Sunday, March 21, 2021

Craniotomy for Brain Mass Excision Case File

Posted By: Medical Group - 3/21/2021 Post Author : Medical Group Post Date : Sunday, March 21, 2021 Post Time : 3/21/2021
Craniotomy for Brain Mass Excision Case File
Lydia Conlay, MD, PhD, MBA, Julia Pollock, MD, Mary Ann Vann, MD, Sheela Pai, MD, Eugene C. Toy, MD

Case 28
A 51-year-old man with a tempero-parietal metastatic melanoma presents for left craniotomy and tumor excision. Over the past few days, he has experienced new-onset right upper extremity weakness and grand mal seizures. The patient’s past medical history is significant for mild systemic hypertension, and melanoma on the right side of his neck. His past surgical history is significant for wide local excision and lymph node dissection of right side of his neck. His current medications include atenolol 25 mg once a day, prednisone 20 mg tid, and dilantin 100 mg tid. The patient’s lab test results are normal. His hemoglobin is 14 g%, platelet count is 140,000, and his INR is 1.0. Serum electrolytes are within normal limits. His ECG is normal with sinus rhythm of 66 bpm. CT scan shows a 3 × 4 cm lesion in the left tempero-parietal cortex with edema around the tumor, and a 2-mm midline shift.

➤ What preoperative information is especially useful for the anesthesiologist regarding patients undergoing a craniotomy?

➤ How can intracranial pressure (ICP) be reduced?

➤ Why are patients observed in an ICU setting postoperatively, and what are the implications of a new abnormal finding?


ANSWERS TO CASE 28:
Craniotomy for Brain Mass Excision

Summary: A 51-year-old man presents with metastatic melanoma, a 2-mm midline shift, and the new onset of a motor deficit.

Preoperative information: In addition to the usual pre-anesthetic assessment, the preoperative assessment for a patient with a space occupying lesion (SOL) includes knowledge of the size and site of lesion and its vascularity, and whether the patient has any neurological deficits, and if so, whether they are stable or worsening in intensity. Any symptoms of an elevated ICP and/or impending herniation warrant special attention.

Ways to reduce intracranial pressure: The anesthetic is designed to actively reduce and avoid any further increases in ICP, and to maintain cerebral perfusion. The elevation of ICP can worsen the cerebral edema, the midline shift, and ultimately, the neurological deficit. Increases in ICP are minimized by ensuring an adequate depth of anesthesia for painful parts of the case such as the application of head pins. ICP can be reduced by moderate hyperventilation, mannitol, and/or furosemide.

Reason for observation in ICU postoperatively: Postoperatively, the strict control of blood pressure and periodic assessment of mental status and motor function are essential. Any acute deterioration in mental status or a new deficit suggests worsening cerebral edema or an intracranial bleed and requires an immediate intervention such as a CT scan or MRI.


ANALYSIS

Objectives
1. Learn the elements of a preoperative evaluation specific for patients with a SOL.
2. Become familiar with the relationship between arterial pressure, intracranial pressure, and cerebral perfusion pressure.
3. Understand the factors that influence intracranial pressure (ICP), and the methods to control ICP.
4. Understand the effects of anesthetic agents on ICP and cerebral metabolic rate for oxygen (CMRO2).
5. Be able to describe an anesthetic plan for craniotomy.


Considerations
This patient has a SOL with a midline shift and new onset of a neurological deficit. He is receiving medical management for the cerebral edema and elevated ICP. The preoperative assessment of this patient includes knowledge of the size and site of lesion and its vascularity. This information can be obtained by physical examination and evaluating the radiological images and medical record.

The goal of the anesthetic is to avoid any further increase in ICP. Further increases in ICP can worsen the cerebral edema and midline shift, and contribute to worsening of the neurologic deficit. Invasive blood pressure monitoring is required. However, in this case, the elevation of ICP is not severe enough to require intraoperative ICP monitoring.

General anesthesia is induced with thiopental or propofol, and muscle relaxation can be achieved with vecuronium. After endotracheal intubation, anesthesia is maintained with nitrous oxide/oxygen and low concentrations of an inhalational agent. A nicardipine infusion is used to treat hypertension, and fentanyl is administered for pain control.

The anesthetic technique is also designed to actively reduce ICP and maintain cerebral perfusion. The careful control of blood pressure, moderate hyperventilation, and use of diuretics such as furosemide and mannitol help to reduce the ICP. To minimize bleeding at the surgical site, the patient is extubated with minimal coughing and bucking, and strict control of blood pressure is maintained during emergence.

This patient will be monitored postoperatively in an intensive care setting to ensure the strict control of blood pressure and periodic assessment of mental status and motor function. Any acute deterioration in mental status or a new onset neurodeficit suggests a worsening of the cerebral edema or an intracranial bleed and must be addressed immediately.


