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| Head Injury | Supratentorial Tumors | Posterior Fossa Surgery| Intracranial Aneurysms |Ischemic Cerebrovascular Diseases |Neuroendocrine Tumors |Epilepsy-Awake Craniotomy-Intraoperative MRI |Spinal Cord Injury and Procedures |Pediatric Neuroanesthesia |Neurosurgery in the Pregnant Patient |Management of Therapeutic Interventional Neuroradiology |Management in Diagnostic Neuroradiology |



I. Anesthesia for supratentorial tumors

Background. Approximately 35,000 new brain tumors are diagnosed per year in the United States. In adults, 85% are primary (9% of all primary tumors); 60% are primary and supratentorial (gliomas approximately 35%; meningiomas approximately 15%; pituitary adenomas approximately 8%). Approximately 12% of intracranial tumors are metastases. Their incidence increases with age, and approximately one-sixth of patients with cancer develop a brain metastasis which is symptomatic in most cases and often the controlling variable for survival.
General considerations
Concerns and problems
1. Patient symptoms result from local mass effect and generalized increased intracranial pressure (ICP) effects.
2. Main surgical concern is brain exposure without retraction or mobilization damage.
3. Main anesthetic concern is the avoidance of secondary brain damage (Table-1). Therefore, understanding the following is vital: pathophysiology of ICP and cerebral perfusion; effects of anesthesia on ICP, cerebral perfusion, and metabolism; and therapeutic options for decreasing ICP, brain bulk, and tension perioperatively.
4. Specific problems are massive intraoperative hemorrhage, seizures, air embolism (head-elevated/sitting position or if venous sinuses are traversed), monitoring brain function and environment, and rapid versus prolonged anesthetic emergence. A concurrence of intra- and extracranial pathologies might also occur (e.g., cardiovascular or pulmonary disease; paraneoplastic phenomena with metastases; chemotherapy/radiotherapy effects).
Pathophysiology of rising ICP. The usual intracranial space-occupying components - brain tissue, intravascular blood, cerebrospinal fluid (CSF) are contained in an unyielding skull. Any volume increase (tumor) must be compensated by parallel volume reduction of one or more of these components, mainly CSF or blood (the brain is largely incompressible). The ability to compensate for the presence of a mass and maintain homeostasis depends on the volume of the mass and its rate of growth (the ICP volume curve shifts to the left for rapidly expanding masses). Homeostatic mechanisms: early (limited capacity) intracranial to extracranial blood shift; late (larger capacity) CSF displacement (ineffective if CSF flow is obstructed); exhaustion with rapid ICP rise and impaired cerebral circulation leading to brain herniation (end stage of compensation).

Table-1. Secondary insults to the already injured brain

Intracranial Systemic
Increased intracranial pressure Hypercapnia/hypoxemia
Epilepsy Hypo-/hypertension
Vasospasm Hypo-/hyperglycemia
Herniation: falx, tentorium, foramen magnum, craniotomy Low cardiac output
Midline shift: tearing of cerebral vessels Hypo-osmolality
 Shivering/pyrexia

Intracerebral perfusion and cerebral blood flow (CBF)
Regulation of CBF is through gradients in wall pressure of cerebral arterioles (result of cerebral perfusion pressure [CPP]) and partial pressure of arterial carbon dioxide (Paco2) concentration (result of ventilation) (Figure -1).
Autoregulation of CBF keeps the CBF constant despite changing CPP via alterations in cerebral vasomotor tone (i.e., cerebrovascular resistance [CVR]). Characteristics are: dominant to ICP homeostasis; normally functional for CPP of 50 to 150 mm Hg; impaired/affected by intracranial (e.g., blood in CSF, trauma, tumors) and extracranial (e.g., chronic systemic hypertension) pathologies and anesthetic drugs. Autoregulation is not immediate in that a sudden increase in blood pressure gives rise to a temporary increase in CBF.
Formulas. CBF = CPP/CVR, CPP = MAP-ICP. Note that normally, ICP CVP (central venous pressure).
Inadequate perfusion. Depends on both the reduction of CBF and its duration when CBF falls under 20 mL/100 g/minute. Inadequate perfusion is also linked to CPP <50 mm Hg with intact autoregulation. Action is to restore CPP and CBF ( MAP [mean arterial pressure],  ICP,  cardiac output); reduce cerebral metabolic demand (deepen anesthesia and hypothermia and treat epilepsy).

Figure-1. Pressure-cerebral blood flow relationships.

(A) Cerebral blood flow (CBF) autoregulation. CBF is maintained at 50 mL/100 g/minute for mean arterial pressure (MAP)/cerebral perfusion pressure = 50 to 150 mm Hg. (B) Linear relationship between partial pressure of arterial carbon dioxide (Paco2) and CBF for Paco2 = 20 to 80 mm Hg. (C) Pao2 and CBF. (D) Intracranial pressure (ICP) and CBF.

