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Questions and Answers
What effect does a rise in PaCO2 have on cerebral blood flow (CBF)?
Which scenario corresponds to increased intracranial pressure (ICP)?
What is the maximum PaCO2 level associated with complete vasodilation of cerebral arterioles?
Which of the following is NOT a known factor that impairs venous drainage from the brain?
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Which condition is characterized by hypertension, bradycardia, and irregular respiratory patterns?
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What is the most common cause of subarachnoid bleeding?
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Which of the following options is least likely to contribute to aneurysmal rupture?
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What is the most common sign associated with subarachnoid hemorrhage (SAH)?
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Which of the following tumors in adults is associated with the highest likelihood of elevated intracranial pressure?
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Postoperative intubation is more frequently required in which type of tumors?
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Which of the following should be avoided during premedication to minimize risks related to respiration?
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Which measures are essential to control during intubation to prevent complications?
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What is critical to minimize during induction regarding cerebrovascular stability?
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Which pharmacological agent is recommended to blunt the sympathetic nervous system response during laryngoscopy?
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What is the recommended infusion rate for hypertonic saline during ICP management?
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Which fluid type is advised for maintenance of anesthesia to achieve euvolemia?
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Which of the following drugs should NOT be used in large doses during maintenance of anesthesia due to their potential to increase ICP?
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Which drug is often used to control hypertension in patients after emergence from anesthesia to prevent the worsening of cerebral edema?
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What is the equation for calculating Transmural Pressure?
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Which of the following factors contributes to the rupture risk of a cerebral aneurysm?
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What intervention should occur within 48 hours following an initial hemorrhage due to a cerebral aneurysm?
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During which surgical phase is the risk of intraoperative rupture of a cerebral aneurysm the highest?
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What is a significant goal during the surgical management of a cerebral aneurysm?
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What is involved in the process of the endovascular coiling procedure for a cerebral aneurysm?
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What significantly increases the transmural pressure in the context of cerebral aneurysms?
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Which aneurysm location has the highest reported occurrence in the Circle of Willis?
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What is the initial bolus dose of heparin given during a neuro-interventional radiology procedure?
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Which of the following outcomes is most commonly linked with cerebral vasospasm after subarachnoid hemorrhage (SAH)?
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What does Triple H Therapy aim to achieve during treatment of cerebral vasospasm?
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What is the purpose of performing a daily transcranial Doppler exam in patients with cerebral vasospasm?
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Which treatment is the only calcium channel blocker associated with decreased morbidity and mortality in cerebral vasospasm?
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In cases of traumatic brain injury, which condition is a significant risk factor that must be managed?
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What should NOT be done when managing intracranial pressure (ICP) in traumatic brain injury?
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What is the indicated management for warfarin reversal in traumatic brain injury?
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What is the effect of increasing cerebral perfusion pressure (CPP) above 150 mmHg on cerebral blood flow (CBF)?
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Which physiological phenomenon describes the effect of intracranial volume changes on intracranial pressure (ICP) according to the Monro-Kellie hypothesis?
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What is the primary outcome of Cushing's triad in response to increased intracranial pressure?
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Which of the following conditions would most likely lead to impaired autoregulation of cerebral blood flow?
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During ischemia and reperfusion injury, which mechanism is primarily responsible for secondary brain injury?
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What is the condition characterized by reduced blood flow to the brain due to low cerebral perfusion pressure?
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Which measure is considered critical in preventing Cushing's Triad in patients with elevated intracranial pressure?
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According to the Monro-Kellie Hypothesis, what happens when intracranial volume increases?
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Which of the following factors has the most significant impact on cerebral blood flow dynamics?
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What is the minimum cerebral blood flow (CBF) rate necessary to avoid cell death in brain tissue?
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Which scenario best describes reperfusion injury in the context of cerebral blood flow?
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What is the primary determinant of cerebral perfusion pressure (CPP)?
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Which type of molecules have higher permeabilities in the area postrema, affecting drug delivery?
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What physiological mechanism is described by the need to decrease one component of intracranial volume when another increases, according to the Monro-Kellie Hypothesis?
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Which intervention is specifically aimed at providing temporary relief from elevated intracranial pressure when hyperventilation is used?
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Which phase is characterized by compensatory failure leading to symptoms of intracranial hypertension and focal ischemia?
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In the context of cerebral blood flow, what occurs when blood pressure is above the autoregulation limit?
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Which of the following factors contributes to the increased volume of blood in the cranial cavity?
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Which clinical condition is indicated by a combination of hypertension, bradycardia, and irregular respirations?
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What is the effect of hyperventilation on intracranial pressure?
