big group discussion group c3b malig-marayag carbuncle with ipsilateral facial cellulitis in a...

Big Group DiscussionGroup C3B

Malig-Marayag

Carbuncle with Ipsilateral Facial Cellulitis in a Diabetic

Infections in DiabeticsDiabetic patients have greater frequency

and severity of infection due to:Diminished vascularizationHyperglycemia

Impairs killing of micro-organisms by neutrophils and macrophages

Interferes with T lymphocyte functionAids in colonization and growth of a variety

of organisms (Candida and other fungal species

Harrison’s Principles of Internal Medicine, 17th ed.

Oxford Textbook of Medicine, 4th ed.

CellulitisAcute suppurative inflammation involving

the subcutaneous tissueCharacterized by:

Localized pain, erythema, swelling, heatDifferentiated from erysipelas:

Lesion is not raisedLine between the involved and

uninvolved tissue is indistinct

Harrison’s Principles of Internal Medicine, 17th ed.Jawetz, Melnick & Adelburg’s Medical Microbiology, 24th ed.

CellulitisMild local erythema and tenderness

Rapidly becomes intense and spreadsArea becomes infiltrated and pits on pressureCentral part may become nodular and

develop a vesicle that ruptures and discharges pus and necrotic material

MalaiseFever and chills

Andrews’ Diseases of the Skin: Clinical Dermatology, 10 th ed.

CellulitisMost 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


CellulitisAssociated with predisposing conditions

Streptococcus agalactiae – diabetes mellitus, peripheral vascular disease

Haemophilus influenzae – causes periorbital cellulitis children with sinusitis, otitis media or epiglottitis


Facial CellulitisPeople with certain risk factors are more

likely than others to develop facial cellulitis. Facial cellulitis risk factors include:Problems in the lymphatic system Upper respiratory infection Infection of the teeth or middle ear

http://skin.emedtv.com/facial-cellulitis/facial-cellulitis-p2.html

Facial Cellulitisin the facial region the most common portals

of entry are dental infections, sinusitis, upper respiratory tract infection, surgery, and trauma

Facial cellulitis associated with Pseudomonas aeruginosa complicating ophthalmic herpes zoster Laura Atzori MD1, Caterina Ferreli MD1, Myriam Zucca MD1, Daniela Fanni MD2, and Nicola Aste MD1 Dermatology Online Journal 10 (2): 20

Patient: M.E. (55 y/o male), unemployed

Chief complaint: Painful erythematous swelling on the face

HISTORY OF PRESENT ILLNESS

PAST MEDICAL HISTORY• Diabetic for 27 years

– Maintained on Gliclazide(Diamicron) for the first 10 years with unrecalled dose taken OD

– Insulin maintenance (Humulin N 20 ’u’ in the morning and 15 ‘u’ in the evening) for the past 16 years

• Cholecystitis- underwent cholecystectomy in 1996

• Underwent 3 operations for the right eye:• 2003- cataract surgery • 2004- glaucoma- trabeculectomy • 2007- corneal transplant; patient developed graft rejection which led to blindness

FAMILY HISTORY

(+) DM – mother(+) HPN - father(+) HPN – brother(-) Cancer, allergy, stroke

PERSONAL AND SOCIAL HISTORY

• Married (with 2 children)• Used to work as a “master cutter” at a tailoring shop until 2003• Currently unemployed•Occasionally smokes and drinks alcohol•Mixed diet

MEDICATIONS

Insulin (Humulin N 20 ”U” in the morning and 15 “U” in the evening)

Vitamin B complex

REVIEW OF SYSTEMSNo headache, vertigo, syncopeNo epistaxis, nasal dischargeNo neck stiffness, masses,

lymphadenopathyNo tinnitus, ear discharge, loss of

hearingNo dyspnea, coughNo chest pain, easy fatigability,

nocturnal dyspnea, orthopnea, palpitations

REVIEW OF SYSTEMS• No nausea, vomiting, hematemesis,

dysphagia, abdominal pain, diarrhea, constipation, melena, hematochezia

• (+) polyphagia, polydypsia, polyuria, (-) dysuria, flank pain, urethral discharge

• No joint stiffness, pain, swelling, muscle pain, cramps, weakness, wasting

• (+) numbness, tingling sensations on both feet

• (+) hyperpigmented scaly plaque on the dorsum of the right foot

• No heat-cold intolerance• No pallor, abnormal bleeding, bruising

ON ADMISSION (SEPT 18, 2009)

