FARMAKOLOGI

PADA KASUS
BEDAH SEPSIS
PPDS ILMU BEDAH
FK ULM / RSUD ULIN
KASUS

• Wanita 17 tahun dibawa ke RS oleh orang tuanya karena mengeluh nyeri

hebat di seluruh lapangan perutnya 6 jam SMRS. 4 hari sebelumnya anak
tersebut mengeluh nyeri perut sekitar pusat yang masih hilang timbul, nyeri
dirasakan tembus ke punggung. 2 hari setelahnya nyeri semakin terasa di
perut kanan, disertai demam, dan anak sulit diberi makan dan minum. 6 jam
SMRS os semakin merasakan nyeri di seluruh perutnya, disertai muntah 2-
3x, badan terasa panas, dan os tampak mengantuk. Selama sakit, orang tua
hanya memberi obat maagh karena pasien memiliki riwayat maagh
sebelumnya, antibiotik (amoxicillin), dan obat penurun panas karena jauh
dari RS.
• RPD : tidak ada riwayat penyakit sebelumnya
PHYSICAL EXAMINATION

Tanda Vital
Kesadaran: GCS E3V4M6
TD : 80/50 mmHg (MAP 60)
HR : 122x/menit, regular, pulsasi lemah
RR: 30x/menit, cepat dan dangkal
T : 40,2°C
SPO2 : 97% without O2
Weight : ± 40 Kg
Physical Examination

• Head : Pale conjunctiva (-|-) light reflex (+|+), Edema palpebra (-/-),
Head • Mouth : Bibir tampak kering
• Neck : Increased level of JVP (-), enlargement of lymph node (-)

• I : symmetrical respiratory movement, retraction (+),

• P : Symmetric VF
Chest • P : Sonor at all regio
• A : symetric VS, no ronchi, no wheezing

• I : distension (-)
• A : bunyi usus menurun
Abdomen • P : defence muscular (+)
• P : tidak dilakukan

Extremities • Akral dingin

PEMERIKSAAN DARAH RUTIN
Lab Normal Client
Hemoglobin 14-18 12,4
Hematocrit 42-52 37.8
Platelets 150-400 160
WBC 4.3-10 27,2
Neutrophils 55-70 88
Lymphocytes 20-40 13
Monocytes 2-8 10
PTT 20-45 22
PT (INR) <2 1.8
Ureum 10-50 34
Creatinin 0.7-1,4 1.1
DIAGNOSIS

Susp. Shock Sepsis ec Peritonitis Akut

APAKAH FARMAKOLOGI YANG
BERLAKU PADA PASIEN INI ?
The Primary Goals of Therapy :
1. Timely diagnosis and identification of pathogen
2. Rapid elimination of the source of infection medically and/or
surgically
3. Early initiation of aggressive antimicrobial therapy,
4. Interruption of pathogenic sequence leading to septic shock
5. Avoidance of organ failure.
 Antibiotic ?

Stress Ulcer Septick Vasopressor ?

Prophylaxis ?
Shock

Corticosteroid ?
INTRODUCTION

Sepsis is life-threatening organ dysfunction caused by a dysregulated host

response to infection.

Early identification and appropriate management in the initial hours after

sepsis develops improves outcomes.
FARMOKOLOGI
1. Antibiotics
2. Vasopressor
3. Corticosteroid
4. Stress Ulcer Prophylaxis

Source :
Rhodes A, Evans L.E, et al. Surviving Sepsis Campaign : International Guidelines
for Management of Sepsis and Septic Shock: 2016. Intensive Care Med 2017 : 43 :
304-377
ANTIBIOTIC
1. Administration of IV antimicrobials be initiated as soon as possible
after recognition and within 1 h for both sepsis and septic shock.
2. Empiric broad-spectrum therapy with one or more antimicrobials
for patients presenting with sepsis or septic shock to cover all likely
pathogens
 The most common pathogens that cause septic shock are gram negative
bacteria, gram positive, and mixed bacterial microorganisms
3. Empiric antimicrobial therapy be narrowed once pathogen
identification and sensitivities are established and/or adequate
clinical improvement is noted
4. Against sustained systemic antimicrobial prophylaxis in patients with
severe inflammatory states of noninfectious origin (e.g., severe
pancreatitis, burn injury)
5. Dosing strategies of antimicrobials be optimized based on accepted
pharmacokinetic/pharmacodynamic principles and specific drug
properties in patients with sepsis or septic shock
 Problems : increased frequency of hepatic and renal dysfunction, a high
prevalence of unrecognized immune dysfunction, and a predisposition to
infection with resistant organisms.
 The clinical success rate for treatment of serious infections correlates with
higher peak blood levels
 Long of treatment based on patient clinical respond (average 5-7 days, and
can be stopped 3-5 days after clinical respond improved)
Several factors must be assessed and used in determining the appropriate
antimicrobial regimen at each medical center and for each patient.
1. The anatomic site of infection with respect to the typical pathogen profile
and to the properties of individual antimicrobials to penetrate that site.
2. Prevalent pathogens within the community, hospital, and even hospital
ward.
3. The resistance patterns of those prevalent pathogens.
4. The presence of specific immune defects such as neutropenia, splenectomy,
poorly controlled HIV infection and acquired or congenital defects of
immunoglobulin, complement or leukocyte function or production.
5. Age and patient comorbidities including chronic illness (e.g., diabetes) and
chronic organ dysfunction (e.g., liver or renal failure), the presence of
invasive devices (e.g., central venous lines or urinary catheter) that
compromise the defense to infection.
SELECTED ANTIBIOTIC