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How does the volume composition of the cranial cavity break down according to the Monro-Kellie Hypothesis?
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What is the effect of decreased PaCO2 on cerebral blood flow (CBF)?
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At what level of PaO2 does cerebral vasodilation begin to be impaired?
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Which factor does NOT affect cerebral blood flow as indicated by the content?
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What occurs when intracranial pressure (ICP) exceeds 20 mmHg?
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What physiologic response is characteristic of Cushing’s triad?
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What is the most common location for cerebral aneurysms in the Circle of Willis?
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What is the primary goal of clipping a cerebral aneurysm during surgery?
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Which factor significantly increases the risk of a cerebral aneurysm rupture?
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During which surgical phase is the risk of intraoperative rupture of a cerebral aneurysm the highest?
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What is the primary concern associated with infratentorial tumors?
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What intervention is recommended immediately following an intraoperative rupture of a cerebral aneurysm?
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Which statement accurately describes transmural pressure in the context of cerebral aneurysms?
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Which clinical sign is commonly referred to as the 'worst headache of my life' in cases of subarachnoid hemorrhage?
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Which medication is typically used to control blood pressure during brain clipping procedures?
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What surgical intervention is considered for treating cerebral aneurysms?
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What is a major potential effect of using excessive crystalloids during cerebral aneurysm surgery?
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Which of the following is NOT considered a risk factor for cerebral aneurysm rupture?
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Which mechanism is primarily responsible for elevated intracranial pressure (ICP) following cerebral trauma?
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What is the primary function of cerebrospinal fluid (CSF)?
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What structure is primarily responsible for producing cerebrospinal fluid?
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What role do astrocytes play in the central nervous system?
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Which of the following substances can cross the blood-brain barrier freely?
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Which pair of structures connects the lateral ventricle to the third ventricle?
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Which cells act as macrophages in the central nervous system?
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What is the primary consequence when intracranial pressure (ICP) increases according to the Monro-Kellie Hypothesis?
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What is the typical range of intracranial pressure (ICP) in mmHg?
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Which statement is true regarding the reabsorption of cerebrospinal fluid?
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Which intervention would best help lower intracranial pressure immediately after a traumatic brain injury?
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How does hyperglycemia affect cerebral injury during ischemia?
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What is the approximate volume of cerebrospinal fluid present in an average adult at any given time?
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Which of the following components is typically higher in plasma than in cerebrospinal fluid?
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What characteristic differentiates focal ischemia from global ischemia?
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Which of the following treatments is NOT recommended for managing elevated intracranial pressure?
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What is the effect of excessive NaCl in fluid management during cerebral conditions?
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What is the recommended tidal volume setting for ventilation management in patients with cerebral issues?
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In the management of cerebral edema, what is the appropriate strategy regarding fluid types?
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Study Notes
Intracranial Pressure
- Normal intracranial pressure ranges from 5 to 15 mmHg.
- Intracranial hypertension occurs when ICP is greater than 20 mmHg.
- Signs and Symptoms of intracranial hypertension include headache, nausea/vomiting, papilledema, decreased level of consciousness, seizures, and coma.
- Cushing's Triad is a late sign of elevated ICP and includes hypertension, bradycardia, and decreased respiratory effort.
- Limit use of drugs that depress respiration to avoid increased PaCO2, which can worsen intracranial hypertension.
- Continue steroids and anticonvulsant therapy.
Cerebral Blood Flow
- PaCO2 directly correlates with cerebral blood flow (CBF).
- Increased PaCO2 increases CBF, while decreased PaCO2 decreases CBF.
- A 1 mmHg change in PaCO2 causes a 1-2 mL/100g brain tissue/min change in CBF.
- Maximum vasodilation occurs at 80-100 mmHg PaCO2.
- Maximum vasoconstriction occurs at 25 mmHg PaCO2.
- Note how respiratory acidosis/alkalosis affects CBF.
- Metabolic acidosis does NOT affect CBF because H+ cannot cross the blood-brain barrier.
PaO2 and Venous Pressure
- A PaO2 below 50-60 mmHg causes cerebral vasodilation and increased CBF.
- A PaO2 above 60 mmHg does NOT affect CBF.
- Increased central venous pressure (CVP) decreases cerebral drainage, leading to increased cerebral volume.
- Impaired venous drainage can be caused by:
- Jugular compression (positioning)
- Increased intrathoracic pressure (cough, PEEP)
- Thrombosis
- Vena cava syndrome
Induction and Airway Management
- The goal of induction and airway management is to minimize changes in ICP and CPP.
- Consider preinduction procedures such as arterial line placement, osmotic diuresis, or CSF drainage.
- Avoid hypotension and hypoventilation.
