1. Rubor, calor, dolor, tumor….. M Armstrong
Cellulitis
Rubor, calor, dolor, tumor…..
M Armstrong

2. Is not cellulitis a boring topic?
Why talk about it? It is just inflammation of the skin…. Unfortunately cellulitis is often not managed optimally The sight of any red skin often leads to the over diagnosis of cellulitis The management of bacterial cellulitis (or any red leg) is thought to = antibiotics

3. Some definitions
Cellulitis is a superficial inflammatory condition of the skin and underlying tissues characterized by erythema, warmth, and tenderness of the involved area
The term “cellulitis” refers to an uncomplicated non-necrotizing acute infection of the skin that involves the mid to lower dermis and subcutaneous tissue (or hypodermis). It does not extend more deeply to fascia or muscle
Erysipelas a more superficial version of cellulitis involves the upper dermis and superficial cutaneous lymphatics

4. Cellulitis can be grouped under different terms SSTI/SSSI
-is one entity in the broader category of skin and soft tissue infection, perhaps around 30% of all SSTI but this is likely to be an under representation
Can divide cellulitis into purulent or non-purulent cellulitis
Necrotizing infections should not be classified as “cellulitis”

6. Epidemiology / Demographics
Occurs most frequently in diabetics, immunocompromised hosts, and patients with venous and lymphatic compromise
Incidence- common presentation ~24.6 cases per 1000 person years

7. Pathophysiology
Pathologically “a diffuse area of soft-tissue infection characterized by leukocytic infiltration of the dermis, capillary dilatation, and the proliferation of bacteria” Cellulitis is caused by microbes colonizing the skin or by bacteria introduced through animal contact, including bites Intact healthy skin in non-immunocompromised hosts is a nearly perfect barrier to infection- small breaks in the skin from abrasions, insect bites, burns, splinters, dermatophyte infections, bites, surgery can be responsible, and not immediately apparent

8. Pathophysiology
Cellulitis usually occurs when one or more risk factors are present
Other conditions predispose: chronic venous insufficiency, lymphedema
Other potential sources: contiguous- OM, haematogenous- bacteremia

9. Pathophysiology
Likely that a lot of the clinical signs and symptoms of cellulitis are from potent virulence factors
-cytokines (TNF and IL-1)
-exotoxins

10. Differential diagnosis..
Quite a few things can cause red skin…. “non-bacterial cellulitis” DVT, peripheral vascular insufficiency, thrombophlebitis, acute gout, psoriasis, insect bite, fixed drug eruption, lymphedema, contact dermatitis, erythromelalgia, shingles, lipodermatosclerosis…

11. Work up
Hx, Exam (elevate) Usual inflammatory markers, including CRP Culture (if possible) Blood cultures (before antibiotics), but only around 4% of patients with cellulitis will have positive blood cultures (more likely to be positive in patients with pre-existing lymphoedema or patients with either fresh water or salt water exposure) Punch biopsy/ needle aspiration- if diagnostic confusion (biopsy at leading edge vs area of most inflammation), although only 20% are positive Other- imaging (plain film, US, CT, MRI)

12. Management
-Non-Pharmacologic Elevate, and more elevation, good wound care -Pharmacologic (not just antibiotics) Analgesia, topical antifungals, ? addition of steroids*, ?? aggressive treatment of oedema** * **

13. Management And now to the antibiotics… Per guidelines
Area of redness can spread beyond initial limit despite adequate antibiotic coverage
Once fevers are down/ systemic symptoms reduced (this can sometimes take time despite appropriate antibiotic therapy)- switch to oral antibiotics early, often do not need HITH. Over treatment with IV antibiotics is common, 2 weeks maximum is usually adequate
For the surgeons can change to oral clindamycin!!

14. eTG

15. eTG
Note that cellulitis in diabetic patients is not treated differently from non-diabetics (chronic “diabetic foot” infections being an exception)
Consider adding Vancomycin in cases of treatment failure, or adding in gram negative coverage

16. Specific syndromes
The streptococcal cellulitis patient... Caused by group A > C,G >> B (in the elderly/diabetics/PVD) “perfectly well then the sudden onset of feeling generally unwell with nausea, vomiting and rigors. Often no signs of cellulitis initially then skin signs develop later (on the post take ward round!)” Patients can get good at recognizing this if they have recurrent episodes, big differential to not miss would be meningococcal disease

