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PENCEGAHAN DAN

PENANGANAN INFEKSI
PASCA-TRAUMA
PRESENTAN :
MOCHAMAD AHLIDIN FIRDAUS, DR
MUHAMMAD ALDITO RIVALDI, DR
ANNISA NURFITRIANI, DR
ADI WIBISONO S., DR
SYAFIFAH NOVA AMIZA, DRG.
Pendahuluan
 incidence approximately 25%.
 most trauma-related deaths occur from either
exsanguination or massive injury to the central
nervous system within 24 hours of injury, the leading
cause of later posttraumatic death is infection, usually
manifesting as multiple organ dysfunction syndrome
Temporal Relationships of Trauma Deaths to Causation

ACUTE EARLY LATE


(<24 H) (24 H-7 D) (>7 D)

 Central nervous system 40% 64% 39%


 Exsanguination 55% 9% 0
 Mods <1% 18% 61%

 Adapted from: Asensio JA, Stewart BM, Murray J, et al.: Penetrating cardiac
injuries. Surg Clin North Am 76:685, 1996.
Trauma patients high risk of infection:
• the host immunosuppressive response to injury
• direct inoculation of wounds by clothing, dirt, or
debris
• inadequate infection control practice under emergency
condition
• blood transfusions
• poor control of blood sugar
Infections following injury
• occur in the injured tissue itself (or an incision made
to treat the injury) or as nosocomial infections, such as
pneumonia or catheter-related blood stream infection
(CR-BSI)
• Among the nosocomial infections, pleuro-pulmonary
infections (e.g., pneumonia, empyema) are more
common than CR-BSIs, which in turn are more
common than urinary tract infections.
Overview of the “Stress Response” to Injury
 Activation of the sympathetic nervous system

 Activation of hypophyseal-pituitary-adrenal axis

 Peripheral insulin resistance

 Production of pro-and anti-inflammatory cytokines

 Acute-phase changes of hepatic protein synthesis

 Recruitment and activation of neutrophils, monocyte/macrophages, and lymphocytes

 Upregulation of pro-coagulant activity


Medical Conditions Known to Increase the Risk
of Infection

 Extremes of age
 Malnutrition
 Obesity
 Diabetes mellitus
 Prior site irradiation
 Hypothermia
 Hypoxemia
 Remote infection
 Corticosteroid therapy
 Recent operation, especially of the chest or abdomen
 Chronic inflammation
 Hypocholesterolemia
PREVENTION
Control of Blood Sugar.
• Moderate hyperglycemia (>200 mg/dL) at any time on
the first postoperative day increases the risk of infection
after cardiac and noncardiac surgery.
• The infusion of insulin to keep blood glucose
concentrations <110 mg/dL was associated with a 40%
decrease in mortality among critically ill postoperative
patients, who also had fewer nosocomial infections and
less organ dysfunction
Infection Control
• Hand hygiene
• Universal precautions (i.e., cap, mask, gown, gloves, and
protective eyewear) must be observed whenever there is
a risk of splashing of body fluids (at all times in the
trauma bay)
• Contact isolation
Catheter Care
• appropriate skin cleansing and barrier protection during
insertion,
• proper catheter selection,
• proper dressing of indwelling catheters,
• removal as soon as possible when no longer needed.

 The benefit of catheterization must always be weighed


against the risk of infection.
SOURCE OF INFECTIONS

 The source of the bacteria causing infection:


 the patients' endogenous flora,
 skin surfaces,
 airways,
 gut lumen,
 wounds,
 catheters,
 surfaces within the patient's room
 Any break in natural epithelial barriers (e.g., incisions,
percutaneous catheters, airway or urinary catheters)
provides a portal of entry for pathogenic organisms.
ANTIBIOTIC PROPHYLAXIS

 Antibiotic prophylaxis refers to the prevention of


infection complications using antimicrobial therapy.
 Patients should be selected for prophylaxis if the
medical condition or the surgical procedure is
associated with considerable risk of infection.
ANTIBIOTIC PROPHYLAXIS

