2. Definitions of
infected states
• ■SIRS=isthebody’ssystemicresponsetosevereinfection
• ■MultipleOrganDysfunctionSyndrome=istheeffectthatSIRS
producessystemically,>=2organfailure
3. Definitions of infected
states
• ■MultipleSystemOrganFailure(MSOF)=istheendstageof
uncontrolledMODS
• ■Bacteremia:viablebacteriaintheblood
• ■Septicemia:isaseriousbloodstreaminfection,It’salsoknownas
bloodpoisoning
4. systemic inflammatory response
syndrome
international Sepsis Definitions Conference
systemic inflammatory response syndrome (SIRS)
≥ 2 of
1- temperature > 38.3 degrees C (100.9 degrees F) or < 36 degrees C
(96.8 degrees F)
2- heart rate > 90 beats/minute
3- respiratory rate > 20 breaths/minute or arterial partial pressure of
carbon dioxide (PaCO2) < 32 mm Hg
4- white blood cell count (WBC) > 12,000/mm3 or WBC <
4,000/mm3 or > 10% immature neutrophils (bands)
above abnormalities should represent change from baseline without
other known cause (such as leukopenia due to chemotherapy)
5. Definition
• Sepsis is a serious problem from an infection. It is an
overreaction of the body to the infection. It can lead
to life-threatening organ damage
• sepsis - SIRS due to documented or suspected
infection
6. Severe sepsis
• Severe sepsis - sepsis plus evidence of acute organ
dysfunction or tissue hypoperfusion (any of below
occurring due to infection)
– sepsis-induced hypotension defined as 1 of
• systolic blood pressure < 90 mm Hg
• mean arterial pressure < 70 mm Hg
• systolic blood pressure decrease > 40 mm Hg
• in absence of other causes of hypotension
7. Septic shock
• septic shock
# clinically defined as persistent hypotension
requiring vasopressors to maintain mean arterial
pressure (MAP) ≥ 65 mm Hg and serum lactate
level ≥ 2 mmol/L (18 mg/dL) despite adequate
volume resuscitation
# associated with hospital mortality ≥ 40%
8. Pathophysiology
• if there is some infective material in the
bloodstream >> WBC will encounter this
infective material >> WBC become active
• 1) WBC recruitment
• 2) WBC release NO >> dilate BV >>
increase diameter & decrease the
systemic vascular resistence (SVR)
• 3) increase permeability of the blood
vessel
9. Pathophysiology
• # NOTE: You have the infecious material in the
blood vessels all throughout the body. So, the
vasodilation happen everywhere >> systemic
vascular dilatation. Decreased SVR >>
decreased Blood pressure.
• 4) low tissue perfusion due to 1- decreased BP
2- difficulty to get to the cells ( due to increased
leakiness) So the cells become starved of O2.
10. Pathophysiology
• 5) releasing lytic enzymes and Reactive oxygen
species (ROS )to destroying the infective
material, that may damage BV as well so…
several complications can occur >> damage to
endothelium triggers coagulation cascade
causing micro-clot of :- fibrin, neutrophils,
platelets, RBCs.>> formation of “micro clot” that
my:
• prevents BV rupture >> so blood does not spill
into extravascular space
11. Pathophysiology
• Also, there is coagulation happens in the vascular
system (disseminated intravascular coagulation -DIC-)
>>>>> this mechanisms can not keep up the breakage of
BV. (due to depletion in platlet, fibrin and other
factors)…… So>> blood spilling out of BV >>
simultaneous bleeding
• • poor nutrition
• • Poor O2 delivary.
• • Poor perfusion of vital organs.
12. Pathophysiology
• 6) Cardiac output: initially increase to
compensate BP >> ( increased CO* inc
SVR = normal compensated BP)
• • As septic shock goes on, the heart can
become paralyzed and damage by these
immune molecules so cardiac output start
to be depressed >> so decreased CO *
Decreased SVR >> decreased BP.
