not provide a similar cure rate as it did with a
3-day regimen of ciprofloxacin (cure rate, 82%
ANTIBIOTIC RESISTANCE
CHOICE OF AGENT  tissues, abscesses, or biofilms also can limit
Antibiotics work by either selectively killing
(bactericidal) or inhibiting the growth
(bacteriostatic) of bacteria. Infections with a
high bacterial burden, such as those seen in
infective endocarditis, require treatment with
antibiotics with rapid bactericidal activity. In
most cases, more than 1 antibiotic is used to
provide synergistic activity and rapid killing.
For example, when treating native valve
endocarditis caused by penicillin-susceptible
viridans streptococci, the usual treatment
duration can vary from 2 to 4 weeks. If
penicillin G or ceftriaxone monotherapy is
prescribed, the treatment duration should be 4
weeks; however, if either antibiotic is used in
combination with an aminoglycoside, then the
treatment can be shortened by 2 weeks. 11
Another factor that can affect the efficacy of
antibiotics is their ability to penetrate and
remain (for an adequate time) at the site of
infection. Fosfomycin tromethamine,
quinolones, nitrofurantoin, trimethoprim-
sulfamethoxazole and beta-lactams are some
of the antibiotics used to treat urinary tract
infections. Even though these antibiotics can
concentrate well in the genitourinary tract,
each can differ in duration of treatment. For
example, fosfomycin can be given in a 1-time
dose because a single 3-g oral dose can
provide a peak urinary concentration within 4
hours and remain elevated (>128 mg/L) for
≤48 hours.12 In another example, Hooton et al
found that a 3-day course of cefpodoxime
proxetil, a third-generation cephalosporin, did
vs 93%, respectively; 95% CI, 3%-18%) for
the treatment of acute uncomplicated cystitis. 13 
TYPE AND SEVERITY OF INFECTION 
A patient’s immune status, affected anatomical
site, and pathogen causing the infection also
should be considered when assessing duration
of therapy. Infected patients with no
hemodynamic issues can be treated with short
courses of antimicrobials. For example,
community-acquired pneumonia (CAP) can be
treated in as little as 5 days, but once the
patient’s condition is complicated by
bacteremia or severe sepsis, a longer course of
antibiotics is essential.3
The ability of antibiotics to penetrate necrotic
their efficacy. Infections can be difficult to
treat and require prolonged antibiotic courses.
Unless surgical intervention is undertaken to
remove debris and/ or drain abscesses,
antibiotics cannot reach infected sites. For
example, a course of antibiotics for
intraabdominal infections is no longer than 7
days; however, if it is difficult to perform the
source control procedure (eg, drain infected
foci, control ongoing peritoneal
contamination), a longer treatment course is
necessary.8
ASSESSMENT OF PATIENT’S RESPONSE 
Improvements in hemodynamic status (eg,
heart rate, blood pressure), white blood cell
count, temperature, oxygenation, and/or
radiologic findings should be seen a few days
after starting an effective therapy. Once the
signs and symptoms of infections are resolved,
clinicians can consider terminating therapy. El
Moussaoui et al conducted a randomized,
double-blind, placebo-controlled study
comparing the effectiveness of discontinuing
amoxicillin therapy in mild to moderate-severe
CAP after 3 days compared with 8
days.14 Patients were assessed
regarding4 respiratory symptoms (dyspnea,
cough, sputum production, color of sputum)
and general improvement (not recovered to
complete recovery) based on a 5-point
symptom scale. Patients who improved by ≥2
points, who had a temperature <38°C, and who
were able to take oral medications were
randomized to receive either 750-mg oral
amoxicillin or placebo for 3 to 5 days. They
found that discontinuing antibiotics 3 days
after symptom resolution did not adversely
affect patient outcomes. In addition, there were
no differences in clinical or radiological
outcomes between the 2 groups after 10 days
and 28 days.14
Rechecking for cultures is not always
necessary once a patient begins responding to
therapy, except in the case of bloodstream
infections. Monitoring for bacterial clearance
is crucial because day 1 of antimicrobial
therapy is the first day on which negative
blood cultures are obtained.15 Acquiring
unnecessary cultures should be avoided
because a positive culture having no signs and
symptoms of infection could lead to treating
colonized bacteria.
The use of biomarkers, such as C-reactive
protein (CRP), and the procalcitonin test also
has been instrumental in evaluating antibiotic
response and determining the duration of
antibiotic therapy. Unlike CRP, procalcitonin
is more specific to bacterial infections;
therefore, the test has been used to curtail
unnecessary antibiotic usage. Use of the
procalcitonin-guided algorithm has been
shown to reduce the duration of exposure to
antibiotics by ≤25% in patients with lower
respiratory tract infections 16 and 23% in
patients who are critically ill.17
CONCLUSION  notice any redness, increasing pain,
Pharmacists are vital team members in
antibiotic stewardship. Thus, they should have
a good understanding of the ways in which
antibiotics work and the factors that affect
their efficacy. In addition, they must be able to
monitor for responses to antibiotics to ensure
that patients are treated adequately and
infection relapses are prevented.