- Maintain strict BP control during intubation to reduce the risk of herniation.
- Use propofol as the induction agent.
- Blunt the sympathetic nervous system response to laryngoscopy with fentanyl (1-2 mcg/kg), lidocaine (1-1.5 mg/kg), or esmolol.
Induction and Airway Management: Vascular Access
- Adequate vascular access is mandatory.
- Establish two large-bore IVs and an arterial line (possible central venous line).
- Place Mayfield pins after induction and vascular access.
- Administer propofol, opioids, or esmolol to blunt the SNS response.
- Excessive neck flexion, extension, or rotation can compress the internal jugular vein and impair cerebral venous drainage.
Decreasing ICP and Increasing Exposure
- Avoid PEEP.
- Hyperventilate the patient.
- Limit the use of volatile anesthetics.
- Elevate the head of the bed (HOB).
- Limit intravenous fluid (IVF) to euvolemia.
- Consider a ventriculostomy.
- Administer mannitol (0.25-1 g/kg) or furosemide (0.5-1 mg/kg).
- Administer hypertonic saline (3% at 50-100 mL/hr).
- Consider the use of steroids.
Maintenance of Anesthesia
- Avoid increases in ICP (at least until dura is opened).
- Maintain CPP.
- Monitor neurologic function.
- Maintain fluid balance with dextrose-free, iso-osmolar crystalloids or colloids to achieve euvolemia.
- Aim for rapid emergence from anesthesia using short-acting, easily titratable drugs like propofol, remifentanil, sevoflurane, desflurane, and possibly nitrous oxide (N2O).
Maintenance of Anesthesia: Drugs
- Use volatile gases at less than 0.5 MAC to avoid cerebral vasodilation.
- Administer propofol infusion at 50-300 mcg/kg/min (depending on volatile anesthetic use).
- Administer remifentanil infusion at 0.05-2 mcg/kg/min (ideal body weight).
- Be cautious of opioid-induced hyperalgesia, and consider low-dose ketamine or magnesium sulfate to help reduce this.
Emergence from Anesthesia
- Extubate patients with a normal Glasgow Coma Scale (GCS) score of 13-15.
- Maintain hemodynamic control (hypertension can worsen cerebral edema).
- Keep labetalol, esmolol, nicardipine, etc. on hand.
- Coughing or vomiting can be deleterious.
- Carefully titrate opioids and antiemetics.
- Control pain without obtunding the patient.
- Use short-acting opioids, IV acetaminophen, local anesthetic infiltration by the surgeon, dexmedetomidine, etc.
Intracranial Tumors
- Supratentorial lesions are more common in adults and often arise from CNS support cells (gliomas, astrocytomas, oligodendrogliomas, etc.).
- Melanoma and tumors originating in the lung, breast, or kidney are the most common metastatic tumors to the brain.
- The primary concern with intracranial tumors is typically elevated ICP.
Infratentorial and Posterior Fossa Tumors
- These tumors are located in close proximity to the brainstem.
- They can cause more hemodynamic distress, changes in respiratory control and arousal, altered respiratory patterns, cardiac dysrhythmias, and cranial nerve dysfunction.
- Postoperative intubation and mechanical ventilation may be required more frequently with this type of tumor.
- Patient positioning may be prone, lateral, or sitting.
- Infratentorial tumors have a particular risk of venous air embolism (VAE).
Cerebral Aneurysm
- A saccular aneurysm is the most common cause of subarachnoid hemorrhage (SAH).
- Essential causes of rupture are:
- Increased aneurysmal distention pressure.
- Higher MAP = greater distention = increased aneurysm radius = increased wall tension.
- Lower ICP = decreased distention = decreased aneurysm radius = decreased wall tension.
- The most common sign of a subarachnoid hemorrhage is a sudden, intense "worst headache of my life."
- Other signs and symptoms include syncope, nausea/vomiting, photophobia, fever, obstructive hydrocephalus, etc.
Aneurysm and Perfusion Pressure
- The transmural pressure (TMP) is calculated as: MAP - ICP.
Cerebral Aneurysm: Location and Risk Factors
Cerebral Aneurysm: Locations
- Common locations for aneurysms in the Circle of Willis are:
- Anterior cerebral artery (ACA) = 40%
- Middle cerebral artery (MCA) = 25%
- Posterior cerebral artery (PCA) = 25%
- Basilar artery (BA) = 10%
Cerebral Aneurysm: Risk Factors
- Increased transmural pressure (TMP = MAP – ICP).
- A diameter greater than 2.5 cm (Laplace law).
- Smoking.
- Excessive alcohol consumption.
- Recreational drug use.
- Age older than 40 years.