Conscious, coherent and oriented to time, place and person

Vital Signs: BP: 130/70mmHg PR - 109bpm, RR-20cpm, Temp: 36.7°C

Weight= 66 kg Height= 170cm BMI=23 HEENT: (+) periorbital swelling,

nonhyperemic conjunctivae, anicteric sclerae, cornea opaque, OU, retina pigmented OU, lens cannot be assessed, (+) light perception, OD, (+) hand movement, OS

No nasoaural discharge, (+) swelling with violaceous discoloration of the lower lip and surrounding skin topped with multiple erosions, crusts and pus, buccal mucosa cannot be assessed

NECK: supple neck, no masses, (-) palpable cervical LN,right, LN on the left cannot be assessed due to swelling over the submandibular area, (-) neck vein distension




nonhyperemic conjunctivae, anicteric sclerae, cornea opaque, OU, retina pigmented OU, lens cannot be assessed, (+) light perception, OD, (+) hand movement, OS

No nasoaural discharge, (+) swelling with violaceous discoloration of the lower lip and surrounding skin topped with multiple erosions, crusts and pus, buccal mucosa cannot be assessed


SEPT 19, 2009 Conscious, coherent and oriented to

time, place and person Vital Signs: BP: 120/80mmHg PR -

90bpm, RR-24cpm, Temp: 37.3°C Weight= 66 kg Height= 170cm BMI=23 HEENT: (+) periorbital swelling,

nonhyperemic conjunctivae, anicteric sclerae, cornea opaque OU

No nasoaural discharge (+) swelling with ruptured carbuncle on

the left lower lip sorrounded by cellulitis, buccal mucosa cannot be assessed





nonhyperemic conjunctivae, anicteric sclerae, cornea opaque OU

No nasoaural discharge (+) swelling with ruptured carbuncle on

the left lower lip sorrounded by cellulitis, buccal mucosa cannot be assessed


THORAX & LUNGS: Symmetric chest expansion, (-) retractions (-) lagging, equal vocal tactile fremiti, resonant on all lung fileds, clear breath sounds

CARDIAC: Adynamic precordium, (-) heaves, thrills and lifts, S1>S2 at the apex, S2>S1 at the base, (-) murmurs

Pulses full and equal on all extremities ABDOMEN: soft, globular abdomen, non-

tender, normoactive bowel sounds; Liver-smooth, non-tender, vertical span- 6 cm at the MCL; spleen & kidneys not palpable

EXTREMITIES: Motor strength grade 5/5 on all extremities, no sensory deficits

(+) 16X7cm pruritic, hyperpigmented plaque with scaly surface on the dorsum of the right foot and distal third of the leg

THORAX & LUNGS: Symmetric chest expansion,

(-) retractions (-) lagging, equal vocal tactile

fremiti, resonant on all lung fileds, clear breath

sounds CARDIAC: Adynamic precordium, (-) heaves,

thrills and lifts, S1>S2 at the apex, S2>S1 at the

base, (-) murmurs Pulses full and equal on all extremities ABDOMEN: soft, globular abdomen, non-tender,

normoactive bowel sounds; Liver-smooth, non-

tender, vertical span- 6 cm at the MCL; spleen &

kidneys not palpable EXTREMITIES: Motor strength grade 5/5 on all

extremities, no sensory deficits, tingling sensation

on both feeth (+)16X7cm pruritic, hyperpigmented plaque with

scaly surface on the dorsum of the right foot and

distal third of the leg

ON ADMISSION (SEPT 18, 2009) SEPT 19, 2009

CLINICAL IMPRESSIONCarbuncle, Left lower lip with

Ipsilateral Facial Cellulitis Diabetes Mellitus, Type 2, Insulin

Requiring

DIFFERENTIAL DIAGNOSIS:Erysipelas

Cellulitis vs ErysipelasCellulitis Erysipelas

Etiology Staphylococcus spp.Streptococcus spp.

Various other bacteria

Streptococcus pyogenes

Characteristics of lesion

Localized pain, erythema, swelling, heat, lesion is not raised, line between the involved and uninvolved tissue is indistinct

Local redness, heat, swelling with a characteristic

raised, indurated border

Accompanying signs and symptoms

Malaise, chills, fever Malaise, chills, high fever, headache,

vomiting, joint painsHarrison’s Principles of Internal Medicine 17th ed.