Vasodilatory and vasoconstrictive cascades. If autoregulation is intact:
MAP cerebral arteriolar vessel dilatation →↑CBV (cerebral blood volume) →↑ ICP →↓ CPP (vicious circle!). Conversely, MAP→↑ CPP →↓ ICP via cerebral vasoconstriction (positive circle).
Paco2. Hypocarbia results in vasoconstriction, reducing CBF, CBV, and therefore ICP, making hyperventilation a favorite tool for the acute control of intracerebral hyperemia and elevated ICP. However, the relative reduction of CBF is larger than the reduction of cerebral metabolic rate for oxygen consumption (CMRo2), inducing a risk of cerebral ischemia.
Anesthesia and intracranial pressure, perfusion, and metabolism. Anesthesia affects the intracranial environment through drug and nondrug effects, all sensitive to the intra- and extracranial state (e.g., cerebral compliance, intracranial pathology, volemic state).
Intravenous anesthetics (barbiturates, propofol, etomidate) reduce CMRo2 dose dependently by depressing electrical and neurotransmitter synthesis (not basal metabolic) activity of the neurons with a ceiling effect at electroencephalographic (EEG) burst suppression. They are cerebral vasoconstrictors →↓ CBF, CBV, and ICP. Cerebral flow-metabolism coupling, autoregulation, and Paco2 vessel reactivity remain intact. In contrast to volatile anesthetics, propofol suppresses the cerebrostimulatory effects of nitrous oxide.
Volatile anesthetics (e.g., isoflurane, sevoflurane, desflurane) decrease CMRo2. They are all cerebral vasodilators (desflurane > isoflurane > sevoflurane). For <1 to 1.5 minimum alveolar concentration (MAC) and in the normal brain (flow/metabolism coupling intact), CBF decreases compared to the awake state and autoregulation is maintained. Above 1 to 1.5 MAC, there is a dose-related increase in CBF with impaired autoregulation (Figures -2 and -3). Maintained Paco2 reactivity allows hypo-capnic control of this type of vasodilatation. A situation to avoid is brain pathology + high volatile MAC impaired/abolished carbon dioxide (CO2) reactivity.
Nitrous oxide (N2O) is cerebrostimulatory →↑ CMRo2, CBF, and sometimes ICP, particularly with volatile anesthesia. For the normal brain, this cerebral vasodilatation can be controlled by hypocapnia or intravenous anesthetics (volatiles - no attenuating effect). CMRo2 and CBF are higher for 1 MAC anesthesia with nitrous oxide-volatile versus volatile only.

 

Figure-2. Cerebral blood flow (CBF)-cerebral metabolic rate for oxygen consumption (CMRo2) coupling during increasing dose of an intravenous anesthetic. A normal CMRo2 of 4 mL/100 g/minute is coupled to a CBF of 50 mL/100 g/minute. EEG, electroencephalogram.

 

Figure-3. Cerebral blood flow (CBF)-cerebral metabolic rate for oxygen consumption (CMRo2)-cerebral blood volume (CBV) during increasing doses of an intravenous (propofol) and volatile anesthetics. Changes are noted as a percentage value from the awake state. Despite similar changes in CMRo2, changes in CBF and CBV are markedly different among intravenous and volatile agents and among sevoflurane, isoflurane, and desflurane above 1.5 minimum alveolar concentration (MAC). EC50, median effective concentration.

Opioids have been associated with short-term ICP (large doses). However, opioids are only modest direct cerebral vasodilators; therefore, reflex cerebral vasodilatation after MAP/CPP probably causes the transient ICP. Opioids modestly CMRo2 without affecting flow-metabolism coupling, autoregulation, or vessel CO2 sensitivity. Remifentanil is particularly suitable for rapid emergence.

 

Table -2. Intracranial hypertension and brain bulging: prevention and treatment

Prevention Treatment
Preoperative: adequate anxiolysis and analgesia Cerebrospinal fluid drainage (lumbar catheter or ventricle)
Preinduction: hyperventilate on demand, head-up position, head straight, no jugular vein compression Osmotic diuretics
Avoid overhydration Hyperventilation
Osmotic diuretics (mannitol, hypertonic saline); steroids for tumor Augment depth of anesthesia using intravenous anesthetics (propofol, thiopental, etomidate)
Loop diuretics (furosemide) Muscle relaxation
Optimize hemodynamics: MAP, central venous pressure, pulmonary capillary wedge pressure, heart rate; use beta-blockers, clonidine, or lidocaine if necessary Improve cerebral venous drainage: head up, no positive end-expiratory pressure, reduce inspiratory time
Ventilation: Pao2 >100; Paco2 ~ 35 mm Hg, low intrathoracic pressure Mild controlled hypertension if cerebral autoregulation intact (MAP ~ 100 mm Hg)
Use of intravenous anesthetics for induction and maintenance  

MAP, mean arterial pressure.

