Septic shock sirs and mof

Septic shock
Osama Mohamed Omar
student at faculty of medicine
Tanta university

OVERVIEW
• Septic shock is the most common cause of mortality
in the intensive care unit. It is the 10th leading cause
of death overall.
• Despite aggressive treatment mortality ranges from
15% in patients with sepsis to 40-60% in patients
with septic shock.

Reference Diseases
 Incidence in US (cases per 100,000)
 AIDS1 17
 Colon and rectal cancer2 48
 Breast cancer2 112
 Congestive heart failure3 ~196
 Severe sepsis4 ~300
 Number of deaths in US each year
 Acute myocardial infarction5 218,000
 Severe sepsis4 215,000
1Centers for Disease Control and Prevention. 2000. Incidence rate for 1999.
2American Cancer Society. 2001. Incidence rate for 1993-1997.
4Angus DC et al. 2001. Crit Care Med 29:1303-1310.
5National Center for Health Statistics. 2001.

Etiology
Pathophysiology
How To Diagnosis?
How To Manage?
Sepsis syndromes
Objectives

Sepsis syndromes
SIRS
Sepis
Severe sepsis-SIRS
Septic shock
MODS

(Systemic Inflammatory Response Syndrome) is a systemic
inflammatory response to non specific insults
SIRS
SIRS is either due to Infection or others (major burn-
major traume-pancreatitis –hypovolemic shock)
Clinically?!
1. hyperthermia >38°C or hypothermia <36°C
2. • tachycardia >90 bpm
3. • tachypnoea >20 r.p.m. or PaCO2 <4.3 kPa
4. • neutrophilia >12 × 10–9 l–1 or neutropenia <4
000

Clinically?!
• Known or suspected infection,
plus
• >2 SIRS Criteria.
Sepis
•The systemic inflammatory response to infection.
Severe sepsis-SIRS
•Severe sepsis resulting in at least one organ
failure
Clinically?!
•Sepsis plus >1 organ dysfunction.

Septic shock
•Sepsis induced shock with hypotension despite
adequate resuscitation along with the presence of
perfusion abnormalities which may include, but
are not limited to lactic acidosis, oliguria, or an
acute alteration in mental status.
MODS
(multiple organ dysfunction syndrome) The presence of
altered organ function in an acutely ill patient such that
homeostasis cannot be maintained without intervention.

SIRS
systemic
inflammatory
response
syndrome
SEPSIS
SIRS with a presumed or confirmed
infectious process
• Severe sepsis
Sepsis with ≥1 sign of organ failure
Septic shock
SIRS + Infection + Organ
Failure + Refractory
Hypotension

Etiology
Caustive
organisms
•Gram –ve the
commonest
•Staphylococcus
•Candida
Sources of
infection
• Endogenus source
1. Causes ofPeritonitis
2. Perforated viscous
3. Gangrenous bowel
4. Genitourinary
infection
• Exogenus source
 Infected CVP
Predisposing
factors
• Old age
• DM
• Corticosteroid
therpy
• Malignancy
• Major operation

 It is not precisely understood, but it involves a complex
interaction between the pathogen and the host's immune
system.
 Physiological response to localized infection:
o Influx of activated PMN leukocytes & monocytes  release of inflammatory
mediators
o Local vasodilatation & increased endothelial permeability
o Activation of the coagulation cascade.
 The same occurs in septic shock but at a systemic level.
 Diffuse endothelial disruption
 Increased vascular permeability
 Vasodilatation
 Thrombosis of end organ capillaries
Pathophysiology

Infection
Inflammatory
Mediators
Endothelial
Dysfunction
Vasodilation
Hypotension Vasoconstriction Edema
Maldistribution of Microvascular Blood Flow
Organ Dysfunction
Microvascular Plugging
Ischemia
Cell Death

Inadequate
Resuscitation
Preoperative Illness
Trauma or
Operation
Tissue Injury
optimal oxygen
delivery and
support
Recovery
Excessive
Inflammatory
Response
SIRS/MODS
Pathogenesis of SIRS/MODS
in surgical patients

 Lungs
 Kidneys
 CVS
 CNS
 PNS
 Coagulation
 GI
 Liver
 Endocrine
 Skeletal Muscle
 Adult Respiratory Distress Syndrome18%
 Acute Tubular Necrosis 50%
 Shock
 Metabolic encephalopathy
 Critical Illness Polyneuropathy
 Disseminated Intravascular Coagulopathy
38%
 Gastroparesis and ileus
 Cholestasis
 Adrenal insufficiency
 Rhabdomyolysis
Acute Organ Dysfunction

