• Patient: M.E. (55 y/o male) • Chief complaint: – Painful erythematous swelling on the face
Jan 17, 2016
• Patient: M.E. (55 y/o male)• Chief complaint: – Painful erythematous swelling on the face
HISTORY OF PRESENT ILLNESS
HISTORY OF PRESENT ILLNESS
PAST MEDICAL HISTORY• Diabetic for 27 years – Maintained on oral hypoglycemic agents for the first 9
years– Insulin maintenance for the past 16 years
• Had 3 operations on his right eye due to cataract– First was during 2003, and the last was during 2007
where he underwent corneal transplant (patient developed GVHD causing loss of sight on the right eye)
• Glaucoma on his left eye• Underwent cholecystectomy in 1996• Complete immunization
FAMILY HISTORY
• (+) DM – mother• (+) HPN – brother• (-) Cancer, allergy, stroke
PERSONAL AND SOCIAL HISTORY
• Married (with 2 children)• Roman Catholic• Used to work as a “master cutter” at a tailoring shop but is currently unemployed•Occasionally smokes and drinks alcohol•Mixed diet
MEDICATIONS
• Insulin• Vitamin B complex
REVIEW OF SYSTEMS
• (+) hyperpigmented scaly plaque on the dorsum of the right foot
• No headache, vertigo, syncope• No epistaxis, nasal discharge• (+) swollen lips, no bleeding gums, sores, fissures• No neck stiffness, masses, lymphadenopathy• No tinnitus, ear discharge, loss of hearing
REVIEW OF SYSTEMS• No dyspnea, cough• No chest pain, easy fatigability, nocturnal dyspnea,
orthopnea, palpitations• No nausea, vomiting, hematemesis, dysphagia,
abdominal pain, diarrhea, constipation, melena, hematochezia
• No urinary urgency, dysuria, flank pain, urethral discharge
• No joint stiffness, pain, swelling, muscle pain, cramps, weakness, wasting
• No heat-cold intolerance• No pallor, abnormal bleeding, bruising
PHYSICAL EXAMINATION• Weight• Height• BMI• BP: 120/80mmHg PR - 90bpm, RR - 24cpm,Temp: 37.3°C• Patient is awake, conscious, coherent and oriented to time,
place and person• PE of the FACE- describe the lesion• Supple neck, no masses, no lymphadenopathies• Apex beat at 5th LICS, S1 louder than S2 at the apex, S2 louder
than S1 at the base• No heaves, lifts, thrills, murmurs• Symmetric chest expansion, no chest wall deformities, no tactile
or vocal fremitus, no abnormal breath sounds
PHYSICAL EXAMINATION
• Globular abdomen, bowel sounds – 9/min, no tenderness on all quadrants
• Liver span 6 cm with smooth border• Spleen and kidney non-palpable• No fracture, swelling, bone malalignment,
swelling of joints. No muscle atrophy or weakness. Motor strength grade 5/5 on all extremities
Clinical Impression
• Carbuncle?? with Cellulitis of the Left half of the Face & Neck
• Diabetes Mellitus, Type 2, Insulin Requiring???
DIFFERENTIAL DIAGNOSIS
• Cellulitis• Erysipelas
Cellulitis vs Erysipelas
CELLULITIS• Etiology-• Characteristic of lesion-
• Accompanying signs & symptoms-
• ASO titer elevation- (-)
ERYSIPELAS
Erythematous swelling with raised margins/ borders
(+)
Cellulitis• inflammatory process caused
by bacterial infection of the dermis and underlying subcutaneous tissues of the skin
• trauma or underlying dermatitis
• Bacteria commonly found on the skin are most often the cause of cellulitis– although bacteria from the
environment may also cause disease
• erythema, pain, swelling, and warmth
• history of trauma or surgery causing a break in the skin or may have no discernible dermal injury.
• infection typically develops over a period of several days.
• Hallmarks – Warmth, erythema, edema,
and tenderness of the affected area
– Regional lymphadenopathy may be present.
– The margin of cellulitis is not palpable. A disease similar to cellulitis, but with a sharply defined, palpable margin is erysipelas.
– Fever may be present.
Risk Factors
• Patients with altered immune response– diabetes mellitus– Immunodeficiency– Cancer– venous stasis– chronic liver disease– peripheral arterial disease– chronic kidney disease higher risk for both recurrent and more severe infection
Etiology• In individuals with normal host
defenses, the most common causative organisms are group A streptococci and Staphylococcus aureus.
• In immunocompromised hosts, gram-negative rods or fungi may cause cellulitis, though fungal cellulitis is rare.