APPROACH TO
Craniotomy for Brain Mass Excision

DEFINITIONS
ICP: Normal ICP is 5 to 15 mm Hg and reflects the relationship between the rigid cranial vault and its contents; that is, the brain, blood, and the CSF. Sustained ICP of 15 to 20 mm Hg is considered elevated ICP.
CEREBRAL COMPLIANCE: When intracranial volume increases such as with a SOL, one of the other components (eg, CSF) is initially displaced, and ICP remains relatively normal. But as these “buffering mechanisms” are exhausted and intracranial volume continues to increase, intracranial pressure then increases as well potentially resulting in brainstem herniation (Figure 28–1).
CEREBRAL AUTOREGULATION: Autoregulation maintains a constant level of cerebral blood flow (CBF) over a wide range of mean arterial pressures. Autoregulation is impaired by cerebral edema, brain injury, and inhaled

Volume of expanding mass

Figure 28–1. Pressure-volume compliance curve.

anesthetics. The autoregulatory curve is shifted to the right in patients with systemic hypertension. (Figure 28–2). Hypercarbia and hypoxia can increase cerebral blood flow irrespective of autoregulation.
CEREBRAL PERFUSION PRESSURE (CPP): It is the net pressure gradient between the force facilitating brain-blood flow (mean arterial pressure) and

Cerebral blood flow

Figure 28–2. Effect of PaO2 and PaCO2 on CPP and ICP.

the force impeding flow (ICP). Cerebral perfusion pressure is directly related to cerebral blood flow. CPP must be maintained within narrow limits, because too little pressure could cause brain tissue to become ischemic or too much could raise intracranial pressure (ICP). CPP is normally between 70 and 90 mm Hg in an adult human, and should not fall below 70 mm Hg for a sustained period. Some authorities, however, regard a CPP between 50 to 150 mm Hg to be within the normal range for adults since this approximates the range of autoregulation in the normal brain.
Cerebral blood flow is approximately 50 mL/100 g of brain tissue/min. It remains fairly constant over a wide range of pressures, due to autoregulation. However, outside the bounds of autoregulation, cerebral blood flow changes according to the cerebral perfusion pressure.
CMRO2: Cerebral metabolic rate for oxygen is coupled with CBF. When the metabolic rate in a particular region increases, CBF to that region will also increase. Increase in CMRO2 increases CBF globally. Factors that increase CMRO2 are hyperthermia, seizures, and some anesthetic agents. Some inhalational agents can cause uncoupling of CBF and CMRO2, that is, though they do reduce the CMRO2, the CBF remains unchanged or is even increased by cerebral vasodilatation.


CLINICAL APPROACH
The SOL may cause seizures and other neurologic deficits, depending on its size and location. Often, the normal physiologic mechanisms which offset dayto- day increases in intracranial volume, such as displacing cerebrospinal fluid from the brain, will have been exhausted. Thus, patients with SOLs have a reduced intracranial compliance, meaning that even small increases in intracranial volume result in large increases in ICP. As ICP increases, the level of consciousness may be compromised, and the brain’s anatomy distorted. Pressure on the brainstem can lead to herniation of the brainstem and death.


Preoperative Evaluation
In addition to the usual preoperative evaluation, patients with brain tumors warrant special examination of their neurological status. Neurological deficits may be new in onset, and/or changing. Clinical signs and symptoms of an elevated ICP are headache, vomiting, blurred vision, somnolence, and papilledema. The signs of impending brain herniation include bradyarrhythmia, hypertension, ipsilateral fixed dilated pupil (from oculomotor and abducent nerve palsy), and contralateral hemiparesis or hemiplegia.

A review of the patient’s CT scan or MRI is invaluable. It gives an idea of the size and position of the tumor, the extent of cerebral edema, and the possible presence of a midline shift signaling a significantly elevated ICP. The size of the tumor, and proximity to dural venous sinuses can give an idea of possible intraoperative blood loss. Cross-matched blood should be available in the blood bank.


Management of Elevated ICP

The following strategies can be used to lower ICP:
a. Reduction of cerebral blood volume: Hypercarbia and hypoxia profoundly increase cerebral blood volume. So proper airway management is crucial in patients with altered intracranial compliance. Hyperventilation to a moderate hypocarbia of a PaCO2 of 25 to 30 mm Hg produces cerebral vasoconstriction and is very useful in acute reduction of elevated ICP. Excessive hyperventilation should be avoided, since it can cause cerebral vasoconstriction in areas of the brain where blood flow is already compromised by cerebral edema. Hypoxia causes cerebral vasodilatation, and thus an increase in ICP. Again, meticulous attention to control of the airway and ventilation is essential. Venous drainage is facilitated by head elevation and avoiding high intrathoracic pressures.
b. Reduction in brain tissue volume is accomplished by diuretics and steroids. Mannitol is an osmotic diuretic administered in the dose of 0.5 to 2 g/kg body weight. It increases the serum osmolality (305-320 mOsm/L) and thus removes the excess water from the brain. Mannitol increases blood volume acutely, and can thus precipitate volume overload and even heart failure in susceptible individuals.