13. Pathophysiology
• Acid base disturbances:
** Lactic acid is elevated due to tissue ischemia (acidosis) **
Acidosis + cytokines: tachypnea (develops due to acidocis,
cytokines, and fever) which will lead to respiratory alkalosis
** Metabolic acidosis develops just before or with hypotension; it
signals the beginning of a fatal downward course
Cytokines involves in sepsis: TNF-alpha IL-1, 6, 8 Complement
Coagulation pathways Gamma interpheron
14. Causes
• a. Infectious —m.c=TB and other
mycobacterial infection, Occult abscesses
(e.g., hepatic, retroperitoneal)
UTI/complicated ,UTI, Endocarditis Sinusitis
HIV, Infectious mononucleosis, and ,Malaria
parasite , Infection of the digestive system
(which includes organs such as the stomach
and colon)
• Infection of the kidney, bladder and other parts
of the urinary system
15. Causes
- Cellulitis , apendicitis , peritonitis infection
of brain or spinal cord
-immunosuppressive drugs,
-chemotherapy) invasive lines (venous line or
arterial ),
- urinary catheters
...etc.
Non-infectious: pancreatitis
16. • Risk Factors for sepsis
Weakened immune system from illness or
medical treatment
Age under 1 year
Age 65 years or more
• HIV, diabetes, cancer, kidney or liver disease
17. Clinical Features
• Fever (first and m.c manifestation)or may
hypothermic ( more common in very young, elderly,
immunocompromised ….)
• 2. sign of SIRS (tachypnea , tachycardia )……..(
TACHYCARDIA is the 1st manifestation)
• 3. sign of shock ( hypotension, oliguria, lactic acidosis)
------ (hypotension and hypoxia)
• 4. manifestation related to the cause of sepsis. ( e.g
pneumonia / breathing difficulty, UTI / urination
problem.....)
• 5. flushing, warm skin due to BV dilatation ------
increase sympathetic innervation >> tries to increase
BP by vasoconstriction to improve Systemic vascular
resistance ------ so, with progression of septic shock,
patient will eventually have cooler skin.
18. Diagnosis
• 1. Careful history and physical examination—
with attention to medications, travel,immune
system competency, and review of systems
• 2. Laboratory tests
a. CBC with differential
b. Urinalysis
c. Cultures of blood, sputum, CSF, urine, and stool
when indicated by clinical
19. Diagnosis
• ABG, chemistry
• o DIC work up by the following tests:
- CBC –platelets are low.
- PT–prolonged as coagulation factors are
consumed –
PTT– may be prolonged
- D-dimer –protein that results from clot break-
down; it is markedly elevated with DIC
-Fibrinogen – one of the clotting factors; is low
20. sofa score = Sequential (sepsis-
related) organ failure
assessment score
• previously known as the sepsis related organ
failure assessment score, is used to track a
person's status during the stay in an intensive
care unit (ICU) to determine the extent of a
person's organ function or rate of failure.
21.
22.
23. Sofa Score
• A change in the SOFA score of 2 or more is
now a defining characteristic of the sepsis
syndrome, and the European Medicines
Agency has accepted that a change in the
SOFA score is an acceptable surrogate
marker of efficacy in exploratory trials of
novel therapeutic agents in sepsis.
• The requirement to detect modest serial
changes in a patients’ SOFA score therefore
means that increased clarity on how the
score should be assessed in different
circumstances is required
24. quickSOFA
• The qSOFA score = quickSOFA) is a bedside
prompt that may identify patients with
suspected infection who are at greater risk for
a poor outcome outside the intensive care unit
(ICU).
• It uses three criteria, assigning one point for
low blood pressure (SBP≤100 mmHg),
high respiratory rate (≥22 breaths per min),
or altered mentation (Glasgow coma
scale<15).
25. quickSOFA
• The presence of 2 or more qSOFA points near the onset of infection
was associated with a greater risk of death or prolonged intensive
care unit stay.
• These are outcomes that are more common in infected patients
who may be septic than those with uncomplicated infection.
• Two points is a positive qSOFA, with increasing points patient
outcomes are associated with higher mortality rates
• Based upon these findings, the Third International Consensus
Definitions for Sepsis recommends qSOFA as a simple prompt to
identify infected patients outside the ICU who are likely to be septic.