• Facial cellulitis is frequently associated with Haemophilus influenzae type B and Streptococcus pneumoniae.
Erysipelas
• acute streptococcus bacterial infection of the dermis, resulting in inflammation.
• Historically, the face was most affected; today the legs are affected most often
Signs and Symptoms
• high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness within 48 hours of the initial infection.
• The erythematous skin lesion enlarges rapidly and has a sharply demarcated
raised edge.
Signs and Symptoms
• red, swollen, warm, hardened and painful rash, similar in consistency to an orange peel.
• can result in vesicles, bullae, and petechiae, with possible skin necrosis
• Lymph nodes may be swollen, and lymphedema may occur
Signs and Symptoms
• may occur on any part of the skin including the face, arms, fingers, legs and toes, but it tends to favor the extremities.
• Fat tissue is most susceptible to infection, and facial areas typically around
the eyes, ears, and cheeks.
Erysipelas
• Etiology– beta-hemolytic group A
streptococci– May also be caused by
non-group A streptococci– can enter the skin through
minor trauma, eczema, surgical incisions and ulcers, and often originate from strep bacteria in the subject's own nasal passages.
• Risk Factors– immune deficiency– Diabetes– Alcoholism– skin ulceration– fungal infections– mpaired lymphatic
drainage
Diagnosis
• Can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titre occurs after around 10 days of illness.
CELLULITIS
Cellulitis
• Acute suppurative inflammation involving the subcutaneous tissue
• Characterized by:– Localized pain– Erythema– Swelling– Heat
Harrison’s Principles of Internal Medicine, 17th ed.
Cellulitis
• Mild local erythema and tenderness– Rapidly becomes intense and spreads– Area becomes infiltrated and pits on pressure– Central part may become nodular and develop a
vesicle that ruptures and discharges pus and necrotic material
• Malaise• Fever and chills
Andrews’ Diseases of the Skin: Clinical Dermatology, 10 th ed.
Cellulitis
• Most commonly caused by indigenous flora– Staphylococcus aureus – usually associated with
an abscess, folliculitis, or foreign body– Streptococcus pyogenes – spreads more rapidly;
associated with fever and lymphangitis
• Bacteria may gain access to the epidermis through:– Cracks in the skin, abrasions, cuts, burns, insect
bites, surgical incisions, intravenous catheters
Harrison’s Principles of Internal Medicine, 17th ed.
Cellulitis
• Associated with predisposing conditions Streptococcus agalactiae – diabetes mellitus,
peripheral vascular disease Haemophilus influenzae – causes periorbital
cellulitis children with sinusitis, otitis media or epiglottitis
Harrison’s Principles of Internal Medicine, 17th ed.
COURSE IN THE WARD
DIAGNOSTIC AND THERAPEUTIC APPROACH
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
• *As clinically indicated; • †Ulcerated lesions should be cleaned and debrided before having wound base swabbed; • ‡Most useful if vesicle/bullae or fluid abscess present; • §Seek out bone trauma and air fluid levels; • ¶Indications –neurological deficits, vision nonassessable, proptosis/deteriorating acuity or colour/bilateral edema/ophthalmoplegia, no improvement
after 24 h and swinging pyrexia not resolving within 36 h (for head only); • **Only if central nervous system involvement suspected
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
Diagnosis• Based on appearance of the skin and patient history
– Drainage from an abscess or weeping wound associated with cellulitis should be sent for culture and sensitivities.
– Material from needle aspiration of inflamed skin or skin biopsy can be cultured in cases of cellulitis without purulence, abscess, or a necrotic
– Indications for blood cultures include significant fever and chills, severe immunocompromise, periorbital cellulitis, and cellulitis superimposed on lymphedema.
• A polymorphonuclear leukocytosis is often present with cellulitis; a complete blood cell count and differential may help gauge the severity of infection and the hematologic response.
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
• oral therapy for mild infections
• intravenous therapy for severe infections – achievement of high
drug levels with rapid delivery.
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
Management: Facial Cellulitis
Mild to Moderate Infection – Augmentin 875 mg PO bid – Cefazolin (Ancef) 1 g IV every 8 hours
Severe Infection – Nafcillin 2 g IV every 4 hours – Oxacillin 2 g IV every 4 hours – Vancomycin 1.0-1.5 g IV qd
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
Duration of therapy
• response to drug therapy• follow-up is of utmost importance• 10 to 14 days of antibiotic therapy– Absence of response/worsening after five days of
the initiation of therapy prompts a change in the antibiotic regimen or other investigations to verify the diagnosis
Ki and Rotstein. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.
Diabetes Mellitus
• Insulin therapy?• Diet recommendation