SEPSIS

Definitions

1.Bacteremia : the presence of bacteria in blood

2.Septicemia: presence of microbes or toxins
3.SIRS ( systemic inflammatory Syndrome)
the presence of two or more of the ff conditions:
A. Fever ( oral T0 >380c) or hypothermia (<350c)
B. Tachypnea (>24pm)
C. Tachycardia ( >90bpm)
D. Leukocytosis (>12,000) or Leukopenia (<4000) or >10% bands
* may have infectious or noninfectious cause
Definitions

4. Sepsis: SIRS that has a proven or suspected

microbial etiology
5. Sever Sepsis: Sepsis with one or more signs of
organ dysfunction (oliguria, hypoxemia
encephalopathy, metabolic acidosis, DIC)
or hypotension
6. Septic shock: sepsis with hypotension that is
unresponsive to fluid resuscitation,
along with organ dysfunction
Definitions

7. Refractory septic shock: Septic shock that persists

more than 1 hr and does not respond to fluid or
pressor.

8. Multi organ Dysfunction Syndrome (MODS):

Dysfunction of more than one organ, requiring
intervention to maintain function.
EPIDEMIOLOGY

• The most common cause of death in ICU

• Incidence and prevalence are increasing
• Contributing factors are:
• Aggressive therapy of cancers
• Surgical factors
• Increased life span
• Anti-microbial therapy
Etiology

• Microbial invasion of blood is not essential for the

development of sepsis
• Blood Culture is positive in 20-40% of sever sepsis
cases and 40-70% of cases with septic shock
• Gram negatives account to 40%
• Gram positives account to 31%
• Fungi account to 6%
• Polymicrobial account to 16%
• Classic pathogens <5%
 Risk factors
• Risks for Gm neg sepsis:
• Cirrhosis, burns, Lymphoproliferative disorders, diabetes mellitus, invasive procedures
and devices, neutropenia
• Risks for Gm +ve sepsis:
• IV catheters, burns
• Fungemia is common in neutropenic patients
Incidence of sepsis according to source of infection
(Clinical Infectious Diseases 2005; 41:S490–7)
 Pathogensis
• Complex inflammatory/anti-inflammatory response of
the body to infection
• It is the result of:
• The host response
• The role of the endothelium
• The disequilibrium between the pro –
inflammatory and anti-inflammatory responses
• The activation of the coagulation pathway
Pathophysiology

infection

Activation of the immunologic system

Inflammatory Cytokines Anti-inflammatory Cytokines

TNF alpha, IL-1, IL-8

Secondary mediators:
-PGs, Txs, NO,
-Vasodilation and hypotension
-Disseminated thrombosis
-Organ dysfunction
Clinical presentation

• Clinical continuum starting as SIRS then progressing

to sever sepsis to septic shock and to MODS
• Appear superimposed on signs and sx of patient’s
underlying illness and primary infection
• Starts with nonspecific symptoms of fever, chills,
myalgia, malaise, anxiety, and confusion
• Fever may not be present in elderly, uremic,
neutropenic patients, alcoholic
Clinical presentation

• With progression of sepsis, there are sx and signs of

organ hypoperfusion
• Respiratory: tachypnea, increasing effort of breathing, cyanosis, apnea or
respiratory arrest
• CVS: hypotension, tachycardia, arrythmia
• Neurology: altered sensorium, irritability, confusion, coma
• Renal: oliguria, anuria
• Hematology: Leukemoid Rx, neutropenia, thrombocytopenia, DIC
 Clinical presentation
• With septic shock
• Warm Shock Cold Shock
Peripheries warm, flashed cold, clammy, cyanotic
Pulse bounding narrow
HR tachycardia tachycardia/bradycardia
BP normal Hypotension
Clinical presentation

• Look for localizing signs

CNS: Meningitis, encephalopathy
Head neck: sinusitis, OM, exudative pharyngitis
Chest: pneumonia
Heart: changing mumur of IE
GIT: guarding, tenderness, mass
Skin: pustules, erythema/scalding
Bone and soft tissues: focal erythema, effusion
Complications

• ARDS
• ARF
• CNS Dysfunction
• Hepatic failure
• DIC
• Stress ulcer and bleeding
Diagnosis

• Diagnosis requires

• High index of suspicion

• Meticulous history
• detailed physical exam
• Extensive lab work up
Laboratory investigation

• Purpose is to make etiologic dx, assess complications

• Blood culture ( with sensitivity): at least two in 24 hrs
• When indicated culture: urine, CSF, tracheal aspirates,
body fluids, pus; fungal culture
• CBC, CRP
• Monitoring severity and progress
• BUN, Creatinine
• Transaminases, ALP, Bilirubine
• Bicarbonate, lactate
• RBG
• PT,PTT, fibrinogen, FDP
• Electrolytes: K, Na, Cl
Laboratory investigation

• With indication: x-ray, US, CT scan

PCT as a response to infection and in predicting
development of sepsis
Treatment

• 1. Stabilization of the patient

• the ABC : Airway, Breathing, Circualtion

• Aggressive fluid resuscitation (crystalloids)
• Inotropic support: dopamine, adrenaline
• Intubation and mechanical ventilation ( if indicated)
• Whole blood or PRBC if HB <10g%
• Platelet or FFP
• Bicarbonate if refractory acidosis
Treatment

• 2. Remove the source of infection

• evaluate to identify focus of infection
• Remove and replace indwelling catheters
• Debride dead tissues
• Drain pus
Treatment

• 3. Anti-microbial treatment
• Should be administered immediately after taking blood
culture
• Choice is empiric, broad spectrum to cover Gram positive
and negative bacteria
• Selection is based on: risk factors of patient and
underlying illness, local organism prevalence and
sensitivity pattern , and institutional protocol
Prevention

• Reduce the number of invasive procedures

• Limit the duration and use of IV and urinary

catheters
• Early and aggressive treatment of nosocomial
infections
• Control indiscriminate use of broad spectrum
antibiotics and glucocorticoids
• Optimal infection prevention practices
Prognosis

• Mortality: sever sepsis is 30%

septic shock is upto 70%
• Depends on
• setting where it occurred
• Gm –ve associated with high death
• Underlying risk