Preoperative Evaluation in Neurosurgery DR. behdad Supratentorial Tumors
Preoperative Evaluation in Neurosurgery DR. behdad Supratentorial Tumors Craniotomies for excision or biopsy, or both, of supratentorial tumors are common neurosurgical procedures. Gliomas and meningiomas are among the most frequent tumors. Relevant preoperative considerations include the
patient's ICP status and the location and size of the tumor. Location and size give the anesthesiologist an indication of the surgical position and the potential for blood loss, and occasionally reveal a risk of air embolism. Patients with a significant tumor-related mass effect, especially if there is tumor-related edema, should receive preoperative steroids. A 48-hour course is ideal, although 24 hours is sufficient for a clinical effect to be evident. Dexamethasone is the most commonly used agent; a regimen such as 10 mg intravenously or orally
followed by 10 mg every 6 hours is typical. Because of the concern about producing CO 2 retention in a patient whose intracranial compliance is already abnormal, patients with any substantial mass effect are usually not premedicated outside of the operating room. Aneurysms and Arteriovenous Malformations Contemporary management of intracranial aneurysms calls for early intervention after SAH, ideally within 24 hours and definitely
within 48 hours. Intervention may entail either operative clipping or an endovascular approach. Early intervention was originally undertaken only in patients in the better neurologic gradesgrades I through III and perhaps IV of the World Federation of Neurosurgeons classification ( Table 63-8 ) or grades I through III of the Hunt-Hess classification ( Table 63-9 ) but more recently has been extended to patients of higher grades.
If early intervention is not feasible, and a surgical approach is intended, surgery is usually delayed for 10 to 14 days to be safely beyond the period of maximal vasospasm risk (i.e., days 4 to 10 post-SAH). Many patients scheduled for intracranial aneurysm clipping come directly from the ICU, and elements of their management in the ICU may influence their immediate preoperative status.
Fluid Management. Some patients develop the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after SAH and are appropriately managed with fluid restriction. However, hyponatremia after SAH is more likely to be the result of the cerebral salt-wasting syndrome, which probably occurs as a result of the release of a natriuretic peptide by the brain. Cerebral salt-wasting syndrome is characterized by the triad of hyponatremia, volume contraction, and high urine sodium concentrations (>50 mmol/L).
The distinction between this syndrome and SIADH is important. SIADH, which is characterized by normovolemia or mild hypervolemia, is treated by volume restriction. Cerebral salt wasting is associated with a contracted intravascular volume. Fluid restriction and further volume contraction may be especially deleterious in a patient after SAH and should be avoided. Although the clinical distinction between these two causes of hyponatremia (SIADH and cerebral salt-wasting syndrome) may be difficult, management of both is simple:
administration of isotonic fluids using intravascular normovolemia as the end point. Vasospasm The anesthesiologist should determine whether vasospasm has occurred, and what, if any, therapies for it have been undertaken. Vasospasm is thought to be caused by the breakdown products of hemoglobin from the blood that has accumulated after SAH. A specific mechanism/mediator has not been identified, but the current focus is on endothelin. A trial of
the endothelin A receptor antagonist clazosentan indicated effective reversal of established vasospasm and a substantial reduction in the incidence of new infarctions , and a preliminary report of drug-related reductions in vasospasmrelated hypoperfusion in those patients has appeared. When there is a clinical suspicion of vasospasm (typically because of a change in sensorium or new neurologic deficit), surgery is deferred, and TCD, angiography, or other imaging is performed. Confirmed vasospasm is commonly treated with the triple H therapy (hypervolemia,
hemodilution, and hypertension ) and sometimes by balloon angioplasty or intra-arterial vasodilators. For patients proceeding to surgery, CPP should be maintained intraoperatively in a high-normal range. Despite the former popularity of induced hypotension, the potential for induced hypotension to cause or aggravate cerebral ischemia in a patient with some degree of vasospasm is now recognized. This concern extends even to a patient classified as
World Federation of Neurosurgeons grade I who may have regions of cerebral ischemia that are subclinical when the patient is normotensive. In the ICU, the regimens employed to treat vasospasm usually involve some combination of hypervolemia, hemodilution, and hypertension. Phenylephrine and dopamine are the most commonly employed pressors; the specific pressor choice should be governed primarily by systemic cardiovascular considerations.
The end point for pressor administration varies. Most commonly, the objective is an increase in MAP of approximately 20 to 30 mm Hg above baseline systolic pressure. It has been reported, however, that augmentation of cardiac output with dobutamine, without simultaneous MAP increase, augments CBF in vasospastic territories. Some authors believe that the hematocrit should be reduced to the low 30s. Commonly, hematocrit reduction occurs
secondarily as a result of attempts to produce hypervolemia (usually with colloid solutions) as a part of the effort to increase blood pressure. Calcium Channel Blockers. Calcium channel blockers are now an established part of the management of SAH. Administration of nimodipine has been shown to decrease the incidence of morbidity from cerebral ischemia occurring after SAH.