Identifying Acute Organ Dysfunction
as a Marker of Severe Sepsis
Tachycardia
Hypotensio
n
 CVP
 PAOP
Jaundice
 Enzymes
 Albumin
 PT
Altered
Consciousness
Confusion
Psychosis
Tachypnea
PaO2 <70 mm
Hg
SaO2 <90%
PaO2/FiO2 300
Oliguria
Anuria
 Creatinine
 Platelets
 PT/APTT
 Protein C
 D-dimer

How To Diagnosis?
• You must suspect sepsis in patient with predisposing
factors,dont wait for septic shock
• The diagnosis of sepsis requires the taking of an
EXCELLENT history, physical examination,
appropriate laboratory tests, and a close follow-up
of hemodynamic status
• Early recognition is live saving in such rapid
overwhelming situation

How To Diagnosis?
Hyperdynamic- Warm- Early
Septic Shock
Restlness & confusion
Vitals
1. Temperature fever
more than 38 chills
2. Mild decrease ABP
3. Tachycardia
4. Tachypnea
Skin warm ,dry ,flushed
High cardiac output
Hypodynamic- Cold- Late
Septic Shock
 Semicomatosed
 Vitals
1. Temperature
decreased
2. Tachycardia
3. Tachypnea
4. SBP<90mmHg
 Oliguria & low COP
 Multiorgan failure start at
this stage

How To Diagnosis?
Work-up…
 Laboratory studies
o CBC
o Coagulation studies
o Blood & urine cultures
 Imaging studies
o Chest radiography
o Abdominal radiography
o Others according to the suspected cause.

• Glucose control is important in the management of sepsis,
with hyperglycemia associated with higher mortality
• LFTs and bilirubin, alkaline phosphatase, and lipase
levels are important in evaluating multiorgan
dysfunction or a potential source (eg, biliary disease,
pancreatitis, hepatitis).
• Serum lactate …It is the best serum marker for tissue perfusion.
Lactate levels >2.5 mmol/L are associated with an increase in mortal

How To Manage?
Septic Shock & MODS
Septic
•Control Infection Source
Shock
•Optimize Organ Perfusion
(Resuscitation)
MODS
•Support Dysfunctional
Systems & Monitoring

Shock
•Optimize Organ Perfusion
(Resuscitation)
1)Circulatory support
I. Fluid replacment to achieve
cvp 10-12 cm H2o
II. Packed RBCS if low HCT
III. Drugs Inotropes &
vassopressor
2)Respiratory support
3)Renal support haemodyalisis in ARF
4)TTT of DIC fresh frozen plazma
The most important is
Early goal directed therpy

The most important is
Early goal directed therpy
EGDT is a 3-step protocol aimed at optimizing tissue
perfusion

Septic
•Control Infection Source
Eliminate surgical causes?!
 Huge abscess
 Peritonitis
 gangernous bowel
Antibiotic therapy
Parentral ,compined ,broad spetrum.

• Antibiotics should be administered within the first hour of
recognition of septic shock, and delays in antibiotic
administration have been associated with increased
mortality.
• Selection of particular antibiotic agents is empirically based
on
 an assessment of the patient's underlying host defenses,
 the potential source of infection, and
 the most likely responsible organisms.
• One regimen for septic shock of unknown cause is
ogentamicin or tobramycin 5.1 mg/kg IV
once/day
o3rd generation cephalosporin “cefotaxime 2 g q
6 to 8 h or ceftriaxone 2 g once/day”
oor if pseudomonas is suspected ceftazidime 2
g IV q 8 h”

•Renal replacement therapies (dialysis).
•Cardiovascular support (pressors,
inotropes).
•Mechanical ventilation.
•Blood Transfusion for hematologic
dysfunction.
MODS
•Support Dysfunctional
Systems & Monitoring

Steroid therapy…?!
Recent guidline is that steroids should be administered only in
patients with septic shock whose hypotension is poorly
responsive to fluid resuscitation and vasopressor therapy.
NEVER resuscitate with glucose 5%

References......
 http://emedicine.medscape.com/article/168402-overview
 http://www.atsu.edu/faculty/chamberlain/Website/lecture
s/lecture/sepsis.htm
 http://en.wikipedia.org/wiki/Septic_shock
 http://www.medscape.com/viewarticle/738317
 Surgery_At_a_Glance_2nd_Ed_2002
 Kaser El-Aini 7th Edition part 1

Septic shock sirs and mof

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