Pathophysiology of Lung Injury

in Sepsis

• Sepsis is a clinical syndrome that complicates severe

infection and is characterized by systemic inflammation and
widespread tissue injury

• Multiple organ dysfunction is a continuum, with incremental

degrees of physiological derangements in individual organs;
it is a process rather than an event
• The term MODS is defined as a clinical syndrome in which
the development of progressive and potentially reversible
physiological dysfunction in 2 or more organs or organ
systems induced by a variety of acute insults, including
sepsis, is characteristic.

• Sepsis  SIRS plus a culture documented infection

• Severe Sepsis  Sepsis plus organ disfunction, hypotension
or hypoperfusion (including but not limited to lactic acidosis,
oliguria or acute mental status changes)
• Septic Shock  Hypotension ( despite fluid resuscitation)
plus hypoperfusion

• The pathogenesis of sepsis involves complex interaction of :

• inflammatory mediators
• activations of host cells to release counter
inflammatory mediators
• role of tissue factors in triggering
coagulant response
• supression of endogenous fibrinolysis

• The lung seem to be particularly vulnerable to the septic

inflammatory response
• sepsis is the underlying cause in about 40% patients
with acute respiratory failure
 Pathophysiology of lung injury
1st phase 2nd phase
Administration
1 hour endotoxin >2-4 hour
• Mean pulmonary Endothelial
artery pressure ↑↑ Permeability ↑
• Pulmonary vascular
resistance ↑↑ Protein content of
Pulmonary lymph ↑

1. Hydrostatic pressure gradient
across the endothelium ↑↑
2. Pulmonary lymph flow with
a low protein content ↑↑
3. Extravascular lung water
accumulates
Interstitial onkotic
Pressure ↑
Interalveolar oedem
If alveolocapillary Promote further
membrane is severely extravasation of fluid
damage