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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. Adelaide, Australia. 2. Last accessed 25th February 2011, available at: http://etg.hcn.net.au.ezproxy1.canberra.edu.au/ 3. Last accessed 25th February 2011, available at: https://www.mimsonline.com.au.ezproxy1.canberra.edu.au/Search/Search.aspx 4. Walker R, Edwards C. (2003). Clinical Pharmacy and Therapeutics. Churchill Livingstone 4th edition; (chapter 37). 5. Groote De M.A. And Johnson P. (2004). Skin, bone and soft tissue infections. World health organisation; (chapter 8). 6. McNamara, D.R., I.M. Tleyjeh, E.F. Berbari, B.D. Lahr, J.W. Martinez, S.A. Mirzoyev, and L.M. Baddour. "Incidence of Lower-Extremity Cellulitis: A Population-Based Study in Olmsted County, Minnesota." Mayo Clin Proc. 82.7 July 2007: 817-821. 7. Cellulitis. Last accessed 25th February; available at: http://www.merckmanuals.com/home/sec18/ch211/ch211b.html 8. Bisno AL, Stevens DL. (1996). Streptococcal infections of skin and soft tissues. N Engl J Med 334: 240-245. 9. Treatment of soft tissue infections. Last accessed 25th February , available at: http://www.who.int/water_sanitation_health/emerging/en/patmycrobact8.pdf. 10. Hersh AL, Chambers HF, Maselli JH, Gonzales R. National trends in ambulatory visits and antibiotic prescribing for skin and soft-tissue infections. Arch Intern Med. Jul 28 2008;168(14):1585-91. 11. Cellulitis. Last accessed 25th February 2011, available at: http://emedicine.medscape.com/article/1053686-overview 12. Skin image. Last accessed 28th February 2011, available at: http://www.cancer.umn.edu/cancerinfo/NCI/Media/CDR0000579036.jpg. 13. Cephalosporin. Last accessed 28th February 2011, available at: http://www.emedexpert.com/compare/cephalosporins.shtml 14. Ellis Simonsen SM, van Orman ER, Hatch BE, et al. Cellulitis incidence in a defined population. Epidemiol Infect. Apr 2006;134(2):293-9. 15. Davies HD, McGeer A, Schwartz B, et al. Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study Group. N Engl J Med. Aug 22 1996;335(8):547-54. 16. NF. Last accessed 25th February 2011, available at: http://www.medscape.com/viewarticle/444061_5 17. Types of debridement. Surgical debridement. Last accessed 25th February 2011, available at: http://medicaledu.com/debridhp.htm. 18. Hyperbaric oxygen therapy. Last accessed 30th February 2011, available at: http://www.drcranton.com/hbo.htm 19. Kaul R, McGeer A, Norrby-Teglund A, Kotb M, Schwartz B, O’Rourke K, Talbot J, Low DE, and The Canadian Streptococcal Study Group. Intravenous Immunoglobulin Therapy for Streptococcal Toxic Shock Syndrome – A Comparative Observational Study. Clinical Infectious Disease. 1999; 28:800-807. 20. Cellulitis image. Last accessed 28th February 2011, available at: http://www.google.com.au/imgres?imgurl=http://findmeacure.com/wp-content /uploads/2008/03/cellulitis_left_leg.jpg&imgrefurl=http://findmeacure.com/2008/03/0 4/cellulitis/&usg=__3Suw8XSrbscuH0f5a-_XFQfhdTc=&h=482&w= 640 &sz=80&hl=en&start=2&zoom=1&um=1&itbs=1&tbnid=1jtZEaU3zf_m4M:&tbnh= 103&tbnw=137&prev=/images%3Fq%3Dcellulitis%26um%3D1%26hl%3Den%26sa %3DN%26tbs%3Disch:1&ei=QbKGTdrpJI-lcfO3kJUD. 21. Cellulitis image. Last accessed 28th February 2011, available at: http://www.google.com.au/imgres?imgurl=http://rpmedia.ask.com/ts%3Fu%3D/wikip edia/commons/thumb/6/60/Cellulitis3.jpg/190px-Cellulitis3.jpg&imgrefurl =http://www.ask.com/wiki/Anaerobic_cellulitis&usg= __5YFjswgembbFYmdiky 7Sbr6CeW8=&h=1632&w=1224&sz=271&hl=en&start=25&zoom=1&um=1&itbs= 1&tbnid=-Hsyhm_7Ffmx_M:&tbnh=150&tbnw=113&prev=/images%3Fq%3 Dcellulitis%26start%3D20%26um%3D1%26hl%3Den%26sa%3DN%26ndsp%3D20 %26tbs%3Disch:1&ei=MbOGTaSIPIzQcdHlqbQF