Best practice & research. Clinical anaesthesiology
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Best Pract Res Clin Anaesthesiol · Dec 2007
ReviewCardiovascular therapy of neurosurgical patients.
The causes of postoperative cardiovascular disturbances in neurosurgical patients include direct cardiac neurogenic effects, clinical situations where brain tissue is underperfused, and hyperdynamic states. EKG and echographic abnormalities are common in subarachnoid hemorrhage where cardiac troponin I is the most useful predictor of cardiac risk after SAH. Neurogenic pulmonary edema is short lived and often resolves with resolution of the neurologic problem. ⋯ Induced hypertension improves blood flow through vessels compromised by cerebral stenting, angioplasty, microcatheters, thrombolysis, carotid clamping, intracranial bypass and cerebral vasospasm. Hyperdynamic lesions include vascular breakthrough after elimination of cerebral arteriovenous malformations, but also emergence hypertension and hyperemia. Pharmacologic agents and adjunctive measures are effective in controlling both the systemic and the cerebral circulation.
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Best Pract Res Clin Anaesthesiol · Dec 2007
ReviewPostoperative management of adult central neurosurgical patients: systemic and neuro-monitoring.
Postoperative neurosurgical patients are at risk of developing complications. Systemic and neuro-monitoring are used to identify patients who deteriorate in order to treat the underlying cause and minimize the impact on outcome. Hypotension and hypoxia are likely to be the most frequent insults and can be detected easily with blood pressure monitoring and pulse oximetry. ⋯ Intracranial pressure monitoring, cerebral blood flow monitoring, electroencephalography, and brain imaging are often used postoperatively. Despite the numerous publications on this topic only few studies address the impact of postoperative monitoring on outcome. Accordingly, in most patients the decision on which monitors are to be used must be based on the patient's presentation and clinical judgment.
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Best Pract Res Clin Anaesthesiol · Dec 2007
ReviewPrevention and treatment of intracranial hypertension.
Intracranial pressure (ICP) is the pressure exerted by cranial contents on the dural envelope. It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF). Normal intracranial pressure is somewhere below 10 mmHg; it may increase as a result of traumatic brain injury, stroke, neoplasm, Reye's syndrome, hepatic coma, or other pathologies. ⋯ When intracranial hypertension persists, second-tier treatments may be indicated. These include 'forced hyperventilation' (paCO2 < 25 mmHg), barbiturate coma or experimental protocols such as tris buffer, indomethacin or induced hypothermia. The last resort is emergent bilateral decompressive craniectomy; once taken into consideration, it should be performed without undue delay.
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Osmolality is the primary determinant of water movement across the intact blood-brain barrier (BBB), and we can predict that reducing serum osmolality would increase cerebral oedema and intracranial pressure. Brain injury affects the integrity of the BBB to varying degrees. With a complete breakdown of the BBB, there will be no osmotic/oncotic gradient, and water accumulates (brain oedema) consequentially to the pathological process. ⋯ In patients with brain pathology, volume depletion and/or hypotension greatly increase morbidity and mortality. In addition to management of intravascular volume, fluid therapy must often be modified for water and electrolyte (mainly sodium) disturbances. These are common in patients with neurological disease and need to be adequately treated.