17. Specific syndromes
The recurrent cellulitis patient…(often streptococcus) Once you have had one attack of streptococcal cellulitis, scarring of lymphatics increases the chance of getting further infection Tinea and other factors can be added to the mix Prophylactic treatment of fungal infections or prophylactic oral penicillin mg BD can be considered in patients with more then 2 episodes of cellulitis in the same place

18. https://medicswriter. wordpress

19. “Purulent” cellulitis (associated with purulent exudate or drainage)
Usually associated with Staphylococcal aureus cellulitis including MRSA Purulent infection that spreads from a localized infection/ wounds such as an abscess, folliculitis, surgical wound or infected foreign body (splinter, IVC, prosthetic device) MRSA is becoming increasing common, specific risks include diabetics patients, athletes, people living in public housing, and incarcerated people, IVDU Usually do not get as sick as quickly (C/F Streptococcal cellulitis)

20. Erysipelas Specific variant of cellulitis
-Erysipelas involves the outer layer of the epidermis, defined by acute onset of abrupt onset of fiery red well defined painful swelling across face or extremities
-Erysipelas is caused by GAS (S pyogenes) or C/G strep, clinical signs are secondary to exotoxins and host response

22. More specific causes of cellulitis to be aware of
Haemophilus influenzae cellulitis: area involved is a blue-red/purple-red color; occurs mainly in children; generally involves the face in children and the neck or upper chest in adults, less common post Hib vaccination
V. vulnificus: higher incidence in patients with liver disease and in immunocompromised hosts. Association with salt water exposure and seafood consumption (leading cause of death related to seafood consumption in the U.S.)
Clinically- large hemorrhagic bullae/ blisters, cellulitis, lymphadenitis, myositis; often patients critically ill in septic shock (Rx doxycycline)
Shewanella: Brackish seawater, often associated with ulcers

23. Erysipelothrix rhusiopathiae: common in people handling poultry, fish, or meat (occupational exposure)
Aeromonas hydrophila: generally occurs in contaminated open wounds in fresh water
Pseudomonas aeruginosa: Hot tub exposure, penetrating wounds (IVDU), immunocompromised patients
Mycobacterium marinum: Fish tank exposure

24. Bites (often polymicrobial, including anaerobes): Human (Eikenella corrodens), dog (Pasteurella multocida, C. canimorsus), cat (P. multocida),rat (Streptobacillus moniliformis)
Gram-negative rods (Serratia, Enterobacter, Proteus, Pseudomonas): may be present in immunocompromised or neutropenic patients
Fungi (Cryptococcus neoformans): in immunocompromised neutropenic patients

26. Necrotising fasciitis
Group A Streptococcus or mixed aerobic-anaerobic bacteria
Clostridium perfringens
MRSA with PVL toxin
Often presentation is pain out of proportion to clinical findings. Often rapid progression to swelling, brawny edema, dark red induration and bullae. Sepsis and MOF.
Mx- Surgical therapy, broad spectrum antibiotics until cultures known- Pip-Taz or Meropenem plus Clindamycin (decreased toxin mediation), IVIG, hyperbaric O2 (not much evidence)

27. eTG- necrotising fasciitis

28. Diabetic feet Often deeper then you think…
Neuropathic, poor vascular supply…Often infection can track up tendons
Often polymicrobial
Broad spectrum
Ulcers- colonized by pseudomonas

29. Bilateral “red leg syndrome”

30. Lipodermatosclerosis
Due to poor oxygenation of fat cells with apoptosis and inflammation (panniculitis- a mild inflammatory condition) High venous pressures likely significant underlying factor. 2/3rds of patients obese. It is often bilateral
Results in:
-Skin induration
-Increased pigmentation
-Oedema
-Erythema
-“Inverted champagne bottle” legs
-Leg pain

31. Episodic exacerbations of pain and erythema are commonly confused with cellulitis. It can also seem to respond to IV antibiotics, which may be because legs are elevated and patients rested while in hospital
Bilateral involvement and the absence of systemic symptoms are useful pointers to differentiate this condition from cellulitis
Inflammatory markers are not raised or only slightly
Compression stockings and weight reduction are the most important aspect of management

33. Thank you References: 5 minute consult
RACP written exam lecture series (Melbourne)
Harrison’s- 18th Edition
Netter’s infectious diseases
NEJM cellulitis clinical practice article 2004
The American Journal of Medicine cellulitis review article 2011
Various internet sources