Sepsis &

ARDS
Written by: Lea Sichilia
Advisor: Dr. dr. Erwin Mulyawan, Sp. An-KMN,
FIPM
Definition of Sepsis
● Sepsis is characterised as a potentially fatal organ
dysfunction brought on by an dysregulated host response
to infection
● Septic shock is characterised by underlying circulatory,
cellular, and metabolic abnormalities that raise the
mortality risk over that provided by sepsis alone
Epidemiology

● WHO declared sepsis a global health

priority
● 49 million cases of sepsis and 11
million fatalities from sepsis
globally in 2017.
● 2009-> severe sepsis and septic
shock accounted for 10.9% of
intensive care diagnoses with a
mortality rate of 44.5%.
 Etiology

Gram-positive Gram-negative Fungal

Staphylococcus Escherichia coli, Candida spp. ->
aureus and Klebsiella, and long-term
Streptococcus Pseudomonas chemotherapeutic and
pneumoniae spp. immunosuppressive
medication treatment
 Etiology
01 02 03
Respiratory
urinary system (16%) abdomen (14%)
tract/pulmonary
parenchyma (43%),

04 05

the head which is linked other sites/causes (13%)

to a fever of are the primary sites of
undetermined origin infection
(FUO) (14%)
Diagnostic Criteria of Sepsis

● Sepsis is characterised as a potentially fatal organ

dysfunction brought on by an dysregulated host
response to infection.
● An overall mortality risk of about 10% in a general
hospital population with a suspected infection is
indicated by a SOFA score of ≥ 2
Organ system SOFA score
0 1 2 3 4
Respiratory, ≥400 <400 (53.3) <300 (40) <200 (26.7) with respiratory <100 (13.3) with
PO2/FiO2, mmHg (53.3) support respiratory
(kPa)
Coagulation, ≥150 <150 <100 <50 <20
Platelets, ×103/mm3
Liver, Bilirubin, <1.2 1.2–1.9 2.0–5.9 6.0–11.9 >12.0
mg/dL
Cardiovascular MAP ≥70 MAP <70 Dopamine <5 or Dopamine 5.1–15 or Dopamine >15 or
mmHg mmHg dobutamine (any epinephrine ≤0.1 or epinephrine >0.1 or
dose)b norepinephrine ≤0.1b norepinephrine >0.1b
Central nervous 15 13–14 10–12 6–9 <6
system, Glasgow
Coma Scale
Renal, Creatinine, <1.2 1.2–1.9 2.0–3.4 3.5–4.9 >5.0
mg/dL. Urine output, <500 <200
mL/d
 Screening (qSOFA)

Respiratory rate Change in mental Systolic blood

≥22/min status pressure ≤100 mmHg

Organ dysfunction is indicated by a

qSOFA score ≥ 2.
Diagnostic Criteria: Septic Shock
presence of sepsis with persistent hypotension
requiring vasopressors to maintain mean arterial
pressure (MAP) ≥ 65 mmHg

lactate levels ≥ 2 mmol/L despite

adequate fluid resuscitation
Pathophysiology of Sepsis

vascular endothelium
(microvascular injury,
thrombosis, and
capillary leak)

endothelial disorder->
organ dysfunction and
global tissue hypoxia
Resuscitation Bundle Treatment (1 hour)

Measuring the getting a blood

lactate level culture before giving
antibiotics

administration of 30 starting rapid

mL/kg crystalloid fluid administration of
for hypotension broad-spectrum
antibiotics

giving vasopressors if the patient becomes

hypotensive during or after fluid
resuscitation-> MAP≥65 mmHg
Treatment
2016 SSC guideline: 30 mL/kg (ideal body weight) of IV crystalloids
Re-evaluation of the response to treatment:
● Dynamic measurements: passive leg lifting in conjunction with the measurement
of cardiac output (CO), fluid challenges against stroke volume (SV), systolic
pressure, or pulse pressure
● indicators of tissue perfusion: Capillary refill time (CRT), skin mottling, and
extremity temperature

Measuring lactate: lactate cutoffs used to define a high level was 1.6–2.5
mmol/L,
Blood cultures before beginning antimicrobial therapy (less than 45 minutes)

The panel advises aiming for a MAP ≥65 mm Hg-> improves the supply side of tissue
perfusion
Treatment ● Procalcitonin: early detection
of dangerous bacterial
Antimicrobial Timing infections and the prescription
of antibiotics

Risk factors for MRSA:

● Prior MRSA infection or
colonisation
● recent IV antibiotics
● a history of recurrent skin
infections or chronic wounds
● the presence of invasive
devices, hemodialysis
● recent hospital admissions
● the severity of the illness
Treatment
High risk for MDR organisms-> two gramme negative medicines
for empiric treatment
Low risk for MDR organisms-> single agent.

