Download A 52 year old woman who weighs 110 kg was brought in by

A 52 year old woman who weighs 110 kg was brought in by ambulance to the Canberra
hospital. She presents with the following symptoms; painful, swollen and erthematous left
lower leg. She is febrile (38.5 C), tachycardic (HR 118/min), mild hypotension (BP 105/65)
and hyperglycaemis BGL (23mmol/L). After the first examination and her systemic
symptoms where all suggestive of cellulitis.
The patients history included NIDDM, hypertension, GORD, past ulceration of the lower leg
hypothyrodisim hypercholesterolemia, depression and osteoarthritis.
Current medication at the time of admission included;
Medications
Dose
Indications
Metformin
1000mg 1 tds
NIDDM
Gliclazide
80mg 1 bd
NIDDM
Ramipril
10mg 1 d
Blood pressure
Esomeprazole
40mg 1 d
GORD
Thyroxine
50 mcg 1 d
Hypothyroidism
Atorvastatin
40 mg 1 d
Hypercholesterolemia
Sertraline
50mg 1 d
Depression
Diazepam
1 d prn
Anxiety
Paracetamol
665mg 2 tds
Osteoarthritis
Allergy to penicillin was reported but the type of allergic reaction was not indicated. At no
stage during the patients stay despite multiple culturing was an organism cultured from this
wound.
The patient denied any recent trauma to the leg and the history of infection onset was unclear.
Laboratory tests revealed a high WCC, neutrophils and CRP which are all indicators of an
infection.
Test
16/03/09
15/03/09
12/03/09
Reference Range
WCC
25.3 x 109/L
22.2 x109/L
19.7 x 109/L
5-15 x 109/L
Neutrophils
14.3 x 109/L
12.3 x109/L
10.1 x 109/L
2.1-7 x 109/L
Creatinine
93 umol/L
89 umol/L
90 umol/L
60-140 umol/L
Hb
127g/L
130g/L
129 g/L
120-155 g/L
CRP
389 mg/L
343mg/L
290 mg/L
< 10mg/L
Cellulitis is a bacterial infection mainly caused by two types of bacteria streptococcus and
staphylococcus[2,5,6,7]. These types of bacteria are normally present on the skin and in
otherwise healthy cadicats cause no harm, it is when the skin barrier is broken due to a cut,
wound, surgical incision and other methods that these bacteria lead to the development of
cellulitis by affects the dermis and subcutaneous tissue[2,5,6,7,11].
Figure 1: skin layers[12].
Cellulitis occurs anywhere on the body but the infection is most commonly seen on the lower
leg[5,6,7]. Cellulitis is characterised by localised pain, swelling, erthema, tenderness and
warmth[2,5,6,7,11]. Mortality and morbidity rates are low ~5% as most patient recover
completely when treated appropriately[11].
As with every treatment it is important to take into account the patients comorbidities to
ensure an adequate treatment plan[5,6,7,11].
Treatment:
1st line = di/flucloxacillin 500mg Q6H for 7-10days[2].
If the patient is hypersensitive to penicillin the following should be used[2]:
Cephalexin 500mg Q6H for 7-10 days[2]
Immediate penicillin hypersensitivity[2]:
Clindamycin 450mg Q8H for 7-10 days[2]
Given this patients’ history of allergies, she was started on ceftriaxone IV along with actrapid
for hyperglycaemia and IV fluids on the 11/03.
Ceftriaxone belongs to the antibacterial group Cephalosporins and it is one of the broad
spectrum antibiotics[1,3]. This group of antibiotics contain a beta-lactam ring that interferes
with the bacterial peptidoglycan synthesis[1,3]. It is therefore bactericidal and effective against
gram-negative and gram positive organisms[1,3].
Throughout the next six days the patient remained intermittently febrile and her leg failed to
show any significant signs of improvement with increasing oedema of the subcutaneous
tissue and pustule development which began to spread rapidly over the dorsum of the foot
and upper leg with signs of fat necrosis.
Necrotising faciitis (NF) more commonly known as “flesh eating disease” is a rare and life
threatening bacterial infection leading to the necrosis of the subcutanouse tissues[15,16].
Patients at risk of developing NF are the elderly, obese, immunosuppresent, neonates and
malnutrition, but it is more commonly seen in immune compromised and diabetic patients it
may also develop after chronic venous leg ulceration and skin blister and accounts for ~75%
mortatlity[15,16]. There are two types of NF these include;
Type 1:
Is most commonly associated with multiple bacteria such as Clostridia and Bacteroides[15,16].
Type 2:
Is most commonly associated with group A beta haemolytic streptococcus and can develope
with or without coexisting staphylococcal infection[15,16]. This type of necrotising fasciitis is
the one exhibited by this patient.[15,16]
The following are bacteria that maybe responsible for NF[15,16];





Group A streptococcus (Streptococcus Pyogenes),
Staphylococcus aureus (MRSA),
Clostridium Perfringens,
Bacteroides fragilis,
Vibrio yulnificus.