Neuromuscular blocking agents (NMB). The effect of succinylcholine on ICP is controversial, but fasciculations may increase ICP. Succinylcholine may be used for difficult intubation or rapid sequence induction in patients with brain injuries. Other NMB have no effect on ICP.
Other drugs. Avoid vasodilating antihypertensive agents (nitroglycerin, nitroprusside, hydralazine) cerebral vasodilatation. Take into account pharmacologic interactions, particularly with antiepileptic agents.
Reducing ICP, brain bulk, and tension (Table-2). The effectiveness of these techniques depends on intact intracerebral homeostatic mechanisms and/or structures.
Intravenous anesthetics →↓ CMRo2, CBF →↓ CBV, ICP →↓ brain bulk. Cerebral vasoconstriction depends on intact CMRo2-CBF coupling (Figure-2) and is dose related up to neuronal electrical silence (EEG burst suppression). Like autoregulation, CMRo2-CBF coupling is impaired by brain contusion and other intracerebral pathologies.
Hyperventilation - hypocarbia - cerebral vasoconstriction (acute effect lasting for a maximum of 24 hours). For intact autoregulation, CBF is linearly related to Paco2 from 20 to 70 mm Hg (3% to 4% change/mm Hg Paco2). Factors impairing CO2 reactivity are head injury, other intracerebral pathology, high-inspired volatile anesthetic concentrations, N2O (especially with already dilated vessels). Typical target: Paco2 of 30 to 35 mm Hg; based on arterial blood gas analysis rather than end-tidal CO2 (ETco2: possibility of large arterio-alveolar CO2 gradients in neurosurgical patients). Side effects of hyperventilation include linear reduction in coronary artery flow and cardiac venous return as well as hypokalemia.
Diuretics. Osmotic diuretics (e.g., mannitol, hypertonic saline)  acutely  blood osmolality →↓ brain water content (mainly healthy brain tissue with intact blood-brain barrier) →↓ brain bulk, ICP, compliance. Also: better blood rheology ( endothelial edema; erythrocyte edema →↓ erythrocyte deformability). Typical regimen: mannitol, 0.5 to 1 g/kg intravenously (i.v.), (split between rapid precraniotomy dose and slower infusion until brain dissection is complete). ICP effect: prompt, lasts for 2 to 3 hours, removes approximately 90 mL brain water at peak effect. Problems: hypernatremia, acute hypervolemia. Compensate urinary losses due to mannitol with isotonic saline.
CSF drainage. Can be accomplished either by direct puncture of the lateral ventricle by the surgeon or lumbar spinal catheter by the anesthesiologist preoperatively; this is effective only without caudal block to CSF outflow. Acute brain herniation might occur; therefore, lumbar CSF drainage should be used cautiously and only when the dura is open and the patient is at least mildly hyperventilated. Draining 10 to 20 mL CSF effectively reduces brain tension; up to 50 mL can be drained if necessary.
  Use the vasoconstrictive cascade. Mild MAP →↑ CPP →↓ CBV.
Avoid other factors causing cerebral vasodilatation: hypovolemia, hypoxia, patient positioning (head-down, extreme turning of the neck →↓ cerebral venous drainage, rotation of the head on one side and jugular venous thrombosis on the other side major brain swelling), volatile anesthetics >1 to 1.5 MAC.

 

Table -3. Preoperative neurologic evaluation

History
Seizures, level of consciousness
ICP: headache, nausea, vomiting, blurred vision
Focal neurology: hemiparesis, sensory deficits, etc.
Hydration: duration of bed rest, fluid intake, diuretics, syndrome of inappropriate secretion of antidiuretic hormone
Medication: steroids, antiepileptic drugs
Associated illnesses, trauma
Physical Examination
Mental status, level of consciousness
Papilledema (CP), Cushing response (hypertension, bradycardia)
Pupil size, speech deficit, Glasgow Coma Scale score, focal signs
Investigations (Computed Tomographic/Magnetic Resonance Imaging Scans)
Size and location of the tumor: e.g., silent or eloquent area?, near major vessel?
Intracranial mass effects: midline shift, ā†“ ventricle size, temporal lobe herniation, cerebrospinal fluid space surrounding the brain stem, edema, hydrocephalus
ICP, intracranial pressure.

