The incidence of perioperative stroke without predisposing factors is approximately 0.1%, but specific risk factors and procedures can increase the risk by 10-fold or more.
Cerebrovascular reserve refers to the capability of the brain's vasculature to dilate in order to compensate for perioperative physiologic stresses.
Attention to the maintenance of a normal physiologic milieu is the first principle of brain-oriented perioperative care.
Fever kills vulnerable neurons, and hypothermia is protective in cases of cardiac arrest and possibly traumatic brain injury.
Glycemic control improves outcome after severe critical illness and probably optimizes neurologic outcome.
Some anesthetics are neuroprotective, but some anesthetic drugs may have neurotoxic potential.
Neural function is the essence of human existence. Thus loss of any neural element in the course of a critical illness represents a major loss to a given individual. Neurons or supporting elements may be lost in a small, virtually unnoticeable manner, or they may perhaps manifest as cognitive or behavioral deficit, or there may be widespread selective neuronal loss or tissue infarction with more apparent and disabling deficits. Based on the notion that neural function is essential for acceptable survival from critical illness, it is crucial for perioperative management to include considerations of neural viability and the impact and interactions of the primary diseases and therapeutics on the nervous system.
There are numerous perioperative scenarios wherein a patient may be at risk for neurologic damage. These scenarios often involve ischemia, trauma, or neuroexcitation. Each of these, as they progressively worsen, involve a period of decreased cerebral perfusion pressure (CPP), either regionally or globally, the latter of which is usually associated with elevated intracranial pressure. The eventual result is a compromise in global or regional cerebral blood flow (rCBF) sufficient to produce permanent neuronal loss, infarction, and possibly brain death. A variety of biochemical pathways play a major role in this potential damage. This chapter reviews the important pathophysiologic factors and intracranial pressure (ICP) considerations and neuroprotective therapeutic options critical to contemporary perioperative care of the surgical patient at risk for central nervous system (CNS) injury.
Stroke is the third leading cause of death in the United States. For every patient who dies of a stroke, there are about 13 survivors who carry on with the effects of their loss of neural tissue.1 The 2-year incidence of stroke is 10 per 1000 people and the incidence due to atherothrombotic brain infarction is 4.4 per 1000.1
Strokes are either ischemic or hemorrhagic. Hemorrhagic strokes are caused by subarachnoid hemorrhage (SAH), intraparencyhymal (intracerebral) hemorrhage, or subdural/epidural hemorrhage. Eighty-four percent of strokes are ischemic and 16% are hemorrhagic (6% SAH; 10% intracerebral hemorrhage, ICH). Ischemic strokes are caused by embolism, thrombosis, or hemodynamic factors such as anemia or hypotension in the setting of proximal stenosis or brain edema. Atrial fibrillation is a major risk factor for embolic ischemic stroke, comprising about 18% of first ...