These studies failed to show any reduction in the incidence of vasospasm, however, as detected by angiography. The beneficial effect of these agents may be the result of effects on neurons, rather than vascular smooth muscle. Patients coming to the operating room after SAH should be receiving nimodipine. Nimodipine must be administered orally; nicardipine has been evaluated as an intravenous alternative. The
multicenter nicardipine trial revealed a reduced incidence of symptomatic vasospasm, but no improvement in outcome. Magnesium, Statins, and Endothelin Antagonists The endothelin antagonist clazosentan was mentioned earlier in this section. A randomized, blinded, placebo-controlled trial reported fewer new ischemic deficits and improved outcome among patients who received magnesium sulfate starting within 4 days of SAH.
Two trials have examined the post-SAH administration of statins. Together, these trials showed reductions in vasospasm, delayed ischemic deficits, and improvement in outcome. Although some centers have already implemented some of these therapies as part of the local routine, widespread adoption is not likely until the completion of larger trials that confirm these initial results. Antifibrinolytics Antifibrinolytics have been administered in an attempt to reduce the incidence of rebleeding.
Meta-analysis suggests, however, that although they accomplish the latter, they do so at the cost of an increased incidence of ischemic symptoms and hydrocephalus with the result being no net improvement in outcome. Subarachnoid HemorrhageAssociated Myocardial Dysfunction SAH can result in a reversible myocardial injury. The severity of the dysfunction correlates best with the severity of the neurologic injury, and occasionally is
sufficient to require pressor support. The mechanism is uncertain, but it is thought to be catecholamine mediated. Troponin elevation occurs commonly, although typically reaching levels less than the diagnostic threshold for myocardial infarction. Peak troponin levels correlate with the severity of neurologic injury and echocardiographic myocardial dysfunction. ECG abnormalities are common after SAH. In addition to the classic canyon T waves ( Fig. 63-14 ), nonspecific T-wave changes, Q-T prolongation, ST-segment depression, and U waves have been
described. There is typically no relationship between the ECG changes and echocardiographic myocardial dysfunction. ECG abnormalities do not herald evolving or impending cardiac disease. When ECG patterns other than those that are typical of myocardial ischemia are observed, no specific interventions or modifications of patient management are warranted, other than attention to the possibility of dysrhythmias. In particular, an increased Q-T interval (>550 msec) occurs frequently after SAH, especially in patients with more severe SAH, and has been associated with an increased incidence of malignant ventricular rhythms, including torsades de pointes.
Head Injury Intubating a Head-Injured Patient The anesthesiologist's first encounter with a patient who has sustained a traumatic brain injury (TBI) may come as a result of a request for assistance with airway management. Patients with GCS scores of 7 or 8 or less require intubation and controlled ventilation for ICP or airway control or both. Patients with less severe head injuries also may require intubation because of trauma-related cardiopulmonary dysfunction or, when uncooperative, to facilitate diagnostic procedures.
In choosing the intubation technique, the anesthesiologist may encounter numerous conflicting constraints , including (1) elevated ICP, (2) a full stomach, (3) uncertain cervical spine status, (4) uncertain airway status (e.g., presence of blood, possible laryngotracheal injury, possible skull base fracture), (5) uncertain volume status,
(6) an uncooperative or combative patient, (7) hypoxemia. There is no correct way, and the best approach is determined by the relative weight of these various factors along with the degree of urgency. The anesthesiologist must not become distracted by placing an excessive initial emphasis on ICP. The anesthesiologist needs to keep sight of the ABCs of resuscitation: Securing the airway, guaranteeing gas exchange, and stabilizing the circulation are higher initial
priorities than ICP. One must not risk losing the airway or causing severe hypotension for the sake of preventing coughing on the tube or brief hypertension with intubation. Cervical Spine The possibility of causing or aggravating an injury to the cervical spine is a relevant concern. Approximately 2% of blunt trauma victims who survive to reach a hospital and 8% to 10% of TBI victims with GCS less than 8 have a fracture of the cervical spine. This incidence suggests that a hypnotic-relaxant-direct
laryngoscopy approach for all patients with a closed-head injury might convey a measurable risk of injuring the cervical cord. Nonetheless, although the literature contains contradictions, several published series have concluded that a rapid-sequence induction does not convey significant risk of neurologic injury. It is possible, however, that the incidence of intubation-related neurologic injury is underreported. An informal survey reported by Criswell and colleagues indicated that
there have been more such events than one can infer from the published literature. Nonetheless, the literature argues that we will get away with it most of the time, and most TBI patients requiring airway control are intubated using a hypnoticrelaxant-direct laryngoscopy sequence. It is our (probably minority) opinion, however, that the possibility of devastating spinal cord injury exists, probably most so with injuries in the atlanto-occipital region, which are also difficult to identify radiologically, and that the anesthesiologist should identify
circumstances in which time latitudes allow more detailed examination or radiologic evaluation. When there is any uncertainty regarding the airway or the cervical spine, direct laryngoscopy (with vigorous atlanto-occipital extension) should probably be avoided, unless the exigencies of airway control demand it (which often is the case). The nasal route can be considered if the clinical context warrants, bearing in mind that risk of infection may be increased with skull base fracture and CSF leak.
