Harrison`s Principles of Internal Medicine, 17 th ed. Cellulitis
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Transcript Harrison`s Principles of Internal Medicine, 17 th ed. Cellulitis
Carbuncle with Ipsilateral Facial
Cellulitis in a Diabetic
Big Group Discussion
Group C3B
Malig-Marayag
Infections in Diabetics
Diabetic patients have greater frequency and severity of
infection due to:
Diminished vascularization
Hyperglycemia
Impairs killing of micro-organisms by neutrophils and
macrophages
Interferes with T lymphocyte function
Aids in colonization and growth of a variety of organisms
(Candida and other fungal species
Oxford Textbook of Medicine, 4th ed.
Harrison’s Principles of Internal Medicine, 17th ed.
Cellulitis
Acute suppurative inflammation involving the
subcutaneous tissue
Characterized by:
Localized pain, erythema, swelling, heat
Differentiated from erysipelas:
Lesion is not raised
Line between the involved and uninvolved tissue is
indistinct
Harrison’s Principles of Internal Medicine, 17th ed.
Jawetz, Melnick & Adelburg’s Medical Microbiology, 24th 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, 10th 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.
Facial Cellulitis
People 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 Cellulitis
in 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
3 days PTA
2 days PTA
• Papule about the size of mongo seed at the border of the left
lower lip; no fever, no accompanying pain, erythema, swelling
no other symptoms
• No medications taken. No consult was done.
• Increase in size of the papule with central suppuration,
surrounding erythematous plaque, swelling of the left half of
the lower lip and mild pain
• fever (Tmax- 38.5°C) and generalized body malaise
• Self medicated with amoxicillin 500mg tab bid and
paracetamol 500mg/tab 1tab OD which provided minimal
relief of fever
HISTORY OF PRESENT ILLNESS
1 day PTA
Few hours
PTA
• Progression of swelling involving the entire lower
lip, left cheek, left periorbital region and
submandibular area
• Consultation at a nearby community center and
was advised to go a hospital.
• Further swelling on the left side of the face
accompanied by severe pain (4/10) admission
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 SYSTEMS
No headache, vertigo, syncope
No epistaxis, nasal discharge
No neck stiffness, masses, lymphadenopathy
No tinnitus, ear discharge, loss of hearing
No dyspnea, cough
No 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
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
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
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
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, nontender, 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, nontender, 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
CLINICAL IMPRESSION
Carbuncle, Left lower lip with Ipsilateral Facial
Cellulitis
Diabetes Mellitus, Type 2, Insulin Requiring
DIFFERENTIAL DIAGNOSIS:
Erysipelas
Cellulitis vs Erysipelas
Etiology
Characteristics of lesion
Accompanying signs and
symptoms
Cellulitis
Erysipelas
Staphylococcus spp.
Streptococcus spp.
Various other bacteria
Streptococcus pyogenes
Localized pain,
Local redness, heat, swelling
erythema, swelling,
with a characteristic
heat, lesion is not
raised, indurated border
raised, line between
the involved and
uninvolved tissue is
indistinct
Malaise, chills, fever
Malaise, chills, high fever,
headache, vomiting, joint
pains
Harrison’s Principles of Internal Medicine 17th ed.
DIAGNOSTIC PLANS:
CBC
CBG
Blood Chemistry
creatinine
Lipid profile
HBA1c
Sodium
Potassium
Arterial Blood Gas
THERAPEUTIC PLANS
ANTIBIOTIC- what?
INSULIN THERAPY ACCORDING TO CBG
RESULTS(SLIDING SCALE)/INSULIN DRIP?
DIETARY MANAGEMENT- DIABETIC/RENAL DIET
specific diet: kilocalories/day, protein & carbohydrate
requirement
HYDRATION-PLAIN NSS (HOW MUCH
INFUSION/MIN)
Laboratory Results
Blood Chemistry
CBC
Hgb
RBC
Hct
MCV
MCH
MCHC
Plt
WBC
Neutrophils
Bands
Monocytes
Eosinophils
Basophils
Lymphocytes
141
4.8
0.42
87.7
29.3
33.4
280
27.3
0.86
0.01
0.13
120-170 g/L
4-6 X 1012/L
0.37-0.54
87 ±5 U3
29 ±2 pg
34 ±2 g/dL
150-450 x109/L
4.5-10 x109/L
0.50-0.70
0-0.05
0.00-0.07
0.00-0.05
0.00-0.01
0.20-0.40
Creatinine
Urea Nitrogen
Choloesterol
Triglycerides
HDL
LDL
HBA1c
SGPT-ALT
Na
K
Cl
Acetone
2.3
35.6
150
135
31.7
87
9.18
27
129
3.4
99
Neg
0.5-1.2 mg/dL
9-23 mg/dL
131-239mg/dL
0-210
30-90 mg/dL
66-178mg/dL
4.8-6%
U/L
137-147mmol/L
3.8-5mmol/L
98-110 mmol/L
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.
