Sepsis - Infeksi App Antibiotika

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    Sepsis Infection:

    The Appropriate Antibiotics

    Dr. Veronica Wiwing, SpMK

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    Introduction

    Causes of death (RSCM, 2010)

    1) SIRS & MODS 47.05%

    2) Inhalation Injury 39.70%

    3) Shock 30.90%

    4) ARDS 26.5

    5) Sepsis 23.5%

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    Introduction

    Sepsis @ causa Infection

    1) Contributing factors

    a) Predisposing:

    b) Precipitating: Immunocompromise2) Port dentree

    a) Wound infection

    b) Bacterial translocation

    c) Instrumentation

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    The concept of SIRS & MODS

    SIRS

    Infection

    BacterimiaViremia

    Parasytemia

    Fungemia

    T r a u m a

    B u r n

    Ischemia

    Pancreatitis

    Sepsis

    Diagram: the concept of SIRS and sepsis

    Baue, AE, Faist, E, Fry, ED. Multiple organ failure, pathophysiology, prevention, and therapy. New York : Springer, 2000.

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    The concept of SIRS & MODS

    SIRSsystemic Inflammatory response syndrome

    SepsisSIRS due to objective (laboratory evidenced)

    of infection: bacteremia (toxemia)

    MODS

    multi system organ dysfunction syndrome(previously: multiple organ failure)

    2 or more organs involved

    Baue, AE, Faist, E, Fry, ED. Multiple organ failure, pathophysiology, prevention, and therapy. New York : Springer, 2000.

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    The concept of SIRS & MODS

    Shocklack of perfusion

    Septic shocksepsiswith hypotension despite adequate

    fluid resuscitation

    Severe Sepsissepsisassociated with organ dysfunction

    Baue, AE, Faist, E, Fry, ED. Multiple organ failure, pathophysiology, prevention, and therapy. New York : Springer, 2000.

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    Predisposing

    Precipitating

    Local effect of Anti

    Inflammatory response

    Localeffect of Pro

    Inflammatory response

    Cardiovascular

    compromised

    Equal CARS-SIRS

    Homeostasis Apoptosis

    SIRS Predominant SIRS Predominant

    Organ

    dysfunction CARS Dominant

    immune

    Suppression

    C H A O SCARS Compensatory Anti-inflammatory Response Syndrome MARS Mixed Antagonistic Response Syndrome

    Pro Inflammatory response

    enter the systemiccirculation

    Anti Inflammatory response

    enter the systemiccirculation

    SIRS Predominant

    Systemic Response

    CARS

    MARS

    SIRS

    Diagram the cascade of SIRS

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    Exaggerated response

    Tissue injury SIRS

    Immunere

    sponsetoinjury

    time

    recruitmentneutrophil

    arachidonic acid production

    free radicals

    anti-inflammatorypro-inflammatory

    compensation

    3-5 days

    5-21 days

    The diagram of the nature of SIRSwith the host immune response to injury point of view

    The concept of SIRS & MODS

    (ARDS)

    32 days

    CARS

    immunosuppressive

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    The concept of SIRS & MODS

    Predisposing factors:

    Host / Injury ex : burns devastating injury /

    Management (early, advanced)

    Precipitating factors (Initiation):

    Epithelial damage:

    Endothelial (capillary permeability)

    Mucosa (disrupted airway mucosa, gut mucosal

    disruption, acute tubular necrosis, etc)

    Skin-soft tissue necrosis: eschar

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    Infection @ causa burns injury

    Host defence Immunosuppresion

    Epithelial damage

    Port dentre:

    Wound infection

    Bacterial translocation

    Instrumentation

    Defenceaggressor homeostasis

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    Bacterial Translocation

    Splanchnic hypoperfusion lead to ischaemic and

    mucosal disruption (epithelialdamage) Altered gut mucosal and intraluminal environment due

    to:

    Fasting the injured pts

    The use of Antacids The use of certain Antimicrobial

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    Instrumentation

    Disobeyed a and antiseptic handling in procedure of

    insertion and maintenance of: Endotracheal tube, tracheostomy tube, suction catheter,

    etc

    IV lines, CVP lines, syringes

    Indwelling catheter Wound management

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    Wound infection

    Non vital tissue (eschar)