Furosemide is a loop diuretic which is very effective in reducing ICP alone or when used in combination with mannitol. Furosemide reduces blood volume as well as CSF production.

Steroids appear to be helpful in reducing the edema surrounding a SOL.

They are ineffective in reducing edema due to hypoxia or hypercarbia.
c. A reduction of CSF can be achieved by surgical placement of a ventriculostomy catheter or a lumbar drain.


Anesthetic Management
It is ideal to have two large-bore peripheral venous accesses and an arterial line. A central line or pulmonary artery catheter is indicated based on the coexisting medical conditions, and is not an absolute requirement for supratentorial craniotomies. Excessive sedation from premedications can cause hypercarbia and hypoxia, thus elevating the ICP. Therefore, sedative premedication should be used with caution or avoided all together in patients with elevated ICP. Normal saline is the ideal maintenance fluid. Hypotonic solutions such as Ringer lactate and dextrose containing solutions should be avoided.

Routine intraoperative monitoring and invasive monitoring of arterial pressure is utilized for craniotomies. Central venous pressure monitoring is not routine, and indeed, may either expose the patient to an unnecessary risk of pneumothorax, or impede venous drainage from the neck. Moreover, placing a patient with altered intracranial compliance in Trendelenburg for line placement could also cause a dangerous increase in ICP. The one situation where a central venous catheter is indicated is during craniotomies in the sitting position, where the head is higher than the heart. In this position,
there is a risk of venous air embolism potentially necessitating the aspiration of air through a central venous catheter to prevent its entry into the pulmonary circulation. The risk of venous air embolism is relatively low with supratentorial tumors, provided the tumor is not adhered to large dural venous sinuses.

Induction is typically performed with sodium thiopental, since thiopental reduces CMRO2. However, propofol and etomidate are also suitable for induction. Ketamine should not be used as it increases ICP and CMRO2. Following induction, hyperventilation is established to avoid hypercarbia. Either depolarizing or (more commonly) nondepolarizing muscle relaxants are used to obtain relaxation for intubation. Succinylcholine does minimally increase ICP, but when administered after an induction agent, this elevation does not appear to be clinically significant. Succinylcholine should be avoided in patients with motor deficit because of the risk of hyperkalemia from neuronal depolarization.

Narcotics do not directly affect ICP unless patients are breathing spontaneously, and they are quite useful to help blunt the response to laryngoscopy and intubation. Blunting this response is one of the crucial goals of induction, since patients with a SOL may already have a reduced intracranial compliance, and increases in arterial pressure can further increase ICP. The events that cause most intense pressor response are laryngoscopy and intubation, the placement of pins (which hold the head), the skin incision, and stimulation of the periosteum. Fentanyl, lidocaine, additional doses of the induction agent, and moderate hypocarbia aid in avoiding any rapid increases in cerebral blood flow which may result. Remifentanil, an ultrashort-acting opioid, can be also used as an infusion from induction to extubation. Long-acting opioids are best avoided. Before the dura is opened, it is essential to optimize operating conditions and to avoid a “tight” or “full” brain from cerebral edema, or an excess of cerebral blood flow. This can be accomplished by moderate hyperventilation in combination with the administration of mannitol, furosemide, and steroids.

Low concentrations of a potent inhalational agent can be added to an oxygen/nitrous oxide mixture for maintenance of anesthesia. Though nitrous oxide reduces the concentration of inhalational agents required to maintain anesthesia, recent evidence, though controversial, suggests that it increases CMRO2, though this effect is blocked by hyperventilation. On the other hand, inhalational agents attenuate autoregulation, and in high concentrations increase cerebral blood flow. Ideally, after establishing moderate hypocarbia a low dose of an inhalational agent or propofol infusion are used to maintain anesthesia. Muscle relaxation and moderate hyperventilation to an end-tidal CO2 concentration of 25 to 30 is continued during the craniotomy.

Hyperglycemia increases intracellular acidosis and facilitates cell ischemia. Therefore, hyperglycemia should be treated aggressively with insulin as required, and glucose-containing solutions should be avoided. Steroids can also contribute to hyperglycemia.

Elevations in blood pressure can cause an intracranial bleed at the surgical site requiring re-exploration. At the time of extubation, hypertension, coughing, and straining are to be avoided at all costs. Intravenous lidocaine has been used to prevent the stress responses to extubation. A short-acting opiate, such as remifentanil, can suppress the cough response and facilitates a smooth wakeup. In addition, autoregulation is impaired in areas with cerebral edema. Therefore, blood pressure is carefully controlled, the head elevated, and the patient is extubated awake.