26. TRIAGE of Sepsis At EmerGency
department (TRIAGE)
• Emergency departments play a vital role in
identifying, treating, and managing septic
patients.
• Early identification and appropriate management
in the initial hours after sepsis develops
improves outcomes, .
• SIRS and qSOFA, are sepsis recognition tools
=triage screening tool.
27. TRIAGE of Sepsis At EmerGency
department (TRIAGE)
• Randomized control trials or meta-analysis strengthen
the claim for SIRS over qSOFA in ED triage screening
tool for sepsis recognition.
• SIRS criteria has greatest sensitivity to sepsis
recognition ,,with qSOFA showing higher sensitivity to
mortality.
• . The evidence leads to septic patients benefiting from
an additional screening tool, the qSOFA, if they have
2+ SIRS criteria to rule out higher mortality and critical
care need.
• A triage model at the ED with special attention to
severe sepsis patients, led to sustained improvements
28. Treatment
ABCs
• 2 large IV bore
• Fluid resuscitation (IV fluids at a dose of 30 mL/kg given within
the first 3 h)
• oxygen
• Empiric antibiotics, Levofloxacin used in suspected patient
with pneumonia since its cover most Aminoglycosides(eg.
Gentamycin), Ceftriaxone in UTI suspected Ampicillin,
Amoxicillin, Tetracyclines Vancomycin For MRSA >>> After the
culture result >> specific antibiotic to the organism.
• if not get better with antibiotics>> Antifungal (for candidemia)
• Vasopressors as needed as following:
29. Treatment
• • Steroids: they are given for patients who develop
adrenal insufficiency.
• # monitor progress of the patient
• 1) CRP(c- reactive protein) normal < 1 mg/dL
• 2) ESR (erythrocyte sedimentation rate normal
< 20-25 ml/h
• **Both markers increased in inflammation and
downtrend(decrease) in resolution of septic shock
30. Treatment
• sodium bicarbonate may reduce need for
renal replacement therapy in patients
admitted to intensive care unit with severe
acidemia
• 2 JUN 2020
• vasopressin and vasopressin analogues
might reduce need for renal replacement
therapy compared to norepinephrine in
critically ill adults with septic shock.
31. Treatment
• ABC
• 2 IV large bore
• giving antibiotics giving fluids intravenously
• giving oxygen if levels are low
• blood transfusion
• mechanical ventilation
• Dialysis
• Admission to ICU , ---
corticosteroids medic
ation ???
32. Sepsis Treatment in Adults,
Dynamed , corticosteroids ???
• treatment bundle of hydrocortisone, ascorbic
acid, and thiamine may reduce time to
resolution of shock in adults with sepsis or
septic shock admitted to intensive care
• 21 FEB 2020
• corticosteroids may increase shock reversal
and reduce 28-day mortality in patients with
sepsis, with mortality benefit potentially
limited to those with ARDS, community-
acquired pneumonia, or septic shock
• corticosteroids may reduce 28-day mortality,
ICU mortality, and hospital mortality in adults
33. Corticosteroids ????
• Upon study was done in December 2018 - Maria
Vargas, MD, Giuseppe Servillo, MD, Department of
Neurosciences, Reproductive and
Odontostomatological Sciences, University of Naples
• And they found that the ,results may suggest that the
evidences about the relationship between the use of
corticosteroids and the reduction of mortality in septic
critically ill patients are very weak, and the messages
coming from these randomized clincal trial RCTs),--
concluded that corticosteroid may result in a small
absolute reduction in mortality of approximately 2%--,
should be carefully interpreted.
• Furthermore, they found no effect of corticosteroid on
short-term mortality
34. • Reference for SOFA score =Lambden,S ,et al , The SOFA score—development,
utility and challenges of accurate assessment in clinical trials, 23, Article number:
374 (2019)
• Reference For triage =November 2018. Triage Tool for Sepsis Recognition. [online].
Available from: https://nursinganswers.net/essays/sepsis-triage-tool.php?vref=1
[Accessed 23 August 2020].
