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Septic shock
Dr. M. A. Sofi MD; FRCP
(London); FRCPEdin;
FRCSEdin
Septic Shock
• Septic shock- once a uniformly fatal
condition with 100% mortality.
• Present recovery rates are up to 50%.
• Significance: Frequent occurrence and high
mortality.
Septic Shock
I.
II.
Introduction.
Pathophysiology
III. Clinical Manifestations
IV.
Management
Introduction.
• What is shock?
Shock is a state of acute disruption of circulatory function,
resulting in insufficiency of tissue utilization and cellular
energy production.
“Sepsis is a clinical syndrome characterized by systemic
inflammation due to infection. There is a continuum of
severity ranging from sepsis to severe sepsis and septic
shock”
Septic shock refers to sepsis with cardiovascular dysfunction
(ie, hypotension, reliance on vasoactive drug
administration to maintain a normal blood pressure, or
two of the following:
“prolonged capillary refill, oliguria, metabolic acidosis, or
elevated arterial lactate) that persists despite the
administration of ≥40 mL/kg of isotonic fluid in one hour.
Terminology
 Systemic Inflammatory Response Syndrome (SIRS)
 Temp > 38 or < 36
 HR > 90
 RR > 20 or PaCO2 < 32
TWO out of four criteria
 WBC > 12 or < 4 or Bands > 10%
acute change from baseline
 Sepsis
 The systemic inflammatory response to infection.
 Severe Sepsis
 Organ dysfunction secondary to Sepsis.
 e.g. hypoperfusion, hypotension, acute lung injury,
encephalopathy, acute kidney injury, coagulopathy.
 Septic Shock
 Hypotension secondary to Sepsis that is resistant to adequate fluid
administration and associated with hypoperfusion.
Infection, SIRS & Sepsis
Comparable global Epidemiology
• 95 cases per 100,000
– 2 week surveillance
– 206 French ICUs
• 95 cases per 100,000
– 3 month survey
– 23 Australian/New Zealand ICUs
• 51 cases per 100,000
– England, Wales and Northern
Ireland.
• Over 1,665,000 cases of sepsis occur in
the United States each year, with a
mortality rate up to 50 percent .
• Even with optimal treatment,
mortality due to severe sepsis or septic
shock is approximately 40 percent and
can exceed 50 percent in the sickest
patients
SIRS
• SIRS – systemic inflammatory response
syndrome
• Must have at least 2 of the following:
– Temperature >38.5ºC or <36ºC
– Heart rate >90 beats/min
– Respiratory rate >20 breaths/min or PaCO2 <32
mmHg
– WBC >12,000 cells/mm3, <4000 cells/mm3, or >10
% immature (band) forms
• SIRS is the body’s response to infection,
inflammation, stress.
Sepsis and Severe Sepsis
Sepsis – SIRS + suspected or confirmed infection
(documented via cultures or visualized via physical
exam/imaging)
Severe Sepsis – Sepsis + at least one sign of organ
hypo-perfusion or dysfunction
Areas of mottled skin
Disseminated intravascular
coagulation
Capillary refill > 3 secs
AKI
UOP < 0.5cc/kg /hr
ARDS or acute lung injury (ALI)
Lactate > 2mmol /L
Cardiac dysfunction on echo
Altered mental status
Plt < 100
Abnormal EEG
Troponin Leak
Septic Shock
• Septic Shock - Severe sepsis plus one of the
following conditions:
– MAP <60 mm Hg (<80 mm Hg if previous
hypertension) after adequate fluid resuscitation
– Need for pressors to maintain BP after fluid
resuscitation
– Adequate fluid resuscitation = 40 to 60 mL/kg
saline solution (NS 5L-10L)
– Lactate > 4mmol /L
Noninfectious mimics of sepsis
Acute myocardial
Overzealous diuresis
infarction
Acute pulmonary embolus Transfusion reactions
Acute pancreatitis
Adverse drug reactions
Procedure-related transient
Fat emboli syndrome
bacteremia
Acute adrenal
Amniotic fluid embolism
insufficiency
Acute gastrointestinal
hemorrhage
Pathophysiology
• The nidus of infection:
– Localized infections ( otitis, pneumonia,
meningitis etc.,)
– Colonization of mucosal and invasion
(meningococci)
– Occult bacteremia ( 3mo to 3 years )
– Nosocomial : ‘at risk patients’
Pathophysiology
The Pathogen:
• Neonates: GBHS, enterobacteriacae, listeria,
Staph aureus, HSV.
