolones or TMP/SMX are preferred because of cyst penetration. Beta-lactam and aminoglycoside penetration is relatively poor.

In failure of medical therapy (prolonged symptoms, fever, sepsis) or in cases where the presumed culprit cyst is greater than 5cm in diameter, percutaneous or surgical drainage is often required.

See the recently published case series here.

In our case today we elected to use high-dose ceftriaxone (since CIP/TMP-SMZ/AMP/CEF were resistant) to try and maximize intracyst concentration.