 A single dose of a first-generation cephalosporin


(e.g., cefazolin) prevent infections following
emergency tube thoracostomy.
 Antibiotics (e.g., minocycline/rifampin) are effective
in reducing the incidence of catheter-related
bloodstream infection.
 Surgical site infection is prevented by antibiotic
prophylaxis.
 Antibiotic prophylaxis more than 24 hours beyond
injury increases the risk of nosocomial infection.
 Catheter insertion procedures require only a single
dose of prophylactic antibiotics, except perhaps for
emergency tube thoracostomy.
FACTORS INFLUENCING
ANTIBIOTIC ADMINISTRATION

 Shock, hypoperfusion, and hemorrhage complicate


the pharmacokinetics of prophylactic antibiotic
administration immediately following trauma.
 Shock, hypovolemia, and hypoperfusion may also
increase the risk of organ dysfunction caused by
antibiotics (e.g., aminoglycosides and renal injury).

Increase the dose of drug administered to patients in


shock.
FACTORS INFLUENCING
ANTIBIOTIC ADMINISTRATION

 Young injured patients have higher GFR → more


rapid clearance in the urine → need higher doses
for prophylaxis therapy.
 Tissue edema associated with resuscitation will
change volume of distribution of drugs.
 Hypoalbuminemia associated with hemodilution,
plasma loss can affect tissue antibiotic
concentrations.
ABDOMINAL INJURIES

 Prophylaxis < 24 hours of a second-generation


cephalosporin (e.g., cefoxitin) for penetrating
abdominal trauma with injury to a hollow viscus.
 Penetrating trauma that does not injure a hollow
viscus needs only a single dose of antibiotics given
prior to operation.
 For blunt abdominal trauma, if managed
nonoperatively no antibiotics are required.
CHEST INJURIES

 If antibiotics are started they should be discontinued


within 48 hours if the development of pneumonia is
unproved.
 Penetrating trauma to the chest should be
governed by the decision administer antibiotic
prophylaxis.
SKIN AND SOFT TISSUE INJURIES

 Risk factors for infection of traumatic lacerations:


 diabetes mellitus,
 age (increased risk per year),
 foreign body, and
 the width of the incision.
 The most common pathogens of infected traumatic wounds
are aerobic gram-positive cocci (e.g., S. aureus).
 Animal and human bites should be presumed to be infected.
 Penicillin or macrolide prophylaxis of dog bite wounds reduce
infection.
 Human bites are likely to cause infection with oral anaerobes
(e.g., anaerobic streptococci, rarely Bacteroides fragilis).
PEDOMAN PEMBERIAN
ANTIBIOTIK PROFILAKSIS
PADA PEMBEDAHAN
 Mempunyai risiko untuk infeksi.
 Ada pengetahuan mengenai kemungkinan flora yang berhubungan
dengan luka operasi.
 Harus dapat memotong aktifitas patogen terhadap luka yang
terkontaminasi atau pada lapangan operasi.
 Bila menggunakan lebih dari satu antibiotik, maka antibiotik terpilih
harus berdasarkan mikroorgnisme terbanyak.
 Diberikan dalam dosis dengan konsentrasi efektif sebelum kontaminasi
bakteri intraoperatif. (30-45 menit sebelum insisi kulit).
 Untuk sefalosporin pada pasien dengan BB >70 kg, dosis sebaiknya dua
kali lipat (contoh, 70 kg: cefazolin 1 g IV, >70kg: cefazolin 2 g IV).
 Pelaksanaan pembedahan ≤ 3 jam → dosis tunggal. Pembedahan >
3jam → dosis efektif tambahan.
 Vancomycin dapat diberikan untuk pasien dengan alergi
penisilin/sefalosporin.
ANTIMICROBIAL RESISTANCE

When microbes are less treatable with one or more


medication used to treat or prevent infection.

 Makes these medication less effective.


 May require other medication or higher doses.
RESISTANCE

Bacteria use 4 mechanisms to develop resistance to antibiotics.