Empiric antifungal therapy in patients at high risk of fungal infection

● febrile neutropenia that does not improve after 4–7 days of
broad-spectrum antibiotic medication, immunosuppressed
patients

Source control:
● Draining an abscess, removing potentially infected equipment,
debriding diseased necrotic tissue, or permanently controlling a
source of ongoing microbial contamination
Treatment (Antimicrobial)
● Antibiotic de-escalation, or ceasing
01 an antibiotic that is no longer required

02 ● Shorter course of antibiotics: for individuals

with a first diagnosis of sepsis or septic

shock and good source control

03 ● Biomarkers to determine duration:

C-reactive protein, procalcitonin

Treatment
Fluid treatment.
● Crystalloids: Normal saline solution (0.9% sodium chloride)
○ potential side effects: hyperchloremic metabolic acidosis,
renal vasoconstriction, increased cytokine secretion, and
concern about acute kidney injury (AKI) have increased
interest in chloride-restrictive solutions, also known as
balanced or buffered solutions.
● Consider albumin in patients who received large amounts of
crystalloids.
 Treatment
● Norepinephrine: strong agonist of the α-1 and β-1
adrenergic receptors
● Epinephrine: high β -1 adrenergic receptor activity
and moderate β -2 and α -1 adrenergic receptor
activity
● Vasopressin: hypothalamus produces the
endogenous peptide hormone -> vasoconstrictor
mechanism involves binding to V1 receptors on
vascular smooth muscle

Inotropic treatment: prolonged hypoperfusion following

adequate fluid resuscitation and in patients with
myocardial dysfunction
● Dobutamine
 Treatment

Corticosteroid use is Red blood cell transfusion

hydrocortisone , dose is given if the hemoglobin is <7
g/dL to achieve a hemoglobin
≤ 300 mg/day
value of 7-9 g/dL.
Intermittent sedation:
achieve the target level
of sedation

The use of muscle ● Sepsis is the main cause of

NICE-SUGAR: target of AKI:
relaxants in the ICU is to 140-180 mg/dL.
facilitate mechanical ● sodium bicarbonate
ventilation therapy-> septic shock,
severe metabolic acidemia
(pH ≤ 7.2) and AKI
Definition of ARDS
● ARDS: rapidly progressing noncardiogenic pulmonary edoema that swiftly
progresses into respiratory failure
● Dyspnea, tachypnea, and hypoxemia are the early symptoms

Berlin criteria:
● The timing of symptom onset (within one week of confirmed clinical insult or
new or worsening respiratory symptoms)
● bilateral chest imaging opacities that cannot be adequately accounted for by
nodules, lobar or lung collapse, or effusions

Classification:
● Mild: PaO2/FiO2 300 mm Hg
● Moderate: PaO2/FiO2 200 mm Hg
● Severe: PaO2/FiO2 100 mm Hg
Treatment of Sepsis with ARDS
ARDS -> Acute hypoxemic respiratory failure
● High flow nasal cannulas (HFNCs) are non-invasive, high
concentration oxygen delivery
● Lung protective strategy:
○ regulation of tidal volume by adjusting plateau
pressure
○ final positive pressure
○ expiration (positive end-expiratory pressure)
○ adjustment with thoracic and abdominal
compartment pressures
Treatment of Sepsis with ARDS
Low tidal volume of 6 mL/kgBW can even be up to 4
mL/kgBW to maintain plateau pressure ≤ 30 cm H2O

The prone position is also considered to help

improve oxygenation

refractory hypoxemia: high-frequency

oscillatory ventilation (HFOV), airway
pressure release ventilation (APRV) and
extracorporeal membrane oxygenation
(ECMO)
Sedation while using mechanical ventilation.

ARDS are very susceptible to pulmonary edema ->

prevent excessive fluid administration
Conclusion
Sepsis-3:
● Sepsis is defined as a potentially fatal organ dysfunction brought on by an dysregulated
host response to infection
● septic shock is characterised by underlying circulatory, cellular, and metabolic
abnormalities that raise the mortality risk over that provided by sepsis alone
● SOFA score of ≥ 2-> mortality risk of about 10%
● Resuscitation bundle treatment, known as the 1-h bundle:
○ Measure lactate level
○ blood culture before giving antibiotics
○ administration of broad-spectrum antibiotics
○ administration of 30 mL/kg crystalloid fluid for hypotension or lactate ≥4 mmol/L
○ vasopressors if the patient becomes hypotensive
● Acute hypoxemic respiratory failure can be caused by ARDS
● Mild, moderate, and severe ARDS (PaO2/FiO2 300, 200, and 100 mm Hg, respectively).
● Treatment of ARDS: lung protection. High PEEP approach, prone positioning, NMBA
injection, and ECMO are available for treatment in patients with intractable hypoxemia.
Bibliography
Thank
You