 General anesthetic management
Preoperative assessment. Anesthetic strategy is based on the patient's neurologic and general state and the planned surgery; both should be discussed with the neurosurgeon.
Neurologic state of patient. Assess (Table-3): ICP increases and intracranial compliance (computed tomographic [CT] scan or magnetic resonance imaging [MRI]); size of ICP/CBF homeostatic reserve (margin before brain ischemia/neurologic impairment); autoregulation impairment (diffuse brain pathology, coma); presence of neurologic damage (permanent/reversible); present drug therapy (especially antiepileptic drugs and their side effects); neurodiagnostic studies.
General state of patient. Cardiovascular system: brain perfusion/oxygenation depends on it; acute intracranial pathologies affect cardiac and lung function (worst situation: neurogenic pulmonary edema); supratentorial surgery (meningioma, metastasis) may result in significant bleeding (hypovolemia, hypotension →↓ CPP/CBF and ICP). Respiratory system: hyperventilation to ICP, CBF, CBV, and brain tension depend on it; 40% of brain metastases are from lung (primary tumor, its chemotherapy/radiotherapy). The head-up/sitting position affects the cardiac and respiratory systems. Other systems: paraneoplastic or chemotherapy/radiotherapy-associated syndromes (hematology, coagulation); renal system, diuretics, and decreased fluid intake; altered endocrine system (intracranial processes; pituitary adenoma or its therapy; steroids); gastrointestinal tract (steroids and mucosa; motility effects of ICP). Coagulation profile must be normal: stop aspirin at least 7 days and clopidogrel 10 days before surgery.
Biology. Coagulation, hemoglobin, platelet count, potassium, sodium.
Planned operative intervention. Clarify surgical approach (tumor size/position, proximal structures and likelihood of vascular involvement, radical excision), resultant patient positioning (supine, prone, sitting, lateral), and tumor type.
(1) Meningiomas. The combination of large size, difficult location, and radical excision (total resection is virtually curative) makes for long, technically demanding operations, often with significant bleeding (surrounding structures, meningioma vascularity). Anesthetic priority: maximal brain tension reduction to facilitate surgical access; compensate blood losses with isotonic saline or colloids (hematocrit >28%).
(2) Gliomas. Often simple debulking with easy surgical access and little risk of bleeding. Risk of postoperative intracranial hypertension due to edema.
(3) Others. Third ventricle colloid cysts, which may result in obstructive hydrocephalus and therefore ICP at induction. Colloid cysts, basal cistern epidermoids, and transcranially resected pituitary tumors need maximal brain relaxation for exposure at skull base.
(4) Pituitary adenoma by transsphenoidal resection. Essentially an extracranial operation in a head-up position.
Determination of anesthetic strategy. Points to be addressed:
(1) Vascular access. Consider the risk of bleeding or venous air embolism, hemodynamic and metabolic monitoring, and infusion needs for vasoactive and other substances.
(2) Fluid therapy. Target normovolemia/normotension; avoid hyposmolar (Ringer's lactate) and glucose-containing solutions (hyperglycemia →↑ ischemic brain injury).
(3) Anesthetic regimen. Simple¯ procedures (low risk of ICP problems or ischemia, little need for brain relaxation): volatile-based technique okay (<1.5 MAC). High-risk procedures (anticipated ICP problems, significant risk of intraoperative cerebral ischemia, need for deep brain relaxation): use total intravenous anesthesia with propofol.
(4) Extracranial monitoring such as cardiovascular or renal, venous air embolism.
(5) Intracranial monitoring. General or local environment versus specific functions: metabolic (jugular venous bulb oxygen saturation [Sjo2], brain tissue oxygen partial pressure [btPo2)], neurophysiologic (EEG/evoked potential), functional (transcranial Doppler).
 Preoperative preparation
Premedication. Risk assessment: sedation hypercapnia, hypoxemia, upper airway obstruction →↑ ICP; stress →↑ CPP/CBF/CMRo2,ICP and the development of vasogenic edema with impaired autoregulation. Best: titrated intravenous analgesia/sedation (e.g., midazolam, 0.5 to 2 mg, ± fentanyl, 25 to 100 mcg, or sufentanil, 5 to 20 mcg) under direct anesthesiologic supervision for vascular access placement, and so on. Patients without signs of ICP can benefit from oral premedication with a small benzodiazepine dose (e.g., 5 mg midazolam). Continue steroids (supplement with pituitary axis suppression) and other regular medication (anticonvulsants, antihypertensives, other cardiac drugs). Consider starting anticonvulsant therapy if not already initiated (e.g., loading dose of phenytoin, 15 mg/kg, or fosphenytoin, 20 mg/kg, over 30 minutes) and H2 blockers (for gastric emptying, acid secretion with steroids, ICP).
Vascular access. Two large-bore peripheral intravenous catheters are typical for full craniotomy.
(1) Central venous access. Recommended for significant risk of venous air embolism (radiographically control catheter tip position at transition of vena cava/right atrium) or bleeding, long-lasting procedures (>6 hours), major cardiovascular compromise (if severe, consider pulmonary artery catheter or transesophageal echocardiography), and continuous infusion of vasoactive drugs. Jugular cannulation technique (conventional or retrograde) must be meticulous, impairment of cerebral venous drainage must be avoided (hematoma, head-down position →↑ICP!).
(2) Arterial cannulation. Obligatory for full craniotomy due to the need for close monitoring and control of CPP (obtain by transducing arterial pressure at mid-ear/circle of Willis level, CPP = MAP - ICP); frequent determination of arterial Paco2 (hyperventilation) and plasma glucose, potassium, and so on, values. Note that ETco2 monitoring is no substitute for Paco2 measurement (correlates poorly, especially with ventilation-perfusion mismatch).
(3) Jugular venous bulb monitoring (JVBM). Permits monitoring (intermittent or continuous with fiberoptic oximetry) of cerebral oxygen extraction (Sao2-Sjvo2), allowing conclusions about the adequacy of global cerebral perfusion (assuming CMRo2 is constant). But frequently difficult to interpret during surgery due to the rotation of the head. Technique: retrograde cannulation of jugular vein; catheter tip should be radiographically verified to be in the jugular venous bulb.
Monitoring
(1) Cardiovascular. Electrocardiographic (myocardial ischemia, arrhythmias); arterial and CVP, pulse oximetry. Others: ETco2 (trend monitor for Paco2, detection of venous air embolism); temperature via esophageal thermistor (modest, passive hypothermia, [approximately 35°C] might confer significant neuronal protection during focal ischemia at small systemic cardiorespiratory risk); urinary catheter.
(2) Air embolism. Sensitively detected by precordial Doppler, end-tidal nitrogen or CO2 (alternative: transesophageal echocardiography).
(3) Neuromuscular block. Do not monitor on hemiplegic extremities ( acetylcholine receptor density of lower motor neuron units innervated by dysfunctional or nonfunctional upper motor neurons resistance to nondepolarizing myorelaxants effective overdose for normal neuromuscular units). Contralateral hemiparesis to a supratentorial tumor is not associated with hyperkalemia as in paraplegic or patients with burns; succinylcholine is therefore not contraindicated.
(4) Blood chemistry. Monitor glucose regularly; hyperglycemia →↑ neuronal damage during ischemia. During general anesthesia, steroids →↑ blood glucose levels; brain retraction focal cerebral ischemia. Others: K, hematocrit, coagulation.
(5) Intracranial environment, cerebral function. JVBM; EEG monitoring (information on CMRo2, cerebral ischemia, depth of anesthesia). Others: evoked potentials (intactness of specific central nervous system [CNS] pathways); btPo2 (information on adequate oxygen supply to brain areas at risk of ischemia).
(6) ICP monitoring. Currently rare for elective neurosurgery due to improvements in perioperative ICP control but still has an important role in neurotraumatology.
Induction of anesthesia
Goals. Ventilatory control (early mild hyperventilation; avoid hypercapnia, hypoxemia); sympathetic/blood pressure control (avoid CNS arousal: adequate antinociception, anesthesia); optimal position on ICP-volume curve (avoid venous outflow obstruction).
  Typical induction scheme. Detailed in Table-4.
Myorelaxants. Modern nondepolarizing drugs have minimal effects on intracerebral hemodynamics. Interaction (doses by 50% to 60%) between pancuronium /vecuronium/ rocuronium/ cisatracurium and chronic (>7 days) phenytoin/carbamazepine treatment can occur due to increased metabolism and resistance to myorelaxants; no neuromuscular transmission monitoring on hemiplegic extremities. Note that because neurosurgical patients are susceptible to myorelaxant hangover (difficult to detect by manual relaxometry), avoid long-acting myorelaxants (e.g., pancuronium); use middle- to short-acting drugs (e.g., vecuronium, cisatracurium, mivacurium, rocuronium).