STERILE PUS
Sterile abscesses are sometimes a milder form
of the same process caused not by germs but
by non living irritants such as drugs. If an
injected drug like penicillin is not absorbed, it
stays where it was injected and may cause
enough irritation to generate a sterile abscess
—sterile because there is no infection
involved. Sterile abscesses are quite likely to
turn into hard, solid lumps as they scar, rather
than remaining pockets of pus.
MANAGEMENT OF WOUND
To take care of a puncture wound:
1. Wash your hands. This helps avoid
infection.
2. Stop the bleeding. Apply gentle
pressure with a clean bandage or cloth.
3. Clean the wound. Rinse the wound
with clear water for five to 10 minutes.
If dirt or debris remains in the wound
after washing, use tweezers cleaned with
alcohol to remove the particles. See a
doctor if you can't remove all of the
debris. Clean the skin around the wound
with soap and a washcloth.
4. Apply an antibiotic. Apply a thin
layer of an antibiotic cream or ointment
(Neosporin, Polysporin). Certain
ingredients in some ointments can cause
a mild rash in some people. If a rash
appears, stop using the ointment and
seek medical care.
5. Cover the wound. Bandages help
keep the wound clean.
6. Change the dressing. Do this at least
once a day or whenever the bandage
becomes wet or dirty.
7. Watch for signs of infection. See a
doctor if the wound isn't healing or you
drainage, warmth or swelling.
Seek prompt medical care
Get immediate medical help if the wound:
 Keeps bleeding after a few minutes of
direct pressure
 Is the result of an animal or human
bite
 Is deep, dirty or caused by a metal
object
If the injured person hasn't had a tetanus shot
in the past five years and the wound is deep or
dirty, your doctor may recommend a booster.
The injured person should have the booster
shot within 48 hours of the injury.
If the wound was caused by a cat or a dog, try
to confirm that its rabies vaccination is up to
date. If it was caused by a wild animal, seek
advice from your doctor about which animals
are most likely to carry rabies.
ABSCESS COMPLICATION
Common complications
As the skin abscess develops, it may appear as
an open or closed lesion or a dome-shaped
nodule (raised bump). According to St.
Vincent Health, a comprehensive health-care
network based in Indiana, the most common
complications that arise from skin abscesses
are pain, redness of the skin (erythema),
swelling and warmth around the area of the
abscess and swollen lymph nodes. The tissue
on and around the skin abscess may harden.
The pus-filled wound may also spontaneously
drain or ooze fluid.
Rare complications
In some cases, abscesses are the result of
infection with multiple types of bacteria,
according to St.Vincent Health. While this
infection may remain localized to the skin, in
rare cases it may spread throughout the body,
signifying a more extensive infection. When
this occurs, people will often develop a fever
or chills. If you notice either of these
symptoms, contact your doctor right away.
Serious complications
The infection that began at the site of the skin
abscess may spread to nearby tissue and
throughout the body, leading to serious
complications. Many new abscesses may form
on the joints or other locations on the skin.
Skin tissue may die as a result of the infection,
leading to gangrene and possible skin loss or
amputation. As the infection makes its way
through the body internally, it can lead to a
condition called endocarditis--an inflammation
of the inside lining of the heart. Endocarditis
can be fatal if not treated early, and many
people will require long-term antibiotic
therapy and hospitalization to treat the
condition. Infection can also spread to the
bone, leading to osteomyelitis--a bone
infection that causes bone pain, fever, nausea,
swelling of the extremities and possibly further
infection that can necessitate amputation or
cause reduced limb or joint function,
according to the NIH.
Recurrence
Some people may experience a recurrence of
skin abscesses after they have healed. St.
Vincent Health advises that people with
recurring skin abscesses should be evaluated
by a doctor to rule out infection with
methicillin-resistant Staphylococcus aureus
(MRSA)--a type of bacteria that is resistant to
commonly used antibiotics. MRSA infections
start off as small red bumps that quickly
become skin abscesses. The abscesses may
then penetrate the body, causing life-
threatening infection that spreads through the
bloodstream and affects internal organs. The
Mayo Clinic recommends seeking medical
care if you notice pus, skin redness or fever,
and that you ask to have the lesion tested
before starting antibiotic therapy.
HAGEMAN FACTORS TO
INFLAMMATION
Coagulation factor XII, also known
as  Hageman factor, is a plasma protein.
Factor XII is part of the coagulation cascade
and activates factor XI and prekallikrein in
vitro. Factor XII itself is activated to factor
XIIa by negatively charged surfaces, such as
glass.
Factor XII  also appears to have a role in
inflammation. Skin windows show reduced
leukocyte migration in XII-deficient
people [51]. FXIIa induces neutrophil
aggregation [52]. XII or XIIa stimulates
monocyte expression of FcγRI [53].
Both factor XII and factor XIIa enhance
proliferation of cultured human
hepatoma cells [54]. XII stimulates ERK1/2
phosphorylation in HepG2 cells and vascular
smooth muscle cells [54,55,56]. We
demonstrated that XII binds to endothelial
cells and has, at least, a multiprotein receptor
complex that consists of urokinase
plasminogen activator receptor (uPAR),
gC1qR, and cytokeratin 1, and competes HK,
single chain urokinase (ScuPA), or vitronectin
binding to uPAR [19,57,58]. We also
demonstrated that XII binding to HUVEC
stimulates ERK1/2 and Akt through β1-integrin
and an ErbB receptor, leading to cell
proliferation and angiogenesis [58]. Last, XII
KO mice have reduced wound repair
angiogenesis [58].
