الفهرس 
Cerebral circulationOnly 14 pages are availabe for public view
 |  | from | 124 |  |  |
| | | from | 124 | | |
Abstract
Septic shock is a clinical syndrome characterized by sepsis and refractory hypotension despite adequate fluid resuscitation
Septic shock and multiple organ dysfunction syndromes are the most common causes of morbidity and mortality amongst critically ill patients.
Different sources of sepsis include respiratory tract infections (pneumonia, lung abscess, empyema), urosepsis, abdominal sepsis (cholecystitis, peritonitis, gastric colonization, clostridium defficile colitis), CNS infection, pancreatitis, wound infection as well as poly traumatized patients.
The mediator network of response to sepsis consists of the interaction of cytokines, adhesion molecules, arachidonic acid metabolites, platelet-activating factor, oxygen-free radicals, nitric oxide, complement and other mediators, all of which induce hypotension, myocardial depression, capillary leak and inflammation. The cytokine cascade is stimulated by endotoxin, TNFα and IL-1. Cytokines include IL-1, IL-6, TNFα and chemokines.
The coagulation cascade has a major role in the pathophsiology of sepsis. Organ dysfunction includes the lung in which ARDS occurs, the cardiac muscle causing myocardial depression, hepatic dysfunction, renal dysfunction, gastrointestinal tract affection, septic encephalopathy, adrenal insufficiency, vasdilation, disturbed oxygen consumption/ delivery, and disturbed peripheral metabolism.
Cerebral autoregulation is a homeostatic process where cerebral blood flow (CBF) remains constant between a mean arterial blood pressure (MAP) of 60 mm Hg and 160 mm Hg. CBF is the determined by dividing cerebral perfusion pressure (CPP) by the cerebral vascular resistance (CVR) (CBF=CPP % CVR).
So lowered cerebral perfusion pressure (CPP) caused by arterial hypotension or increased intracranial pressure (ICP) may cause critical reductions in cerebral blood flow (CBF) to ischemic levels especially in head-injured patients who have poorly functioning or absent autoregulation.
Brain dysfunction is a serious complication of sepsis. The severity of septic encephalopathy or sepsis-associated delirium (SAD) is correlated with the global severity of sepsis and has been reported to be an independent predictor of death.
The etiology of disordered function of the central nervous system in patients with severe sepsis is multifactorial. It includes abnormalities in the blood-brain barrier, alterations in cerebral blood flow, abnormal cellular physiology, and changes in the composition of neurotransmitters in the reticular activating system.
The inflammatory response observed in sepsis triggers profound changes in the brain.
Blood-brain barrier permeability is increased, and substantial changes in regulation of CBF and cerebral perfusion may hypoperfusion due to severe hemodynamic instability which will obviously lead to ischemic brain injury.
The changes in pressure autoregulation may result in an increased vulnerability of the brain to hypoperfusion,however this does not explain the full range of brain dysfunction found in septic patients.
So far it has not been possible to establish a clear link between cerebral perfusion and sepsis-associated delirium.