 Cell wall permeability to antibiotics is decreased by changes in
porin channels (affecting aminoglycosides, beta-lactam drugs,
chloramphenicol, sulfonamides, tetracyclines, and possibly
quinolones).
 Production of specific antibiotic inactivating-enzymes by either
plasmid-mediated or chromosomally mediated mechanisms
affects aminoglycosides, beta-lactam drugs, chloramphenicol, and
macrolides.
 Alteration of the target for antibiotic binding in the cell wall affects
beta-lactam drugs and vancomycin, whereas alteration of target
enzymes can affect beta-lactam drugs, sulfonamides, quinolones,
and rifampin.
 Drugs that bind to the bacterial ribosome (aminoglycosides,
chloramphenicol, macrolides, lincosamides, streptogramins, and
tetracyclines) are also susceptible to alteration of the receptor on
the ribosome.
GRAM-POSITIVE COCCI

 Gram-positive cocci are the most common causes


of infection following injury.
 Include infections following neurosurgery, sinusitis,
device/implant-associated infections.
 Respiratory tract and urinary tract infections may
also be caused by gram-positive cocci.
 60% of hospital-acquired isolates of S. aureus are resistant to
methicillin (MRSA).
 25% of community-acquired strains are now resistant (CA-MRSA).
 S. epidermidis is almost invariably resistant to methicillin (MRSE,
85%).
 About 30% of enterococci are resistant to vancomycin (VRE).
 70% of E. faecium isolated are VRE.
 Risk factors for the acquisition of VRE include prolonged
hospitalization, readmission to the ICU, and therapy with
vancomycin or third-generation cephalosporins.
 Vancomycin remains the most-prescribed antibiotic for resistant
gram-positive cocci.
 Alternatives therapy include linezolid, tigecycline, daptomycin and
quinupristin/dalfopristin.
GRAM-NEGATIVE BACILLI

 Gram-negative bacilli are less common as


pathogens than gram-positive cocci.
 Important in the pathogenesis of skin/skin structure
infection, lower respiratory tract infection, and
intraabdominal infection.
 Enterobacteriaceae (E. coli or Klebsiella spp.)
predominate in intraabdominal infection.
 P. aeruginosa is the second most common ICU
pathogen overall and most closely associated with
death from HAI.
 Enteric gram-negative bacilli mutate to produce a
beta-lactamase.
 Cephalosporin resistance can be the result of induction
of chromosomal beta-lactamases after prolonged or
repeated exposure to the antibiotic.
 Metalloproteinases and carbapenemases threaten the
utility of carbapenems to treat infections caused by
Pseudomonas and Acinetobacter.
 Quinolone resistance is chromosomally by changes in
the target sites for the antibiotic (DNA gyrase or
topoisomerase IV).
 Quinolone resistance is easy to induce if a less than
maximally effective drug or dose is chosen for initial
therapy.
FUNGI AND YEAST

 Fungal infections are usually the result of antibiotic


overuse.
 Prolonged broad-spectrum antibiotic therapy
suppresses host flora → opportunity for overgrowth
of commensal flora.
 The most common health care-acquired fungal
infections are caused by Candida spp., (gut flora in
¼ of patients).
 High-risk patients should be treated prophylactically
with an azole anti-fungal agent (e.g., fluconazole)
to prevent invasive infection.
 Widespread prescribing of fluconazole → resistance
among Candida sp. that are normally susceptible to
fluconazole (e.g., C. albicans, C. tropicalis).
 Fluconazole should not be used until an organism
that is likely to be susceptible to fluconazole is
identified.
 Empiric therapy choices include conventional
amphotericin B, echinocandins, caspofungin or
mica-fungin.
 Comparative studies suggest that the triazole,
voriconazole may be more effective than
amphotericin B for invasive aspergillosis.
Vaksinasi
Revaccination

 CDC suggests a single booster dose for those older


than two years of age who are at high risk for serious
pneumococcal infection and those most likely to
have a rapid decline in antibody titers, which
includes those with either functional or anatomic
asplenia
 Should be given at least five years after the first dose
TERIMA KASIH

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