Septic shock

Septic shock

·        Septic shock is currently the most common cause of death in intensive care units.

·        It results from the spread of microbes from severe localized infections (e.g., abscess, peritonitis, pneumonia) into the bloodstream.

·        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.

·        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.

·        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

·        These reactive features are nonspecific and are present in most bacterial septicemias.

·        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.

·        In the brain the so-called ischemic encephalopathy may develop.

·        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.

·        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.

·        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.

·        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.

·        The abscesses of the liver may take place also.

·        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”.

·        The gastrointestinal tract may suffer patchy mucosal hemorrhages and necroses referred to as “hemorrhagic enteropathy”.

·        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.

·        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.