    Tissue perfusion Wound degradation

    Microorganism: >105/mm3, virulence

    Pro-inflammatory Mediators

    Immune system suppression

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    1. Prevention the development

    2. Breaking the cascade

    In dealing with SIRS, sepsis and MODS, the treatment

    should be:

    Listen to what the cells say

    The strategy

    The management

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    The management

    Bacterial translocation

    The fluid resuscitation:

    Adequate volume replacement regarding ischaemic

    time (gut mocosa: 4 hrs) Peripheral vasodilator (low dose dopamine)

    Gut resuscitation:

    No fasting but early enteral nutrition (when the gutworks: use it! to feed the gut rather than to feed the

    body) No antacids and H2antagonist

    No local antibiotics, no an-aerob antibiotics

    No prophylactic antibiotic is needed

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    The management

    Instrumentation

    Aseptic procedure supported with appropriate antiseptic

    Everything is single use only No prophylactic antibiotic is needed

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    The management

    Wound infection

    Wound cleaning with dressing

    moist dressing for 48 hrs (prevent the wounddegradation)

    Early excision:

    Tangential excision (necrotomy) followed by

    (immediate) skin grafting

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    The management

    Wound infection (cont)

    Haemodynamic stability Limitations:

    Manpower (skill), Facilities, donor

    Impending SIRS & MODS

    The needs for supportive antibiotics

    Problems:

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    The use of antimicrobial

    The rational use of antibiotics:

    Standard : class I level of evidence

    Guidelines : class II level of evidence

    Options : class III level of evidence

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    The use of antimicrobialGuidelines

    Systemic and topical antibiotics:

    Sterile wound

    48hr 5 - 7 day

    Gram positive mo Gram negative mo

    The wound colonization

    Shock phase Second phaseImmune-compromize

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    The use of antimicrobialGuidelines

    Systemic and topical antibiotics should be avoided :

    Antibiotic which is cyto-toxic (visceral organs and

    wounds) Antibiotic interfering the gut normal flora balance.

    Potent antibiotic killing commensal non patogen

    bacteria.

    Refer to general guidelines.

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    Amos F, Grochowski J, Tongol MAS. MIMS antimicrobial guides Indonesia.Singapore: MediMedia Asia. PTE.Ltd.; I(1); 2002

    Burns

    Common pathogen:

    Streptococcus

    pyogenes

    Enterobacter sp

    Staphylococcus

    aureusPseudomonas

    aurugenosa

    Enterococcus sp

    Aeromonas

    Vancomycin 1g IV bid

    &

    Amikacin 10mg/kg IV initial,

    & 7.5mg/kg IV bid

    Piperacillin or 4g IV qid

    Ceftazidim 500mg-2g IV 8-12hror

    Meropenem (single) 500mg-1g IV tid

    Imipenem (single) 500mg-1g tid-qid

    Common pathogen:

    Streptococcus sp

    Topical antibioticswith oral:Silver nitrate 0.5% Moist dressing 2hr

    Mafenide acetate cr apply 2-3 times/day

    Silver sulfadiazine 1%cr apply 2-3 times/day

    Fusidic acid 2% cr/oint apply 2 times/day

    Mupirocin 2% cr apply 2 times/day

    Penicillins:

    Penicillin V 1-2g/day PO devided

    dose qid

    Penicillin G 2-3 MU IV / 4hr

    Macrolides:

    Erythromycin 1-2g/day PO devided

    dose qid

    Wound

    sepsis

    Cellulitis

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    The use of antimicrobialGuidelines

    Systemic antibiotics:

    Sterile wound

    48hr 5 - 7 day

    Gram positive mo Gram negative mo

    Penicillin (V or G)

    Penicillinase resistant

    Vancomycin

    Avoids:

    Carbapenem

    ImipenemAminoglycosides

    According to mo

    succeptibility

    No antibiotics

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    Conclusion(s)

    Guideline for using antibiotic in burns

    Effectiveness, non toxic to visceral organs as well aswound

    No ideal antibiotic

    The use of antibiotic

    is a kind of supportive treatment; accomplishment oftreatment sequence

    refer to: 1) indication, 2) timing, & 3) clinical condition

    supported by a wound biopsy (culture & resistance,histopathology exam)

    should be individual and very selective

    Use your judgment

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    How to manage

    this Infection ??