Patients post craniotomy are monitored overnight in an intensive care setting. Periodic assessment of mental status and motor function is essential to detect any changes in neurological status, and blood pressure is meticulously controlled in the immediate postoperative period. Any acute deterioration in mental status, or a new onset neurologic deficit suggests worsening cerebral edema or an intracranial bleed and requires an immediate intervention including urgent CT scan and possible repeat craniotomy to evacuate an hematoma.


Special Considerations for a Posterior Fossa Craniotomy
Posterior fossa tumors present a special challenge. The tumors can compress the cerebellum, the lower cranial nerves, and the vasomotor and respiratory centers. Involvement of the lower cranial nerves, the glossopharyngeal and vagus can cause vasomotor instability. Indeed, surgical dissections in this area can be associated with arrhythmias and alterations in vasomotor tone. Damage to the glossopharyngeal nerve can impair gag reflex and impair a patient’s ability to protect his airway. Prior to extubation, the ability to protect airway and adequacy of spontaneous breathing should be established.

The sitting position is sometimes required to access a SOL in the posterior fossa, such as an acoustic neuroma. The risk of venous air embolism is significant in sitting position, since the subdural venous pressure is much lower than the atmospheric pressure. These patients often benefit from a precordial Doppler or even a transesophageal echocardiogram as an additional monitor to detect the occurrence and/or severity of a venous air embolism (VAE). Intravascular air is suggested by sudden hemodynamic instability, or a sudden drop in the end-tidal carbon dioxide concentration. These patients benefit from placement of a multiorifice central lumen catheter, which may be used to aspirate venous air from the right atrium. As the sitting position is fraught with risks, modified supine position or prone position is preferable when possible.


Comprehension Questions

28.1. Which of the following factors increase cerebral blood flow?
A. Hypocarbia
B. Hyperoxia
C. Hypercarbia
D. Thiopental sodium

28.2. Methods to reduce an elevated ICP include which of the following?
A. Mannitol and furosemide
B. Hypoventilation
C. Positioning in Trendelenburg
D. Transfusion to increase hemoglobin-carrying capacity

28.3. Which of the following statements regarding cerebral autoregulation is accurate? A. In the presence of intact autoregulation, hypercarbia cannot increase cerebral blood flow.
B. Succinylcholine impairs autoregulation.
C. Cerebral autoregulation can be impaired in the presence of cerebral edema or extreme hypoxia.
D. Cerebral autoregulation in a patient with long-standing systemic hypertension is no different from a normotensive individual.


ANSWERS
28.1. C. Hypercarbia and hypoxia increase cerebral blood flow. Hypocarbia and thiopental sodium reduce cerebral blood flow.

28.2. A. The head up positioning, hyperventilation to mild hypocarbia, the administration of mannitol and furosemide, and placement of a ventriculostomy or lumbar drain help in reducing elevated intracranial pressure.

28.3. C. Autoregulation can be impaired by cerebral edema, severe hypoxia, and long-standing systemic hypertension. In a patient with long-standing hypertension, the autoregulatory curve is shifted to the right so the mean arterial pressure needs to be higher to maintain adequate cerebral perfusion. Hypercarbia can increase cerebral blood flow even in the presence of intact autoregulation.


Clinical Pearls
➤ The preoperative evaluation of a patient for craniotomy should include knowledge of the size, location, vascularity, and nature of the SOL as this can influence positioning of the patient, surgical blood loss, and line placement.
➤ Intracranial pressure is dynamically influenced by blood pressure, PaCO2, and most anesthetics.
➤ Elevated ICP can be reduced by head elevation to 30 degrees in combination with diuretics, that is, furosemide and mannitol, moderate hyperventilation, reducing the mean arterial pressure, and in some cases by drainage of CSF.
➤ The goal of anesthesia for craniotomy is to maintain cerebral perfusion, reduce CMRO2, preserve blood flow and hence oxygenation to “at-risk areas,” and to optimize operating conditions.

References

Cunningham AJ, Hourihan D. The sitting position in neurosurgery-unresolved hemodynamic consequences. Can J Anesth. 2007;54(7):497-500. 

Dinsmore J. Anesthesia for elective neurosurgery. Br J Anaesth. 2007;99(1):68-74. Review. 

Harvey M. Shapiro and John C. Drummond; Neurosurgical Anesthesia; R.D Miller Anesthesia, volume 2, 1994, NewYork: Harvey Livingstone 

Pasternak JJ, Lanier WL. J Neurosurg Anesthesiol. 2008;20(2):78-104.

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