DIAGNOSTIC PLANS:CBCCBGBlood Chemistry

creatinineLipid profileHBA1cSodium Potassium

Arterial Blood Gas

THERAPEUTIC PLANSANTIBIOTIC- what?INSULIN THERAPY ACCORDING TO CBG

RESULTS(SLIDING SCALE)/INSULIN DRIP?DIETARY MANAGEMENT- DIABETIC/RENAL

DIET specific diet: kilocalories/day, protein &

carbohydrate requirementHYDRATION-PLAIN NSS (HOW MUCH

INFUSION/MIN)

Laboratory Results

pH 7.458 7.40 ±0.05

pCO2 27.6 mmHg 40 ±5

pO2 56.5 mmHg 95 ±5

HCO3 19.5 mmol/L

24 ±2

FiO2 21% (room air)

P/F 259

DIAGNOSTIC TEST FOR DIABETES MELLITUS

National Diabetes Group and WHO diagnostic criteria for DM:

Fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/L).

Plasma glucose at or above 200 mg/dL (11.1 mmol/L) two hours after a 75 g oral glucose load as in a glucose tolerance test.

Symptoms of hyperglycemia and plasma glucose at or above 200 mg/dL (11.1 mmol/L).

Harrison’s 17th Edition

Fasting blood glucose test • The most common test for diagnosis of

diabetes.

• blood glucose levels are checked after fasting for between 12 and 14 hours.

• Patients with fasting glucose levels from 100 to 125 mg/dL (6.1 and 7.0 mmol/L) are considered to have impaired fasting glucose

• Patients with diabetes may be asked to delay their diabetes medication or insulin dose until the test is completed.

http://ovennewyork.com/diabetes-mellitus-laboratory-tests-or-diagnostic-tests.html

Random blood glucose test blood glucose levels are checked at various

times during the day, and it doesn’t matter when you last ate.

Blood glucose levels tend to stay constant in a person who doesn’t have diabetes.


Oral glucose tolerance test (OGTT) • FBS is obtained before the ingestion of a 50- to

200-g glucose load (usual amount is 75 g),

• blood samples are drawn at Â½, 1, 2, and 3 hours (may be 4- or 5-hour sampling).

• Blood samples are checked at regular intervals for two hours.

• Glucose tolerance tests are used when the results of the fasting blood glucose are borderline.


• They are also used to diagnose diabetes in pregnancy (gestational diabetes).

• NORMAL: the results of the glucose tolerance test will show that their blood sugar levels fall within the normal range

• Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/L, but not over 200, two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance.

Glycated Hemoglobin (Glycohemoglobin, HbA1c) for Diabetes Mellitus

• Measures glycemic control over a 60- to 120-day period by measuring the irreversible reaction of glucose to hemoglobin through freely permeable erythrocytes during their 120-day lifecycle.

• While not used for diagnosis, an elevated level of glucose irreversibly bound to hemoglobin of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs


GOALS OF THERAPYEliminate symptoms related to

hyperglycemiaReduce or eliminate the long-term

microvascular and macrovascular complications of DM

Allow the patient to achieve as normal a lifestyle as possible


Insulin vs. hypoglycemicsOral hypoglycemics

Should not be used in severly ill patients with type 2 DM

Insulin secretagogues: such as sulfonlyureas are effective in individual with relatively recent onset (<5 yrs) of type 2DM

Biguanides (metformin): should not be used in patients with renal insufficency [serum creatinine > 133umol/L (1.5mg/dL) in men]

Should be discontinued in patients who are severly ill, in patients who can take nothing orally and in thoe receiving radiograohic contrast material

α- glucosidase inhibitors (acarbose and miglitol): should not be used in patients with inflammatory bowel disease, gastroparesis or a serum creatinine >177umol/L (2.0mg/dL)

Insulin

Considered initial therapy in type 2 DM, particularly in lean individuals or those with severe weight loss, in individuals with underlying renal or hepatic disease that precludes oral glucose-lowering agents, or in individuals who are hospitalized or acutely ill

A long acting insulin (lantus) is best for the patient because if his age etc. since you don’t have to take it often.