 Aminoglycosides
 Fluoroquinolones
 Patient with shock usually have one or more forms of
immunocompromise, the initial empiric regimen should be broad enough
to cover most pathogens isolated in healthcare-associated infections. Most
often, a broad-spectrum carbapenem (e.g., meropenem,
imipenem/cilastatin or doripenem) or extended-range penicillin/β-
lactamase inhibitor combination (e.g., piperacillin/tazobactam or
ticarcillin/ clavulanate) is used. However, several third- or high-
gergeneration cephalosporins can also be used, especially as part of a
multidrug regimen.
ANTIBIOTIK PADA PASIEN
INI ?
 Betalactam
 Piperasilin / Tazobaktam 2/0,5 – 4/0,8 gr setiap 8 jam
 Sefalosporin (3rd or higher generation)
 Karbapenem (imipenem, meropenem)
 Monobaktam (aztreonam)
 Glikopeptida (MRSA Suspected)
 Vancomycin
 Metronidazol
 Metronidazol 500 mg iv
VASOPRESSORS

 Recommend norepinephrine (NE) as the first choice vasopressor

 Adding either vasopressin or epinephrine to NE with the intent of
raising MAP, or to decrease NE dosage
 Dopamine only for highly selected patient
 We recommend against using low-dose dopaminefor renal
protection
 Using dobutamine in patients who show evidence of persistent
hypoperfusion despite adequate fluid loading and the use of
vasopressor agents
WHY NOREPINEPHRINE ?
 Vasoconstrictive effects, with little change in heart rate and less increase
in stroke volume compared with dopamine  lower risk for cardiac
arrhythmias
 Norepinephrine is more potent than dopamine and may be more
effective at reversing hypotension in patients with septic shock.
 Epinephrine may increase aerobic lactate production via stimulation of
skeletal muscle β2-adrenergic receptors  preclude the use of lactate
clearance to guide resuscitation.
TREATMENT DOSES
1. Norepinephrine
 Dosis umum: 0,01 - 0,10 μg/kg/menit.
 Dosis awal: 0,05 μg/kg/menit.
2. Dopamin
 1-3 μg/kg/menit : vasodilatasi
 3-10 μg/kg/menit : inotropic & chronotropic positive & conduction
 10-15 μg/kg/menit : increased SVR & PVR, chronotropic positive
3. Epinephrine
 < 0,02 μg/kg/menit : Increased heart rate & decreased SVR
 > 0,02 μg/kg/menit : inotropic positive & chronotropic positive
STRESS ULCER PROPHYLAXIS

1. We recommend that stress ulcer prophylaxis be given to patients with

sepsis or septic shock who have risk factors for gastrointestinal (GI)
bleeding.
 Mechanical ventilation > 48 h
 Coagulopathy

2. We suggest using either proton pump inhibitors (PPIs) or histamine-2

receptor antagonists H2RAs) when stress ulcer prophylaxis is
indicated
3. We recommend against stress ulcer prophylaxis in patients without
risk factors for GI bleeding (BPS).
CORTICOSTEROID
We suggest against using IV hydrocortisone to treat septic
shock patients if adequate fluid resuscitation and vasopressor
therapy are able to restore hemodynamic stability. If this is
not achievable, we suggest IV hydrocortisone at a dose of 200
mg per day (weak recommendation, low quality of evidence).
RESUME
The Primary Goals of Therapy :
1. Timely diagnosis and identification of pathogen
2. Rapid elimination of the source of infection medically and/or
surgically
3. Early initiation of aggressive antimicrobial therapy,
4. Interruption of pathogenic sequence leading to septic shock
5. Avoidance of organ failure.
Terima Kasih