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Pathophysiology of Septic Shock Draft 1

The document discusses the pathophysiology of septic shock. It outlines risk factors, sources of infection from gram-positive and gram-negative organisms, the inflammatory response and how it leads to endothelial dysfunction and multiple organ dysfunction syndrome in septic shock patients.

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Ju Lie Ann
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0% found this document useful (0 votes)
2K views1 page

Pathophysiology of Septic Shock Draft 1

The document discusses the pathophysiology of septic shock. It outlines risk factors, sources of infection from gram-positive and gram-negative organisms, the inflammatory response and how it leads to endothelial dysfunction and multiple organ dysfunction syndrome in septic shock patients.

Uploaded by

Ju Lie Ann
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
  • Pathophysiology of Septic Shock

PATHOPHYSIOLOGY OF SEPTIC SHOCK

Predisposing & Precipitating


> Extremes of age (70 years) > Major surgery, trauma, burns
> Primary diseases (e.g., liver cirrhosis, diabetes mellitus, > Invasive procedures (e.g., placement of catheters,
cardiopulmonary diseases, late stage cancer, intravascular devices, prosthetic devices, hemodialysis
Risk Factors

acquired immunodeficiency syndrome) and peritoneal dialysis catheters, or endotracheal tubes)


> Immunosuppression (e.g., from > Common illnesses and other infections (e.g., lung

EARLY, REVERSIBLE AND COMPENSATORY SHOCK


neutropenia, immunosuppressive therapy [e.g., in organ and bone infections like pneumonia, gastrointestinal infection,
marrow transplant recipients], corticosteroid therapy, injection or urinary tract infections, nosocomial infections, etc.)
IV drug use, complement deficiencies, asplenia)
> Prolonged hospitalization
> Weak immune systems
> Other factors (e.g., childbirth, abortion, and malnutrition)
> Underlying genetic susceptibility

SEPTICEMIA
caused by caused by
GRAM-NEGATIVE GRAM-POSITIVE
ORGANISMS ORGANISMS

FIRST STAGE
Sources of Infection

Release Release
Etiology  

Endotoxins TRIGGERS Exotoxins

example example

Lipopolysaccharide complex Superantigens (Type I toxins);


associated with the outer Response mechanisms occur Exotoxins that damage host cell membranes
(Type II toxins); and.
membrane of Gram-negative
pathogens
during septic shock, but on a systemic scale A-B toxins and other toxin that interfere with
host cell function (Type III toxins)
Release of inflammatory chemical mediators  

Pro-inflammatory Response  
Activation of immunological system

INTERMEDIATE OR PROGRESSIVE SHOCK


CELL-DERIVED PLASMA PROTEIN
LYMPHOCYTES GRANULOCYTES MONOCYTES
MEDIATORS SYSTEMS

SECOND STAGE
Anti-inflammatory Response  
References:
References:
LeMone, P. (2017). Medical-surgical nursing:
Sorenson, M., Quinn, L., & Klein, D. (2019). Critical
Pathophysiology: Concepts of human disease. thinking for person-centred care. Melbourne, VIC:
NY, NY: Pearson. Positive Feedback Mechanism
Result to

Pearson Australia.
Andre Kalil, M. (2020, October 07). Septic McCance, K. L., Huether, S. E., Brashers, V. L.,
Shock. Retrieved October 28, 2020, from
https://emedicine.medscape.com/article/168402- & Rote, N. S. (2019). Pathophysiology: The
ENDOTHELIAL DYSFUNCTION biologic basis for disease
overview
in adults and children. St. Louis: Elsevier
Manifestations  

Capillary Leak Microvascular Trombus Cell Adhesion Tissue Hypoxia Apoptosis Impaired Vascular Tone Free Radical Damage
Clinical

REFRACTORY OR IRREVERSIBLE SHOCK

SEPTIC
MULTIPLE ORGAN DYSFUNCTION
SHOCK
THIRD STAGE
Signs and Symptom

Altered Mental p/f ratio <300 Urine Hypotension Thrombocytopenia Metabolic Acidosis
Lab Test result

Poor Capillary Refill


Status Tachypnea <0.5 ml/kg/hr Tachycardia High 0-dimer High Lactate

DEATH

SEPTICEMIA
> Extremes of age (70 years)
> Primary diseases (e.g., liver cirrhosis, diabetes mellitus,
cardiopulmonary disease

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