MANAGEMENT OF KELOIDS
Occlusive dressings
Occlusive dressings include silicone gel sheets
and dressings, nonsilicone occlusive sheets,
and Cordran tape. These measures have been
used with varied success, and overall the
quality of the studies has been suboptimal.
[4] 
Antikeloidal effects appear to result from a
combination of occlusion and hydration, rather
than from an effect of the silicone.
Previous studies have shown that in patients
treated with silicone occlusive sheeting with
pressure worn 24 h/d for up to 12 months, 34%
showed excellent improvement, 37.5% showed
moderate improvement, and 28%
demonstrated no or slight improvement.
Of patients treated with semipermeable,
semiocclusive, nonsilicone-based dressings for
8 weeks, 60% experienced flattening of
keloids, 71% had reduced pain, 78% had
reduced tenderness, 80% had reduced pruritus,
87.5% had reduced erythema, and 90% were
satisfied with the treatment.
Cordran tape is a clear surgical tape that
contains flurandrenolide, a steroid that is
uniformly distributed on each square
centimeter of the tape, and it has been shown
to soften and flatten keloids over time.
Compression therapy
Compression therapy involves pressure, which
has long been known to have thinning effects
on skin. Reduction in the cohesiveness of
collagen fibers in pressure-treated
hypertrophic scars has been demonstrated by
electron microscopy.
Cellular mechanoreceptors may have an
important role of compression therapy.
Mechanoreceptors induce apoptosis and are
involved in the integrity of the extracellular
matrix. An increase in extracellular matrix
rigidity produced by compression garments
leads to a higher level of mechanoreceptor
activity and therefore more cellular apoptosis.
Migration, proliferation, and differentiation of
cells has been shown to be affected by rigidity;
therefore, the rigidity caused by compression
may also inhibit the differentiation and
proliferation of scar fibroblasts in vivo. [5, 6]  treated using keloidectomy with core fillet flap
Compression treatments include button
compression, pressure earrings, ACE
bandages, elastic adhesive bandages,
compression wraps, spandex or elastane
(Lycra) bandages, and support bandages. In
one study, button compression (2 buttons
sandwiching the earlobe applied after keloid
excision) prevented recurrence during 8
months to 4 years of follow-up observation.
Other pressure devices include pressure
earrings and pressure-gradient garments made
of lightweight porous Dacron, spandex (also
known as elastane), bobbinet fabric (usually
worn 12-24 h/d), and zinc oxide adhesive
plaster. Overall, 60% of patients treated with
these devices showed 75-100% improvement.
Corticosteroids
Corticosteroids, specifically intralesional
corticosteroid injections, have been the
mainstay of treatment. Corticosteroids reduce
excessive scarring by reducing collagen
synthesis, altering glucosaminoglycan
synthesis, and reducing production of
inflammatory mediators and fibroblast
proliferation during wound healing. The most
commonly used corticosteroid is triamcinolone
acetonide (TAC) in concentrations of 10-40
mg/mL administered intralesionally with a 25-
to 27-gauge needle at 4- to 6-week intervals.
Intralesional steroid therapy as a single
modality and as an adjunct to excision has
been shown to be efficacious in various
studies. Response rates varied from 50-100%,
with recurrence rates of 9-50% in completely
resolved scars. When combined with excision,
postoperative intralesional TAC injections
yielded a recurrence rate of 0-100%, with most
studies citing a rate of less than 50%.
Complications of repeated corticosteroid
injections include atrophy, telangiectasia
formation, and pigmentary alteration.
A standardized corticosteroid therapy protocol
has been shown to reduce the recurrence of
keloids and hypertrophic scars after excision.
Intralesional TAC injection was performed
after removal of the sutures and then once
every 2 weeks (total of 5 treatments). In
addition, patients were instructed to apply
corticosteroid ointment twice daily for 6
months to the wounds after suture removal.
Only 3 (14.3%) of 21 keloids and 1 (16.7%) of
6 hypertrophic scars recurred. [7] 
Aradi et al studied 21 earlobe keloids that were
and given intraoperative intralesional steroid
injections. This study showed an efficacy of
87.6%. Immediate recurrence was 9.5%, with
an average of 29.9 months of follow up and
with few complications encountered.
Subjectively, 82.3% of patients were
satisfied. [8] 
Published data show molecular-based evidence
of the clinical benefits of adding 5-fluorouracil
to a steroid injection for improved scar
regression and reduced recurrence of keloids.
5-Fluorouracil–induced G2 cell-cycle arrest
and apoptosis may be associated with p53
activation and p21 up-regulation. 5-
Fluorouracil significantly affects the treatment
when combined with triamcinolone, leading to
more significant cell proliferation inhibition,
apoptosis, Col-1 suppression, and MMP-2
induction.