http://ovennewyork.com/diabetes-mellitus-laboratory-tests-or-diagnostic-tests.html
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 ½, 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.
http://ovennewyork.com/diabetes-mellitus-laboratory-tests-or-diagnostic-tests.html
• 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
http://ovennewyork.com/diabetes-mellitus-laboratory-tests-or-diagnostic-tests.html
GOALS OF THERAPY
Eliminate symptoms related to hyperglycemia
Reduce or eliminate the long-term microvascular and
macrovascular complications of DM
Allow the patient to achieve as normal a lifestyle as possible
Harrison’s 17th Edition
Harrison’s 17th Edition
Insulin vs. hypoglycemics
Oral 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)
Harrison’s 17th Edition
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
Harrison’s 17th Edition
Nutrition
Medical Nutrition Therapy (MNT)
Modest caloric reduction
Reduced fat intake
Increased physical activity
Reduction of hyperlipidemia and hypertension
Harrison’s 17th Edition
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)
Harrison’s 17th Edition
Monitoring the level of glyceminc
control
Plasma glucose measurements by the patient and assessment
of long-term control by the physician
Measurement of A1C and review of the patient’s selfmeasurement of plasma glucose
Harrison’s 17th Edition
Self-monitoring of Blood Glucose
Standard 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
Harrison’s 17th Edition
Assessment of Long-term Glycemic
Control
Measurement of glycated hemoglobin
Plasma glucose is consistently elevated = increase in
nonenzymatic glycation of hemoglobin
Reflects the glycemic history over the previous 2-3 months
Harrison’s 17th Edition
CELLULITIS
DIAGNOSTIC PLANS FOR CELLULITIS
CT scan with contrast of
Blood culture
the paranasal and neck area
pharyngolaryngoscopy
Aspiration
CT 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
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.
Goals of treatment
Eliminate the offending microorganism
Treat/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
www.fpnotebook.com/DER/Endo/SknInfctnsInDbtsMlts.htm
www.emedicinehealth.com/cellulitis
Pharmacologic
Cellulitis in a DM patient
Early or Mild disease
Augmentin 875 mg PO bid
Second Generation Cephalosporin (cefoxitin,
cefacor, cefuroxime)
Third Generation Cephalosporin (cefotaxime,
ceftazidime,m ceftriaxone, cefixime)
Severe disease
Imipenem-Cilastatin (Primaxin)
Ampicillin-sulbactam
Meropenem
Trovafloxacin 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
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=~a
a8X1QFoqoQSyT&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 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
Preventing a recurrence of cellulitis
Cellulitis 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 Infections
John Weigelt,* Kamal Itani,Dennis Stevens, William Lau, Matthew
Dryden, Charles Knirsch,* and the Linezolid CSSTI Study Group
Purpose
The purpose of this study was to compare linezolid to
vancomycin
Clinical efficiency – resolution of symptoms
2. Microbiological efficiency
3. Safety and tolerability
1.
Background of the Study
This 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.
Pathogens
SENTRY 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 Method
Study period: October 2002-March 2003
Inclusions:
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
A medical history, vital signs,
physical examination, wound
description, and baseline
laboratory values were obtained
for each patient upon
enrollment.
Patients were randomized (1:1)
to receive linezolid (600 mg)
every 12 h, either i.v. or orally,
or vancomycin (1 g) every 12 h
i.v.
Clinical observations of the
wound, the patient’s systemic
response to infection,
laboratory values, and culture
follow-up
Record: first 4 days of therapy,
on day 7, at the end of
treatment (EOT), and at the test
of-cure (TOC) visit.
Clinical response to
treatment was determined
by resolution of the signs
and symptoms of infection
that were identified at
baseline.
Statistical Analysis
Microbiological 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).
Results
Clinical Efficacy
Linezolid > Vancomycin
Microbiological Efficacy
Linezolid > Vancomycin
Safety and Tolerability
Linezolid = Vancomycin
Cost
IV
Suspension
Tablet
Linezolid
Zyvox 2mg/mL x 300mL
P 3,418.28
Vancomycin
Vancocin 500mg
P 1,929.00
Zyvox 100 mg/5 mL x 150 mL NA
P 14,637.28
Zyvox 600mg
NA
P 2,950.40
Linezolid
600mg IV or PO every 12 hours
Vancomycin
1g IV every 12 hours
IV: 3,418.28 x 2 = P 6,836.56
PO: 2,950.40 x 2 = P 5,900.80
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