Septic shock
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Septic shock is currently the most
common cause of death in intensive care units.
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It results from the spread of
microbes from severe localized infections (e.g., abscess, peritonitis,
pneumonia) into the bloodstream.
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The majority of cases are caused by
endotoxin-producing gram-negative bacilli - E.coli, Klebsiella pneumonia,
Proteus species, Pseudomonas aeruginosa, Serratia, and Bacteroides - hence the
term endotoxic shock.
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Endotoxins are bacterial wall
polysaccharides, consisting of a toxic lipid A core component and a complex
polysaccharide coat. Gram-positive cocci, such as pneumococci and streptococci,
and certain fungi, as well as gram-positive bacterial toxins produce a similar
syndrome.
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Shock is a progressive disorder that
may lead to death.
Shock tends to evolve through three
stages:
1. An initial nonprogressive phase
during which reflex compensatory mechanisms are activated and perfusion of the
vital organs is preserved.
2. A progressive stage characterized
by tissue hypoperfusion and onset of an ever-widening circle of circulatory and
metabolic imbalances.
3. In finally, an irreversible stage
that sets in after the body has incurred cellular and tissue injury so severe
that even if therapy corrects the hemodynamic defects survival is not possible.
Morphology
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These reactive features are
nonspecific and are present in most bacterial septicemias.
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Shock is characterized by hypoxic
failure of multiple organ systems, and hence the cellular changes may appear in
any tissue. They are particularly evident in the brain, heart, lungs, kidneys,
liver, spleen, adrenals and gastrointestinal tract.
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In the brain the so-called
ischemic encephalopathy may develop.
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The heart may
undergo a variety of changes. Subendocardial hemorrhages and necrosis, or
“zonal lesions”, sometimes appear in all forms of shock. The term zonal lesions
refers to apparent hypercontraction of a myocyte, including shortening and
scalloping of the sarcomere, fragmentation of the Z band, distortion of the
myofilaments, and displacement of the mitochondria away from the intercalated
disc.
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The kidneys may be
severely affected in shock, and that is why oliguria, anuria, and electrolyte
disturbances constitute major clinical problems. The renal changes are referred
to as acute tubular necrosis.
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The lungs are seldom affected in pure hypovolemic shock because
they are resistant to hypoxic injury, but when the vascular collapse is caused
by bacterial sepsis or trauma, changes may appear that are referred to as
“shock lung”. They are referred to as the acute respiratory distress syndrome.
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Splenomegaly
of moderate degree (250 to 350 g) is
common in acute systemic infections and is referred to as “acute reactive
hyperplasia” or “septic splenitis”. The spleen is enlarged and soft, and the
cut surface demonstrates an equal prominence of the red and white pulp.
Lymphoid hyperplasia with germinal center formation is pronounced, and plasma
cell hyperplasia is present in the marginal zone of the white pulp and in the
cords. Histiocytic hyperplasia is equally prominent.
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The abscesses of the liver may take place also.
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The adrenal alterations
encountered in shock comprise in essence those common to all forms of stress
and so might be referred to as “ the stress response”.
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The gastrointestinal tract
may suffer patchy mucosal hemorrhages and necroses referred to as “hemorrhagic
enteropathy”.
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Virtually all of these organs changes
may revert to normal if the patient survives. However, loss of neurons from the
brain and of the myocytes from the heart is, of course, irreversible. However,
most patients who suffer shock so severe as to produce irreversible changes
succumb before these alterations become well developed.
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It is evident that postshock course
of the patient does not lack for threats to life. The prognosis varies with the
origin of shock and its duration.