Patient education about DM, nutrition and exercise• Patient with DM should receive education

about:– Nutrition– Exercise– Care of diabetes during illness– Medications to lower the plasma glucose

• Continuing process with regular visits for reinforcement

• Diabetes self-management education (DSME)


Diabetes education• Self-monitoring of blood glucose• Urine ketone monitoring (type 1)• Insulin administration• Guidelines for diabetes management

during illness• Management of hypoglycemia• Foot and skin care• DM management before, during and after

exercise• Risk-factor-modifying activities


NutritionMedical Nutrition Therapy (MNT)

Modest caloric reductionReduced fat intakeIncreased physical activityReduction of hyperlipidemia and

hypertension


Exercise• CV risk reduction• Reduced BP• Maintenance of muscle mass• Reduction in body fat and weight loss• Lowering plasma glucose• Increasing insulin sensitivity

*ADA recommends 150 min/week (distributed over at least 3 days)


Monitoring the level of glyceminc controlPlasma glucose measurements by the

patient and assessment of long-term control by the physician

Measurement of A1C and review of the patient’s self-measurement of plasma glucose


Self-monitoring of Blood GlucoseStandard of care in diabetes management

and allows the patient to monitor his/her blood glucose at any time

Glucose monitors can rapidly and accurately measure glucose in small amounts of blood (3-10 µL obtained from the fingertip*individuals with type 2 DM who are taking

insulin should utilize SMBG more frequently than than those on oral agents


Assessment of Long-term Glycemic ControlMeasurement of glycated hemoglobinPlasma glucose is consistently elevated =

increase in nonenzymatic glycation of hemoglobin

Reflects the glycemic history over the previous 2-3 months


CELLULITIS

DIAGNOSTIC PLANS FOR CELLULITIS

CT scan with contrast of the paranasal and neck area

pharyngolaryngoscopy

Blood cultureAspirationCT scan

*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

DiagnosisBased 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.

Goals of treatmentEliminate the offending microorganismTreat/manage any underlying conditions

that would increase the chance of cellulitis returning (DM)

Prevent recurrence of cellulitis

oral therapy for mild infections

intravenous therapy for severe infections achievement of high

drug levels with rapid delivery.

Therapeutic approach

Non-pharmacologic

Rest affected area, elevate the area of the body involved (this will help decrease swelling and relieve discomfort)

Clean wound site

PharmacologicCellulitis in a DM patient Early or Mild disease

Augmentin 875 mg PO bidSecond Generation Cephalosporin

(cefoxitin, cefacor, cefuroxime)Third Generation Cephalosporin

(cefotaxime, ceftazidime,m ceftriaxone, cefixime)

Severe disease Imipenem-Cilastatin (Primaxin)Ampicillin-sulbactamMeropenemTrovafloxacin IV Nafcillin 2 g IV every 4 hours Oxacillin 2 g IV every 4 hours Vancomycin 1.0-1.5 g IV qd (ABG)Linezolid

www.emedicinehealth.com/cellulitis

www.fpnotebook.com/DER/Endo/SknInfctnsInDbtsMlts.htm

In a study by Kohno et al, Linezolid was compared with vancomycin; both had a comparable clinical success rate in the treatment of SSTi.

In the lab tests done after the end of the treatment and during follow up, Linezolid had a better microbial eradication rate. Also, for the adverse effects (hematologic), linezolid was safer.

S. Kohno1, K. Yamaguchi2, et al. Linezolid versus vancomycin for the treatment of infections caused by methicillin-resistant. Staphylococcus aureus in Japan. Journal of Antimicrobial Chemotherapy 2007 60(6):1361-1369; doi:10.1093/jac/dkm369

http://jac.oxfordjournals.org/cgi/content/full/60/6/1361

Vancomycin is distributed widely to various tissues and body fluids, however in patient with DM, its penetration in soft tissues is greatly impaired

AUSkhirtladze K; Hutschala D; Fleck T; Thalhammer F; Ehrlich M; Vukovich T; Muller M; Tschernko. Impaired target site penetration of vancomycin in diabetic patients following cardiac surgery. EM SOAntimicrob Agents Chemother. 2006 Apr;50(4):1372-5.

http://www.uptodate.com/patients/content/abstract.do;jsessionid=F7D4E0E035890469420995852E59E973.1102?topicKey=~aa8X1QFoqoQSyT&refNum=8

http://www.uptodate.com/patients/content/topic.do?topicKey=~aa8X1QFoqoQSyT

In a study by Stein et al, Linezolid was effective in the treatment of Staphylococcus aureus in diabetic patients