• Infants: Hib, Strep pneumoniae, Staph aureus.
• Children: Strep pneumoniae, N. meningitidis, S.
aureus, enterobacteriacae, Hib.
• Immunocompromised: Enterobacteria, Staph,
Pseudomonas, Candida.
Pathophysiology
• What ‘type of shock’ is septic shock?
Septic shock has features of :
– Hypovolemic shock
– Cardiac shock
– Distributive shock.
Sepsis Pathogenesis
Unbalanced Immune Reaction
Tissue Factor
Mediators of
Inflammation
Procoagulant State
ROS
Microvascular
Thrombosis
Vasodilation
Capillary
Leak
Severe sepsis
Severe sepsis refers to sepsis-induced tissue hypo-perfusion or
organ dysfunction with any of the following thought to be due to
the infection
• Sepsis-induced hypotension
• Lactate above upper limits
of laboratory normal
• Urine output
<0.5 mL/kg/hr for more
than two hours despite
adequate fluid resuscitation
• Acute lung injury with
PaO2/FIO2 <250 in the
absence of pneumonia as
infection source
• Acute lung injury with
PaO2/FIO2 <200 in the
presence of pneumonia as
infection source
• Creatinine>2 mg/dL (176.8 mi
cromol/L)
• Bilirubin>4 mg/dL (34.2 micr
omol/L)
• Platelet count <100,000
micromol/L
• Coagulopathy (INR >1.5)
Clinical Manifestations.
Staging of Septic Shock:
I. Compensated / Pre-shock / Hyperdynamic
II. Decompensated / Organ hypoperfusion
III. End organ failure / Irreversible
Clinical Manifestations.
Recognition of Septic Shock:
• Inflammatory triad– Fever
– Tachycardia
– flushed skin
• Hypoperfusion
– Altered sensorium
– Urine output
– >CFT
– Wide pulse pressure....bounding pulses
Warm Shock
Clinical Manifestations.
• Hypotension
– Cold and clammy skin
– Mottling
– Tachycardia
– Cyanosis
– Narrow pulse pressure
– Hypoxemia
– Acidosis.
Cold shock
Management
Prevention:
1.
Immunization
2.
Prompt treatment of local infections
3.
Hospitalized patient: look out for nidus
of infection- IV lines, catheters, E. tubes
Management
Recognize septic shock early:
• Remember- Inflammatory triad Signs of
hypoperfusion
• Do not wait for the BP to fall !
• Lower limit for systolic BP = 70 +( age x 2)
Management.
• Two means of death:
1. Shock.
2. Multi organ failure.
• Aims of treatment:
1. Assure perfusion of critical vascular
beds. ( cerebral, coronary, renal)
2. Rx underlying cause.
Management
STEPS
1. Prevent / correct hypoxemia: Supplement
oxygen 95-100%.
2. IV access: peripheral vein.
3. If IV access fails: Interosseous line.
4. Fluid resuscitation: 20mL/Kg NS or RL
as bolus, repeat up to 60 mL/Kg.
End point : Improved perfusion.
Management
STEPS
Improved perfusion =>
a. CFT
b. Warmth
c. Strong pulses
d. mental status
e. Tachycardia
f. BP (ideal = 90 + age x 2; Min = 70+ age x 2)
g. Urine output.
Management
STEPS
5. Establish a 2nd IV line for Dopamine infusion (Draw
blood for culture)
6. Administer IV antibiotics
<2 mo: Ampicillin + gentamicin
or
Ampicillin+ Ceftriaxone/Cefataxime
>2mo: Ceftriaxone or Cefotaxime alone
or
Ampicillin + Chloramphenicol
Fluid therapy
• Central Line Access (Fluid hydration +/pressor)
• 1st line therapy – fluids, fluids, fluids!
• Crystalloid equivalent to colloid
• Initial 1-2 Liters (20mg /kg) crystalloid or 500
ml colloid
• Careful in CHF patients !!
Management
STEPS
7. Correct metabolic derangement:
– Metabolic acidosis.
– Hyper or hypoglycemia : always
correct hypoglycemia.
Management
STEPS
8. DIC:
• Restoration of normovolemia reverses
abnormal activation.
