الفهرس 
Mechanisms of Neurological Insults In Pediatrics With Heart DiseaseOnly 14 pages are availabe for public view
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Abstract
Because of advances in surgical and cardiopulmonary bypass techniques, it is now possible to definitively repair the vast majority of congenital heart disease in infancy or childhood. Although the majority of survivors do not have obvious cerebral squeals, there is increasing disquiet about the high incidence of acute neurological events in the immediate postoperative period, as well as the evidence at long-term follow-up that there are subtle cognitive and motor deficits in many.
Several etiologic factors have been proposed as a cause for such neurological complications. These factors can be confined to preoperative period or extend to intraoperative and postoperative periods. Preoperative mechanisms of neurological dysfunction may be related to fundamental developmental disturbances (chromosomal and dysgenetic) to acquired injury sustained during periods of preoperative cardiorespiratory instability including embolic events, hypoxic insult, low cardiac output, systemic inflammatory response, and altered cerebral blood flow (CBF) and metabolism. Cerebrovascular insults are the predominant form of acquired brain injury in the preoperative period of children with unstable congenital heart disease (CHD) which can be induced by many mechanisms the most important of which is hypoxic ischemic reperfusion (HI/R) injury.
Postoperative, the combination of inotropic dysfunction and arrhythmias (decreasing cardiac output) and transient ”post-pump” pulmonary hypertension (increasing central venous pressure) may be the main mechanisms of injury in this vulnerable period.
Working against prevention of neurological injuries can, also, be differentiated into preoperative, intraoperative and postoperative measures.
Preoperative prevention started from recognition of the population at risk by preoperative evaluation with a careful history and physical examination, laboratory evaluation and necessary investigations.
During pediatric cardiac surgery, cerebral blood flow (CBF) and metabolism can also be affected by factors including arterial PCO2, temperature, anesthesia depth, and perfusion flow rate during cardiopulmonary bypass. In this period special attention must be paid to avoidance of hypoxia, avoidance of thromboembolic complications, use of anaesthetic agents with documented neuroprotecting effects, use of appropriate acid base management strategy during periods of hypothermia and utilizing new therapeutic options for neuroprotection such as remote ischemic preconditioning and the use of erythropoietin. In the same way, utilizing documented protective strategies during (DHCA) and cardiopulmonary bypass (CPB) can minimize risks of such techniques.
Postoperatively, modifiable factors for prevention of neurological injuries include early detection and management of postoperative hyperthermia, clinical and subclinical seizures and low cardiac output syndrome.
The heightened attention toward brain functioning and neurodevelopment has generated increased utility of neurologic monitors that are used for detection of cerebral hypoxia, perfusion abnormalities, and electrophysiological derangements. Numerous intraoperative techniques have been used for monitoring the brain to prevent secondary brain injury due to hypoxia, ischemia, emboli, and electrophysiological derangements. These have primarily included the following modalities in isolation or combination: Near infrared spectroscopy (NIRS) to provide a measure of venous-weighted, tissue oxyhemoglobin saturation; transcranial Doppler to measure arterial flow and resistance; and electroencephalography (EEG) to assess perfusion-related changes in cortical activity. These modalities, in conjunction with conventional physiologic intensive care monitoring, could enhance the ability to prevent injury that results from hypoxia, ischemia, emboli, hypocarbia, hypotension and hyperthermia.