Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
CHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ation, and intracranial pressure. Slowly growing masses are frequently asymptomatic for long periods (despite relatively large size), whereas rapidly growing ones may present when the mass remains relatively small.o Computed tomography and magnetic resonance imaging scans should be reviewed for evid Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ence of brain edema, midline shift greater than 0.5 cm, or ventricular displacement or compression.o Operations in the posterior fossa can injure vitaEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
l circulatory and respirator}' brainstem centers, as well as cranial nerves or their nuclei.o Venous air embolism can occur when the pressure within aCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2o Optimal recovery of air following venous air embolism is provided by a mukiorificed catheter positioned at the junction between the right atrium and the superior vena cava. Confirmation of correct catheter positioning can be accomplished by intravascular electrocardiography, radiography, or transe Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2sophageal echocardiography.o In a patient with head trauma, correction of hypotension and control of any bleeding take precedence over radiographic stEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
udies and definitive neurosurgical treatment because systolic arterial blood pressures of less than 80 mm Hg predict a poor outcome.o Sudden, massive CHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2.comAnesthetic techniques must be modified in the presence of intracranial hypertension and marginal cerebral perfusion. In addition, many neurosurgical procedures require patient positions (eg, sitting, prone) that further complicate management. This chapter applies the principles developed in Chap Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ter 26 to the anesthetic care of neurosurgical patients.Intracranial HypertensionIntracranial hypertension is defined as a sustained increase in intraEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
cranial pressure (ICP) above 15 mm Hg. Intracranial hypertension may result from an expanding tissue or fluid mass, a depressed skull fracture if it cCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2g brain edema (see next section). Multiple factors may be present. For example, tumors in the posterior fossa usually not only are associated with some degree of brain edema and mass effect, but also readily obstruct CSF outflow by compressing the fourth ventricle (obstructive hydrocephalus).Althoug Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2h many patients with increased ICP are initially asymptomatic, they typically develop characteristic symptoms and signs, including headache, nausea, vEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
omiting, papilledema, focal neurological deficits, and altered consciousness. When ICP exceeds 30 mm Hg, cerebral blood flow (CBF) progressively decreCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2his cycle continues until the patient dies of progressive neurological damage or catastrophic herniation. Periodic increases in arterial blood pressure with reflex slowing of the heart rate (Cushing response) can be correlated with abrupt increases in ICP (plateau waves) lasting 1 to 15 min. This ph Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2enomenon is the result of autoregulatory mechanisms periodically decreasing cerebral vascular resistance and increasing arterial blood pressure in resEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
ponse to cerebral ischemia. Eventually, severe ischemia and acidosis completely abolish autoregulation (vasomotor paralysis).CEREBRAL EDEMAAn increaseCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ntry of plasma-like fluid into the brain. Increases in blood pressure enhance the formation of this type of edema. Common causes of vasogenicdownloaded from www.medicalbr.comedema include mechanical trauma, high altitudes, inflammatory lesions, brain tumors, hypertension, and infarction. Cerebral ed Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ema following metabolic insults (cytotoxic edema), such as hypoxemia or ischemia, results from failure of brain cells to actively extrude sodium, causEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
ing progressive cellular swelling. Interstitial cerebral edema is the result of obstructive hydrocephalus and entry of CSF into brain interstitium. CeCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2Treatment of intracranial hypertension, cerebral edema, or both, is ideally directed at the underlying cause. Metabolic disturbances are corrected, and operative intervention is undertaken whenever appropriate. Vasogenic edema— particularly that associated with tumors—often responds to corticosteroi Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ds (dexamethasone). Vasogenic edema from trauma typically does not respond to corticosteroids. Blood glucose should be monitored frequently and controEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
lled with insulin infusions (if indicated) when steroids are used. Osmotic agents are usually effective in temporarily decreasing brain edema and ICP CHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ventilation (Paco2 of 30-33 mm Hg) is often very helpful in reducing CBF, CBV, and ICP acutely, but may aggravate ischemia in patients with focal ischemia.Mannitol, in doses of 0.25 to 1 g/kg, is particularly effective in rapidly decreasing intracranial fluid volume and ICP. Its efficacy is primaril Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2y related to its effect on serum osmolality. A serum osmolality of 300 to 315 mOsm/L is generally considered desirable. Mannitol can transiently decreEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
ase blood pressure by virtue of its weak vasodilating properties, but its principal disadvantage is a transient increase in intravascular- volume, whiCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2acranial aneurysms, arteriovenous malformations (AVMs), or intracranial hemorrhage until the cranium is opened. Osmotic diuresis in such instances can expand a hematoma as the volume of the normal brain tissue around it decreases. Rapid osmotic diuresis in elderly patients can also occasionally caus Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2e a subdural hematoma due to rupture of fragile bridging veins entering the sagittal sinus. Rebound cerebral edema may-follow the use of osmotic agentEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
s.Hypertonic saline (3% NaCl) is sometimes used to reduce cerebral edema anddownloaded from www.medicalbr.comICP. Hypertonic saline should be administCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ration and osmolality should be frequently monitored. In patients with traumatic brain injury, interventions in addition to mannitol to lower intracranial pressure include head elevation. CSF drainage via ventriculostomy, moderate hypocapnia, and metabolic suppression with barbiturates. Decompressiv Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2e craniectomy has been shown to decrease mortality in patients with sustained increases in ICP (> 25 mm Hg) following traumatic brain injury.AnesthesiEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
a & Craniotomy for Patients with Mass LesionsIntracranial masses may be congenital, neoplastic (benign or malignant), infectious (abscess or cyst), orCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2ial cells (astrocytoma, oligodendroglioma, or glioblastoma), ependymal cells (ependymoma), or supporting tissues (meningioma, schwannoma, or choroidal papilloma). Childhood tumors include medulloblastoma, neuroblastoma, and astrocytoma.<0 Regardless of the cause, intracranial masses present symptoms Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2 and signs according to growth rate, location, and ICP. Slowly growing masses are frequently asymptomatic for long periods (despite relatively large sEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
ize), whereas rapidly growing ones may present when the mass remains relatively small. Common presentations include headache, seizures, a general declCHAPTERAnesthesia for NeurosurgeryKEY CONCEPTSo Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, loca Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2plegia, or aphasia, whereas symptoms typical of infratentorial masses may include cerebellar dysfunction (ataxia, nystagmus, and dysarthria) or brainstem compression (cranial nerve palsies, altered consciousness, or abnormal respiration).PREOPERATIVE MANAGEMENTThe preoperative evaluation for patient Ebook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2s undergoing craniotomy should attempt to establish the presence or □ absence of intracranial hypertension. Computed tomography (CT) and magnetic resoEbook Morgan amp; mikhail’s clinical anesthesiology (6/E): Part 2
nance imaging (MRI) scans should be reviewed for evidence of brain edema, midline shift greater than 0.5 cm, or ventricular displacement or compressioGọi ngay
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