• ‘Component replacement’
(Goal - Normal PT, PTT, fibrinogen, PC =
40,000 to 100000 /cu mm.)
a. FFP - most beneficial in early stages.
b. Cryo- consider 1 unit/3 units of FFP
transfused.
c. Platelet concentrate
Management
STEPS
9. Recognize and manage organ failure:
a. Cardiovascular support:
Rate & rhythm- correct 02, acidosis, Ca,
Mg, K variations
Stroke volume - fluid correction & replace
losses
Inotrope support.
Management
STEPS
9. Recognize and manage organ failure:
b. Renal: Volume replacement
Low dose dopamine
?diuretic with volume expansion
Indications for dialysis:
Hyperkalemia
Refractory metabolic acidosis
Anuria despite diuresis
BUN>100mg%
Management
STEPS
9. Recognize and manage organ failure:
c. Respiratory support:
Supplement 02,
Early intubation and PPV ( PEEP)
d. GI:
Antacids, sucralfate, early enteral
nutrition.
Antibiotics
Cultures / Antibiotics / Labs
 Cultures PRIOR to Antibiotics ( 2 Sets, one peripheral
and one from any line older than 48hrs)
 IV Abx within 3 hrs in the ED, within 1 hr in the ICU
 Broad
Spectrum, combination therapy for neutropenic
and patients with pseudomonas risk factors
 Vancomycin PLUS Zosyn
Consider need for Source Control !
 Drainage of
abscess or cholangitis, removal of infected
catheters, debridement or amputation of osteomyelitis
Corticosteroids
• Use in Septic Shock, if NO response to vasopressors
and fluids
– HYDROCORTISONE 200mg -300mg / day
Divided doses (Q6hrs)
• Initial Dose 100mg IV x1
• Consider for patients who received etomidate
• No need for cosyntropin stimulation test
• Wean Steroids QUICKLY once off pressors
Parameters for monitoring organ system function
in patients with sepsis
Organ system
Respiratory system
Renal system
Hematologic system
Central nervous system
Hepatobiliary system
Cardiovascular system
Gastrointestinal system
Respiratory system
Parameter
PaO2/FiO2 ratio
Urine output and serum
creatinine
Platelet count
Glasgow coma score
Serum bilirubin and liver
enzymes
Blood pressure, arterial lactate
Gastric intramucosal pH (pHi),
ileus, blood in nasogastric
aspirate
PaO2/FiO2 ratio
Management- summary.
Five important points
1. ABC, supplement 02 always.
2. IV or IO access and fluid resuscitation up to
60 mL/Kg.
3. Early dopamine infusion @10µg/Kg/min
4. Empirical antibiotic.
5. Frequent monitoring.
SUMMARY AND RECOMMENDATIONS
Therapeutic priorities include securing the airway, correcting
hypoxemia, and administering fluids and antibiotics. Intubation
and mechanical ventilation are required in some patients
 Common signs of hypoperfusion include warm, vasodilated
skin in early sepsis that progresses to cool, vasoconstricted skin
in late sepsis, tachycardia >90 per min, obtundation or
restlessness, oliguria or anuria, and lactic acidosis.
For initial fluid replacement usea crystalloid solution rather
than albumin-containing solution
 Those who remain hypotensive following intravascular volume
repletion, use vasopressors
Prompt identification and treatment of the site of infection are
essential. Sputum and urine should be collected for Gram stain
and culture. Intra-abdominal fluid collections should be
percutaneously sampled. Blood should be taken from two
distinct venipuncture sites and from indwelling vascular access
devices and cultured aerobically and anaerobically.

SUMMARY AND RECOMMENDATIONS
Severe sepsis and
septic shock that are refractory to
intravenous fluid and vasopressor + notropic therapy and blood
transfusions, are administered based on individual assessment.
Blood transfusion for patients with a hemoglobin level <7 g per
deciliter.
Antibiotics should be administered within six hours of
presentation, preferably after appropriate cultures have been
obtained. We recommend empiric broad spectrum antibiotics
when a definite source of infection can not be identified
Antibiotics should be administered within six hours of
presentation, preferably after appropriate cultures have been
obtained. Empiric broad spectrum antibiotics when a definite
source of infection can not be identified
Glucocorticoid therapy, nutritional support, glucose control,
and investigational therapies are additional considerations in
the management of patients with severe sepsis or septic shock
KEY TAKE HOME POINTS
• Recongnize Sepsis EARLY and determine
SEVERITY
• EARLY Antibiotics are critical to resolution of
shock
• RESUSCITATE severe sepsis and septic shock
ASAP
• EARLY GOAL DIRECTED THERAPY