 

Table -4. Suggested anesthesia induction and maintenance scheme

Induction
Adequate preoperative anxiolysis in the anesthetic room
Electrocardiogram, capnometer, pulse oximeter, noninvasive blood pressure
Venous, arterial lines: insert under LA
Furosemide 1 mg/kg
Preoxygenation, then fentanyl, 1-2 mcg/kg, (or alfentanil, sufentanil, remifentanil)
Propofol, 1.25-2.5 mg/kg, or thiopental, 3-6 mg/kg, then nondepolarizing myorelaxant
Control ventilation (Paco2 ~ 35 mm Hg)
Intubation
Maintenance
Propofol, 50-150 mcg/kg/min, or sevoflurane, 0.5%-1.5%, or desflurane, 3%-6%
Maintain analgesia: fentanyl, 1-2 mcg/kg/h, (or alfentanil, sufentanil, remifentanil)
LA, fentanyl 2 mcg/kg (skull-pin head holder placement, skin incision)
Position: head-up, jugular veins free
Mannitol, 0.5-0.75 g/kg, insert lumbar drain
Ensure adequate volemia (NaCl 0.9% or hydroxyethyl starch 6%-not Ringer'slactate)
LA, local anesthesia.


Patient positioning. Pin holder application is a maximal nociceptive stimulus. Block by deeper analgesia (fentanyl bolus, 1 to 3 mcg/kg, sufentanil bolus, 0.2 to 0.3 mcg/kg, alfentanil, 10 to 20 mcg/kg, remifentanil, 0.25 to 1 mcg/kg) or anesthesia (e.g., propofol bolus, 0.5 mg/kg) and/or local anesthetic infiltration of the pin site. Alternative: antihypertensives (esmolol, 0.5 mg/kg, labetalol, 0.075 to 0.15 mg/kg). Remember that pin insertion can introduce venous air embolism! Avoid extreme positions; pad and/or fix regions susceptible to pressure, abrasion, or movement injury. Fix the endotracheal tube securely to avoid accidental extubation and abrasions with movement, and tape the eyes occlusively to avoid corneal damage. A mild head-up position helps venous drainage; mild knee flexion decreases back strain. Avoid severe lateral extension/flexion of head on neck (maintain more than two fingers' space between chin and nearest bone). Extreme flexion of the head may induce quadriparesis or massive swelling of the face and tongue making rapid extubation impossible. If the head is turned laterally, elevate contralateral shoulder (with a wedge or roll) to prevent brachial plexus stretch injury. Lateral/sitting/prone position: specific precautions. Verify cautiously all potential pressure points (eyes), peripheral arterial pulses, nerve compression, and ventilation.
Maintenance of anesthesia (Table-4)
Goals
(1) Controlling brain tension through control of CMRo2 and CBF. Preventing CNS arousal (depth of anesthesia, antinociception); treating consequences of CNS arousal (sympatholysis, antihypertensives); the chemical brain retractor concept¯ (Table-5).
(2) Neuroprotection. Maintenance of an optimal intracranial environment (adequate CPP, Paco2, Sao2: matching cerebral substrate demand and supply); specific neuroprotection is controversial and should not induce adverse effects or delayed recovery.
Choice of technique. Controversy: intravenous or volatile anesthesia for neurosurgery? No study to date has shown significant outcome differences for intravenous versus volatile-based neuroanesthesia. But operative conditions are worse with volatile anesthetic inspired concentration (Fi) >1.5 MAC.
(1) Volatiles. Con: CBF-CMRo2 uncoupling; CBF/ICP/brain bulk. Pro: easy, extensive, successful use; control; predictability (early awakening). Recommendation: use for simple cases (no ischemia, ICP, or brain bulk problems); early moderate hyperventilation; Fi < 1.5 MAC; avoid combination with N2O (cerebrostimulation).