G E. Stein1,* S Schooley1, et al. Linezolid tissue penetration and serum activity against strains of methicillin-resistant Staphylococcus aureus with reduced vancomycin susceptibility in diabetic patients with foot infections. Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkm271

http://jac.oxfordjournals.org/cgi/content/full/dkm271v1

Duration of therapyresponse to drug therapyfollow-up is of utmost importance10 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

Preventing a recurrence of cellulitisCellulitis tends to recur in people with

certain medical conditions that can lead to skin breakdown, such as edema (fluid buildup), fungal or bacterial infections, diabetes, or peripheral arterial disease. edema, support stockings and good skin hygiene

may reduce or eliminate recurrence of cellulitis.fungal infections, regular use of antifungal

medicines may help reduce recurrent cellulitis. high risk for recurring cellulitis, (when with open

wound or cut) taking preventive antibiotics may help

http://www.everettclinic.com/kbase/topic/mini/tr5105/treatmnt.htm

Linezolid versus Vancomycin in Treatment of Complicated Skin and Soft Tissue InfectionsJohn Weigelt,* Kamal Itani,Dennis Stevens, William Lau, Matthew Dryden, Charles Knirsch,* and the Linezolid CSSTI Study Group

PurposeThe purpose of this study was to compare

linezolid to vancomycin1. Clinical efficiency – resolution of symptoms2. Microbiological efficiency 3. Safety and tolerability

Background of the StudyThis was a randomized, open-label,

comparator-controlled, multicenter, multinational study that included patients with suspected or proven methicillin-resistant Staphylococcus aureus (MRSA) infections that involved substantial areas of skin or deeper soft tissues, such as cellulitis, abscesses, infected ulcers, or burns <10% of total body surface area.

PathogensSENTRY Antimicrobial Surveillance Program:

SSTIs may be caused by a wide range of pathogens Staphylococcus aureus 40% 5% of infections included

Pseudomonas aeruginosa (12%)Escherichia coli (10%)Enterococcus spp. (8%)Klebsiella spp. (6%)Enterobacter spp. (6%)

Materials and MethodStudy period: October 2002-March 2003Inclusions:

Required physical findings included (i) erythema with or without induration, (ii) fluctuation, (iii) heat/localized warmth, (iv) pain/tenderness, and (v) drainage/discharge.

at least one of the following symptoms: (i) fever, (ii) hypothermia, (iii) hypotension, (iv) a white blood cell count of 10,000/mm3, or (v) 15% immature neutrophils regardless of white blood cell count

Statistical AnalysisMicrobiological outcomes were categorized

as success (documented or presumed

eradicationof the pathogen present at baseline)

failure (documented or presumed persistence of pathogen present at baseline)

indeterminate (pathogen data indeterminate),

missing (pathogen data missing).

ResultsClinical Efficacy

Linezolid > Vancomycin

Microbiological EfficacyLinezolid > Vancomycin

Safety and TolerabilityLinezolid = Vancomycin

CostLinezolid Vancomycin

IV Zyvox 2mg/mL x 300mLP 3,418.28

Vancocin 500mg P 1,929.00

Suspension

Zyvox 100 mg/5 mL x 150 mL P 14,637.28

NA

Tablet Zyvox 600mgP 2,950.40

NA

Linezolid Vancomycin

600mg IV or PO every 12 hours

IV: 3,418.28 x 2 = P 6,836.56PO: 2,950.40 x 2 = P 5,900.80

1g IV every 12 hours

IV: 1,929.00 x 4 = P 7,716

References Vincent Ki, MD and Coleman Rotstein, MD. Bacterial skin and soft

tissue infections in adults: A review of their epidemiology, pathogenesis, diagnosis, treatment and site of care. Can J Infect Dis Med Microbiol. 2008 March; 19(2): 173-184.

G E. Stein1,* S Schooley1, et al. Linezolid tissue penetration and serum activity against strains of methicillin-resistant Staphylococcus aureus with reduced vancomycin susceptibility in diabetic patients with foot infections. Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkm271

AUSkhirtladze K; Hutschala D et al. Impaired target site penetration of vancomycin in diabetic patients following cardiac surgery. EM SOAntimicrob Agents Chemother. 2006 Apr;50(4):1372-5.

S. Kohno1, K. Yamaguchi2, et al. Linezolid versus vancomycin for the treatment of infections caused by methicillin-resistant. Staphylococcus aureus in Japan. Journal of Antimicrobial Chemotherapy 2007 60(6):1361-1369; doi:10.1093/jac/dkm369

Results

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