The anesthesiologist needs to use discretion (e.g., in the presence of an obvious facial smash, the nasal route should be avoided because of the possibility of entering the cranium) and be sensitive to unusual resistance in passing the endotracheal tube. When a hypnotic muscle-relaxant sequence is used, the standard approach includes the use of cricoid pressure and in-line axial stabilization. Inline traction previously was favored, but has been supplanted by stabilization because of the perceived risk of overdistraction and cord injury in
the event of gross instability. The largest of the clinical series that concluded that oral intubation with anesthesia and relaxation is reasonable used in-line stabilization with the patient's occiput held firmly on the backboard, limiting the amount of sniff that was feasible ( Fig. 63-15 ). There is no question that in-line stabilization, properly performed, makes laryngoscopy more difficult, but it decreases the amount of atlanto-occipital extension necessary to achieve visualization of the glottis. This is
probably because performing the laryngoscopy against the assistant's counter pressure results in greater compression of the soft tissue structures of the tongue and floor of the mouth. Some recommend leaving the back half of the Philadelphia collar in place during laryngoscopy (see Fig. 63-15 ) because it functions as a strut between the shoulder and the occiput limits atlanto-occipital extension. In the resuscitation situation, before initiating a hypnoticrelaxant sequence, the anesthesiologist should confirm the
availability of cricothyrotomy equipment and of someone to make immediate, skilled use of it if necessary. The recently injured brain is very intolerant of hypoxia and hypotension. The occasional failed intubation is inevitable. In the extensive experience of the Cowley Shock-Trauma Center in Baltimore, the cricothyrotomy/tracheostomy rate is 0.3%. As is the case in many other situations, the laryngeal mask may be a useful device for temporizing in the face of a failed intubation, and may provide access for intubation as
an alternative to cricothyrotomy. Although succinylcholine can cause ICP increases, these increments are small; they probably do not occur at all in patients with serious cerebral injuries.Succinylcholine should not be contraindicated in a patient with TBI. If there is an urgent need to secure the airway (to guarantee oxygenation and control PaCO2), and if succinylcholine is in other respects the appropriate drug to achieve that end, it should be used.
The situation of a patient whose cervical spine has not been cleared should arise with decreasing frequency in unconscious patients because of the proliferation of multidetector CT scanners, which allow rapid, thin-slice evaluation, with sagittal reconstruction, of the cervical spine. The combination of a three-view plain film series and CT scanning (and most of these patients require CT evaluation for other reasons) is reported by one reviewer to have a false-negative rate for serious injury of less than 0.1%. Another survey reported, however, that CT
may miss a significant number of ligamentous injuries. With respect to a conscious patient who has not yet undergone complete radiologic evaluation, several clinical surveys have confirmed that patients who are alert, nonintoxicated, and free of significant distracting injuries invariably have pain, midline tenderness, limitation of voluntary movement, or neurologic signs if they have a cervical spine fracture.
Despite the frequency with which an anesthesiologist may encounter a patient still wearing a Philadelphia collar because his or her neck has not yet been cleared, no special precautions seem warranted in an asymptomatic, alert patient. If the clinical situation or examination is suspicious for a cervical spine injury, a normal lateral x-ray (the anteroposterior and through-the-mouth odontoid views are frequently not taken during initial evaluation) cannot provide complete reassurance. The lateral view has been
reported to miss 15% to 26% of fractures. Transsphenoidal Surgery The transsphenoidal approach to the sella turcica is used for the excision of tumors that lie within the sella or that have extended to or originated in the immediate suprasellar area. The most common lesions are prolactin-secreting microadenomas and nonsecreting macroadenomas. Patients with the former are usually women who present with secondary amenorrhea.
Nonsecreting adenomas tend to manifest with mass effects (i.e., headache, visual disturbance, hypopituitarism) and are typically larger at the time of diagnosis. There are three other, less common pituitary tumors: Growth hormonesecreting lesions result in acromegaly, adrenocorticotropic hormone (ACTH) secreting tumors cause Cushing's disease, and a very rare thyroid-stimulating
hormonesecreting lesion results in hyperthyroidism. Preoperative Evaluation The important preoperative considerations relate to the patient's endocrine status. Generally, as a pituitary lesion expands and compresses the pituitary tissue, the sequence in which hormonal function is lost is first gonadotropins; second, growth hormone;
third, ACTH; and fourth and last, thyroid-stimulating hormone. The precise definition of the adrenal status of these patients is often not critical because the patients commonly receive adrenal hormone supplementation at least temporarily. Profound hypocortisolism, with associated hyponatremia, should be corrected preoperatively. It is uncommon for thyroid deficiency to occur. Hypothyroidism should be sought and corrected preoperatively, however, because hypothyroid patients have a diminished tolerance to
the cardiovascular depressant effects of anesthetic agents. Hypertension, diabetes, and central obesity are common concomitants of ACTH-secreting adenomas (Cushing's disease). Patients with advanced acromegaly can develop an enlarged tongue and a narrowed glottis, and the airway should be evaluated accordingly .
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