 

Table -5. The chemical brain retractor concept

Mild hyperosmolalitya
Mild hyperventilation
combined with:
Adequate head-up positioning
Lumbar cerebrospinal fluid drainage
Intravenous anesthetic agent (propofol)
Mild controlled hypertensionb
Avoidance of brain retractors
Venous drainage: jugular veins free
aBefore bone flap removal, give mannitol, 0.5-0.75 g/kg, or 7.5% NaCl, 3-5 mL/kg (NaCl 0.9% = 304 mOsm/kg).
bMean arterial pressure ~ 100 mm Hg.


(2) Intravenous techniques. Con: more onerous use; prolonged/unpredictable awakening (mitigated by target-controlled infusion [TCI]; short-acting, infusion duration-insensitive drugs [e.g., propofol, remifentanil]). Pro: intact CBF-CMRo2 coupling; CBF/ICP/brain bulk; propofol blunts N2O cerebrostimulation. Recommendation: use for cases with high risk of ICP/brain bulk problems or intraoperative cerebral ischemia; use TCI and short-acting drugs.
Management of increases in ICP and brain bulk (Table-2)
Other measures. When CNS and hemodynamic arousal are evident despite adequate anesthesia/analgesia, consider sympatholysis (esmolol, 0.5 to 1 mg/kg; labetalol, 0.075 to 0.15 mg/kg; clonidine, 1 to 1.5 mcg/kg).
Antibioprophylaxis. Oxacillin or second-generation cephalosporin before skin incision.
Fluid therapy. Goals: normovolemia, normotension, normoglycemia, hematocrit approximately 30%, mild hyperosmolality (<320 mOsm/L at end of procedure). Recommendations: avoid glucose-containing solutions, Ringer's lactate (hypo-osmolar); use 0.9% sodium chloride (NaCl) or 6% hydroxyethyl starch.
Emergence from anesthesia causes respiratory, cardiovascular, metabolic/endocrine, and neurologic changes. Emergence is associated with hemodynamic arousal lasting 10 to 25 minutes, weakly correlating with rises in oxygen consumption and mediated by elevated catecholamine levels and nociceptive stimuli. Treatment: antinociception, sympatholysis. Oxygen consumption is increased (up to 5 times) by rewarming (shivering/nonshivering thermogenesis) and pain. As a result of all of these factors, 20% of elective craniotomy patients develop raised ICP in the early postoperative period. Systemic hypertension is frequent and has been associated with an increased risk of postoperative intracranial hemorrhage.
Aims of emergence. Maintain intra- or extracranial homeostasis (MAP-CPP-CBF-ICP, CMRo2, Paco2, Pao2, temperature). Avoid factors leading to intracranial bleeding (e.g., coughing, intratracheal suctioning, ventilator fight, blood pressure). The patient should be calm, cooperative, and responsive to verbal commands soon after emergence.

 
Table-6. Early vs. delayed awakening: pros and cons
Early Awakening Delayed Awakening
Pros Pros
Earlier neurologic examination and reintervention Less risk of hypoxemia and/or hypercarbia
Baseline neurology for subsequent examinations Better respiratory, hemodynamic control
Less hypertension, catecholamine burst Easier to transfer to the ICU
Performed by anesthesiologist who knows patient Stabilization in same state as during surgery
Surgery/recovery period separated, costs Better late hemostasis
Cons Cons
Increased risk of hypoxemia, hypercarbia Less neurologic monitoring
Respiratory monitoring during transfer to ICU More hypertension, catecholamine release→↑bleeding
ICU, intensive care unit.

