Pathophysiology and treatment of septic shock

Abstract

Shock is defined as inadequate circulating blood volume producing decreased peripheral vascular perfusion and cellular metabolic derangements, first in the nonvital tissues (the gastrointestinal tract, muscle, connective tissue, and skin) and later in the vital tissues (the brain, heart, lung, liver, and kidneys). This inadequate microcirculatory perfusion is the common denominator of all types of shock. Septic shock is caused by an immunologic reaction characterized by a hyperdynamic state, which produces increased cardiac output and decreased peripheral resistance. This reaction is secondary to endotoxin-antibody-complement complexing and leukocyte lysis that results in the production of histamine, serotonin, super-radicals, lysosomal enzymes, and kinins. These substances induce a marked capillary permeability and a third space loss, leading to hypovolemia. This is the hypodynamic state of septic shock, which is characterized by decreased cardiac output and increased peripheral resistance. Diagnosis should be established in the hyperdynamic state of septic shock. Monitoring of the patient in septic shock requires continuous evaluation of the status of clinical signs, peripheral perfusion, vital organ function, and volume requirements. There are four principal and equally important objectives in the treatment of septic shock: treatment of sepsis, management of the hypovolemic state, reparation of the metabolic acid-base imbalance, and correction of the nutritional deficit. There are no priorities; all aspects of treatment must be rendered concomitantly and rapidly. It is essential that the septic and hypovolemic processes be treated concomitantly, since preventing the complexing of antigen-antibody and complement will deter vascular permeability and its consequent hypovolemia. Prompt and adequate treatment of hypovolemia prevents the development of attendant cellular metabolic derangements.(ABSTRACT TRUNCATED AT 250 WORDS)