But the most common organism found to cause NF is Group A beta-hemolytic streptococcal
and normally develops from a previous complicated wound, in this patients case from
cellulitis[15,16].
The bacteria spreads from the subcutaneous tissue along the superficial and deep fascial
planes[16]. This facilitation happens by bacterial enzymes and toxins (e.g. collagenase,
streptokinase, hyaluronidase and lipase), which lead to vascular occlusion, ischemia, tissue
necrosis and superficial nerve damage[16].
The following two factors are needed to promote bacterial growth in NF.
1. Surface proteins expression:
M1,3,4,6,12 and 28 surface proteins increase the adherence of streptococci to the tissue,
they also work by protecting the bacteria from phagocytosis by reducing neutrophilic
phagocytosis thereby decreasing the bodys ability to eliminate the infective bacteria[16].
2. Toxin production:
Streptoccoal Pyrogenic exotoxins (SPEs) A,B and C these release exotoxins that activate
the T-cells and lead to the overproduction of cytokines[16].
Most common symptoms of any infection begins with fever and chill with an increase in
CRP, WCC and neutrophils and NF is no different, after 2-3 though erthema is noticed with
redness, swelling and blister formation in patients with NF[16].
Treatment involves the administration of several broad spectrum antibiotics, surgical
debridement, skin grafting and hyperbaric oxygen therapy (HBOT)[2,16].
Empirical therapy includes[2];
Meropenem 1g IV Q8H plus either Clindamycin 600mg IV Q8H or lincomycin 600mg IV
Q8H[2].
Streptococcus pyogenes necrotising faciitis[2];
Benzylpenicillin 1.8g IV Q4H plus either Clindamycin 600mg IV Q8H[2].
Since the patient was allergic to penicillin, ceftriaxone was used along with IV
Clindamycin[2].
I don’t know why the patient was not started on meropenem as it is indicated as the first line
treatment for necrotising fasciitis[2].
The inclusion of clindamycin in the initial antibiotic regimen has been associated with a
better outcome in streptococcal toxic shock, this could possibly be due to its inhibition of
bacterial protein synthesis and thereby reduces toxin production[3,1].
Clindamycin belongs to the antibacterial group lincosamides[1,3]. It works by reversibly
binding to the 50S sub-unit of bacterial ribosome inhibiting its protein synthesis and
preventing peptide bond formation[1,2]. It is bacteriostatic against a variety of gram +ve
aerobic and anaerobic organisms[1,2].
Subsequent rapid deterioration due to ineffective medical treatment and the development of
clinical feature suggestive of necrotising fasciitis has lead to more invasive treatment which
involved immediate surgical interventions.
Debridement of the subcutaneous tissue and deep fascia of all affected areas was performed.
Surgical debridement is a fast and selective procedure that effectively results in the removal
of the patient's dead, damaged, or infected tissue in order to promote healing of the
surrounding healthy tissue[17].
After this procedure was performed the oedema and erthema reduced and no sign of necrosis
was visible.
The patient was later transferred to the Prince of Wales Hospital to commence hyperbaric
oxygen therapy.
The transfer of this patient to Prince of Wales Hospital could be one of two thing either she
became haemodynamically unstable and needed to be commenced on inotropes or it was
done as a precautionary measure to kill off any bacterial that maybe left behind[18].
HBOT is sometimes used in treatment of NF depending on the severity of the infection[18]. It
works by providing 100% oxygen at a higher than atmospheric pressure[18]. The oxygen is
used to inhibit anaerobic bacterial growth and promote tissue recovery[18]. HBOT has been
shown to further reduce morbidity and mortality by about 10%-20% in some patients when
used in conjunction with antibiotics and surgery[18].
The benefits of HBOT is to increase pressure of oxygen in tissues, thus inproving
oxygenation and anaerobes elimination (as it is one of the most common bacterial species
responsible for NF)[18]. This provides wound healing and increases collagen formation[18].
Take home messages:
 Control the infection before the patient is discharged.
 Necrotising fasciitis can commonly be mistaken for cellulitis.
 Provide the patient with preventive measured to inhibit the infection from coming
back (e.g. refer to community wound care clinic)
 Educate on the different signs and symptoms that the patient needs to look out for
especially because she is a diabetic.
 Educate the patient on the importance of QUM and consider Webster pack to help
with compliance.
 Promote healthy eating habits and moderate exercise
References:
1. Australian Medicines Handbook, 2010. Australian Medicines Handbook Pty Ltd.
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Livingstone 4th edition; (chapter 37).
5. Groote De M.A. And Johnson P. (2004). Skin, bone and soft tissue infections. World
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Mirzoyev, and L.M. Baddour. "Incidence of Lower-Extremity Cellulitis: A
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22 1996;335(8):547-54.
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