Early versus late emergence. Ideal: rapid emergence to permit early assessment of surgical results and postoperative neurologic follow-up. However, early emergence is still not appropriate for some categories of patients.
Indications for late emergence. Obtunded consciousness or inadequate airway control preoperatively; intraoperative catastrophe; significant risk of brain edema, ICP, or deranged intracerebral hemo- or homeostasis postoperatively. Risk factors for latter: long (>6 hours) and extensive surgery (particularly with bleeding), repeat surgery, surgery involving or close to vital brain areas, and surgery associated with significant brain ischemia (e.g., long vascular clipping times, extensive retractor pressure). If delayed emergence is chosen, adequate sedation and analgesia should be ensured, preferably with short-acting drugs.

 

Table -7. Check-list before trying an early landing

Adequate preoperative state of consciousness
Cardiovascular stability, normal body temperature, and adequate oxygenation
Limited brain surgery, no major brain laceration
No extensive posterior fossa surgery involving cranial nerves IX-XII
No major arteriovenous malformation removal (avoiding malignant postoperative edema)

Preconditions for early emergence. Anesthesiologic: should be planned (Table-7); use pharmacologically adequate anesthetic technique for early awakening; pay meticulous attention to intraoperative homeostasis (oxygenation, temperature, intravascular volume, cardiovascular function, CNS metabolism); avoid trauma of mechanical brain retraction (pharmacologic ICP/brain bulk control; see Table-5). Neurosurgical: minimization of blood loss (obsessive hemostasis); minimal surgical invasiveness (microsurgery, small operative fields). Craniotomy may be painful after the operation. Postoperative analgesia should be anticipated before awakening, especially if remifentanil is used for maintenance. Under these conditions, early emergence can be associated with less hemodynamic, metabolic, and endocrine activation than for delayed emergence.
Differential diagnosis of unplanned delayed emergence. Within 10 to 20 minutes of cessation of pharmacologically adequate anesthesia with short-acting agents, the patient should be awake enough to obey simple verbal commands. If not, consider and treat or rule out nonanesthetic causes (seizure, cerebral edema, intracranial hematoma, pneumocephalus, vessel occlusion/ischemia, metabolic or electrolyte disturbances). Suspected opioid overhang (fentanyl or sufentanil): try carefully titrated antagonization with small doses of naloxone or naltrexone.
Neurologic evaluation. Perform a baseline simple examination to assess motor responses of arms and legs, size of pupils and reactivity to light, adequate understanding of simple words and verbal response, and orientation to time and space.
Specific anesthetic management
Predicted difficult airway. Avoiding hypoxia is more important than preventing ICP increases. Method of choice: fiberoptic intubation. Technique: well-prepared, informed, cooperative patient; good local anesthesia (nasopharynx, airways); supplemental judicious light sedation (bolus midazolam, 0.5 to 1 mg ± fentanyl, 25 to 50 mcg; alternatively: low-dose propofol infusion at 1 to 2 mg/kg/hour) but avoid deep sedation and hypercapnia; treat hypertension promptly (esmolol, labetalol, clonidine).
Infectious tumors (abscesses) are part of the differential diagnosis of supratentorial mass lesions. They are often accompanied by low-grade fever. Risk factors: contiguous infections (sinus, ear); right-to-left cardiac shunt; immunosuppression (extrinsic/intrinsic); intravenous drug abuse. Initial treatment: antibiotics (infection); corticosteroids (brain swelling). Definitive diagnosis/treatment: craniotomy, abscess aspiration. Surgical and anesthetic management: as for supratentorial neoplasms; aseptic precautions and sterile technique are vital for immunocompromised patients with acquired immunodeficiency syndrome. Note the association between human immunodeficiency virus infection and cerebral non-Hodgkin's lymphomas.
Craniofacial/skull base surgery. Increasingly used for orbital, posterior nasal sinus wall tumors. Particularities: complex, multidisciplinary surgery; tracheostomy/oral intubation frequent. Extensive bony involvement→↑ bleeding, hemorrhagic diathesis, venous air embolism (head-up position). Sensory ± motor neurophysiologic cranial nerve monitoring is common (motor monitoring: avoid neuromuscular blockade). Repeat procedures may be necessary and a difficult intubation (skull base exposure requires extensive temporalis muscle mobilization, which can lead to mandibular pseudoankylosis and limited mouth opening) can result.

