Patient: M.E. (55 y/o male) Chief complaint: – Painful erythematous swelling on the face

HISTORY OF PRESENT ILLNESS 3 days PTA Patient first noticed a painful “pimple” at the left lower lip. There was no associated trauma (e.g., shaving, insect/animal bites), previous dermatoses, rhinitis, otitis media, conjunctivitis, or other oropharyngeal diseases. He self-medicated with mefenamic acid and amoxicillin. No consult was done. 2 days PTA Patient experienced fever (highest recorded measurement at 38.5°C), which was relieved by intake of paracetamol. There was persistence of the “pimple” without any change in size or quality of the pain. Still, no consult was done.

HISTORY OF PRESENT ILLNESS 1 day PTA Patient reported that the lesion on the face developed into a painful erythematous swelling involving the lips, left cheek, eyelid and neck. Patient sought consult at a community center and was advised to go a hospital. Few hours PTA Patient experienced severe pain and more progressive swelling of the face. He was then brought to the hospital and was admitted.

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 5 th 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, 17 th 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, 17 th 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, 17 th ed.

COURSE IN THE WARD

DIAGNOSTIC AND THERAPEUTIC APPROACH

Ki and Rotstein. Can J Infect Dis Med Microbiol March; 19(2):

*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 March; 19(2):

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 March; 19(2):

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 March; 19(2):

Management: Facial Cellulitis Mild to Moderate Infection – Augmentin 875 mg PO bid Augmentin – Cefazolin (Ancef) 1 g IV every 8 hours CefazolinAncef Severe Infection – Nafcillin 2 g IV every 4 hours Nafcillin – Oxacillin 2 g IV every 4 hours Oxacillin – Vancomycin g IV qd Vancomycin Ki and Rotstein. Can J Infect Dis Med Microbiol March; 19(2):

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 March; 19(2):

Diabetes Mellitus Insulin therapy? Diet recommendation