II. Anesthesia for intracranial hematomas

General considerations. The effects of intracranial hematomas on neurostatus and ICP depend particularly on the speed with which they arise. Slow: chronic subdural hematomas- subtle neurologic signs, small ICP; anesthetic technique: similar to supratentorial tumors. Most often seen in elderly patients (>70 years). Fast: acute epidural (e.g., traumatic), subdural, or intracerebral hematoma-massive neurologic impairment, potentially acutely life-threatening ICP; anesthetic technique: aggressive reduction of ICP and measures to preserve brain oxygenation and perfusion, followed by urgent surgical decompression. Situation frequently seen in head trauma or due to anticoagulation or antiplatelet agents. Coagulation should be corrected before surgery (factors II, VII, IX, and X, and vitamin K for patients treated with vitamin K antagonists; platelet transfusion for patients taking clopidogrel.
Anesthetic management of acute intracranial hematoma
Induction.
a. Basics. Ensure oxygenation and then secure airway and hyperventilate with 100% oxygen. Swift, atraumatic intubation (always dangerous if a fractured cervical spine is suspected or confirmed by x-ray); aim for a minimal ICP rise by avoiding coughing and arterial hypertension due to light anesthesia. In polytraumatized, hypotensive, and hypovolemic patients, one should decrease hypnotic, analgesic doses and restore circulating volume. If the patient has a full stomach, use aspiration prophylaxis and cricoid pressure (cautiously if suspected fractured cervical spine).
b. Pharmacologic range of options. Intubation without further use of drugs in the deeply unconscious patient; judicious sedative use (e.g., etomidate, 0.2 to 0.5 mg/kg; propofol, 0.5 to 1.5 mg/kg; or thiopental, 2 to 4 mg/kg) with myorelaxation for a semiconscious, struggling patient; classical rapid sequence induction for the (still) conscious and stable patient. Controversy: what myorelaxant scheme to use? Succinylcholine, perhaps preceded by a small dose of nondepolarizing myorelaxant, remains the classical and time-tested scheme.
c. Control of ICP and brain swelling. Next priority after securing ventilation and airway; should be started as early as possible and continued through to intensive care treatment. Start with large doses of mannitol, 0.7 to 1.4 g/kg (Table -2).
Anesthesia maintenance. Aims: control of ICP and brain swelling; maintenance of cerebral perfusion and oxygenation by matching CMRo2 and CBF.
a. Monitoring
(1) Cardiovascular monitoring for these frequently hemodynamically unstable patients should include invasive arterial pressure monitoring, preferably commenced before induction (close hemodynamic control, repeated laboratory determinations). Electrocardiographic monitoring: interactions between brain damage and myocardial injury, risk of arrhythmias.
(2) ICP monitoring. Generally installed once hematoma is evacuated, mainly for use in intensive care unit.
(3) Laboratory analyses. Blood gas analysis (acid-base balance, ventilation, etc.); glucose (hyperglycemia and brain ischemia); coagulation profile (brain tissue damage→↑ circulating thromboplastin); blood osmolality as guidance for use of osmotic diuretics (e.g., with mannitol, maximum should be 320 mOsm/kg).
Anesthetic technique. Intravenous anesthetics (→↓CMRo2, CBF,CVR) are the mainstay of anesthesia for acute intracranial hematoma. Volatile anesthetics are not recommended because of risk of →↑ICP/brain tension (to the point of acute transtentorial/craniotomy herniation, even with preexisting hypocapnia) and much smaller CMRo2 reduction and neuroprotection against focal ischemia than with intravenous anesthetics (propofol, barbiturates). The following different situations must be evaluated and treated:
(1) Deep coma and signs of brain herniation: myorelaxation and repeated small doses of thiopental titrated to blood pressure
(2) Coma but no sign of herniation, increased ICP: propofol TCI or small doses of thiopental and opioids titrated to blood pressure; myorelaxation
(3) Conscious patient but mass effect on CT-scan: rapid sequence induction, followed by propofol TCI, opioids, and myorelaxation
Cardiovascular control. Avoid arterial hypotension (by using doses of intravenous anesthetics that are too large) to prevent CPP (cerebral ischemia and/or reflex cerebral vasodilatation →↑ICP not controlled by hypocapnia [vasodilatory cascade]). Controversy: control of arterial hypertension and acute intracranial hematoma (Table-2): carefully balance maintenance of CPP to areas of brain rendered ischemic due to compression by hematoma against risk of more vasogenic brain edema or bleeding. Jugular venous bulb oxygen saturation monitoring may help assess adequacy of global CPP. btPo2 can help assess adequacy of local O2 delivery. Globally adequate CPP does not rule out regional CPP inadequacies regional ischemia. If arterial pressure requires reduction, first improve analgesia (i.e., opioids) and/or depth of anesthesia (propofol, barbiturates, etomidate) before instituting specific antihypertensive treatment (usually antisympathetic drugs [e.g., esmolol, labetalol, clonidine]). Avoid cerebral vasodilators. Decrease blood pressure no >15% to 20%. Anticipate severe hypotension after brain decompression due to disappearance of the Cushing response: rapid fluid loading, neosynephrine, noradrenaline, or epinephrine ready to use.
Emergence. Patients with acute cerebral hematoma have significant brain injury with significant actual and potential brain swelling. They should therefore undergo slow weaning and delayed extubation in the neurointensive care unit. Chronic subdural hematoma patients frequently have minimal neurologic impairment preoperatively and can therefore often be awakened and their tracheas extubated immediately after surgery.

III. Conclusions

The main objectives of anesthesia for excision of a cerebral tumor include the following:
Preserving uninjured cerebral territories by global maintenance of cerebral homeostasis and cardiovascular stability as well as neuroprotection.
Balancing CBF autoregulation and MAP and preserving cerebral vasoreactivity to Paco2.
Achieving and maintaining brain relaxation by means of:
CMRo2, CBF, and CBV
moderate hyperventilation (Paco2 ~ 35 mm Hg)
strict maintenance of CPP
osmotherapy
CSF drainage
Timely awakening to facilitate early and continuing neurologic assessment and permit prompt diagnosis and treatment of complications.

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