- Being female.
- Systemic hypertension.
Cerebral Aneurysm: Surgical Options
- Surgical repair is the standard of care, and often involves:
- Aneurysm clipping: Placing a clip at the base of the aneurysm to isolate it from the circulation.
- Endovascular coiling: Transarterial catheterization to thread a coil into the aneurysm sac.
Cerebral Aneurysm: Timing of Intervention
- Intervention should ideally occur within 48 hours of initial bleeding.
Cerebral Aneurysm: Anesthesia Management
- Preinduction:
- Limit sedation to avoid hypercapnia.
- Place an arterial line for monitoring.
- Maintenance:
- TIVA versus volatiles.
- Maintain blood pressure 15-20% below baseline.
- Use a low-dose vasodilator (e.g., nitroprusside) to maintain the target blood pressure.
- Prevent vasospasm.
- Limit excessive crystalloid fluid administration.
- Maintain adequate blood product availability.
- Emergence:
- Rapid wake up required for neurologic assessment.
- Similar considerations as intracranial mass management.
- Maintain BP within 20% of baseline.
- Keep PRBCs available in the operating room.
- Induction:
- Two large-bore IVs.
- Type and crossmatch for at least two units of packed red blood cells (PRBCs) in the room.
- Smooth induction.
- Maintain tight blood pressure control.
- Consider propofol, lidocaine, fentanyl, and esmolol during induction.
- Anticipate a potential increase in MAP during clipping.
- If a clamp is applied on the proximal part of the aneurysm, maintain a MAP of approximately 80-100 mmHg.
Cerebral Aneurysm: Intraoperative Rupture
- Most likely to occur during:
- Dura incision (decreased ICP).
- Excessive brain retraction.
- Aneurysm dissection.
- Clipping or clip release.
- Treatment options include:
- Immediate, aggressive volume replacement (PRBCs).
- Lowering MAP to 40-50 mmHg.
- The surgeon may attempt to clip the feeder vessel.
- Consider adenosine (0.3-0.4 mg/kg) to slow the heart rate and decrease blood flow to the aneurysm.
Cerebral Aneurysm: Clipping
- Involves placing a clip at the base of the aneurysm to isolate it from the MAP, thereby preventing further rupture.
Cerebral Aneurysm: Endovascular Coil
- Involves transarterial catheterization to thread a coil into the aneurysm sac.
- Management is similar to open craniotomy aneurysm clipping, with the following key additions:
- Heparin is required, as foreign metal material is introduced into the body.
- Administer a heparin bolus of 70 units/kg.
- Protamine sulfate is administered at the end of the case to reverse the heparin 1 mg for every 100 units of heparin.
Cerebral Vasospasm
- Linked to significant morbidity and mortality after SAH (affects 1 in 4 patients within 4-9 days).
- Free hemoglobin irritates the cerebral vasculature, leading to hyperactive vasculature, cerebral vasoconstriction, and cerebral infarction.
- Most common presentation is a new neurologic deficit or altered level of consciousness (LOC).
- The gold standard for making the diagnosis of cerebral vasospasm is cerebral angiography.
- Prevention and early detection are important:
- Frequent neurologic assessments.
- Daily transcranial Doppler exams.
Cerebral Vasospasm: Treatment
- Maintain CPP (MAP - ICP or CVP).
- Perfusion to ischemic areas is pressure-dependent.
- Increase MAP 20-30 mmHg above baseline.
- Implement Triple H therapy, which includes:
- Hypervolemia (liberal hydration),
- Hemodilution (decreased blood viscosity)
- Hypertension.
- The goal is to achieve a hematocrit of 27-32%.
- Nimodipine is the only calcium channel blocker (CCB) associated with a reduction in morbidity and mortality.
- Nimodipine doesn't relieve vasospasm but improves collateral blood flow.
Traumatic Brain Injury
- Accounts for 15-20% of mortality in individuals aged 5-35 years old.
- Traumatic brain injury is responsible for 50% of all trauma-related deaths.
- Contributing factors include:
- Hypotension,
- Hypoxemia,
- Intracranial hypertension,
- Hematoma, etc.
Traumatic Brain Injury: Initial Management
- Ensure a stable cervical spine, a protected airway, hemodynamic stability, and cerebral protection.
- Obtain a stat non-contrast head CT to assess for intracranial bleeding.
Traumatic Brain Injury: Key Considerations
- Unstable cervical spine.
- A bloody airway or skull base fracture.
- A full stomach (increased aspiration risk).
- Intracranial hypertension.
Traumatic Brain Injury: Blood Thinners
- If a patient is on warfarin, consider reversal with fresh frozen plasma (FFP), recombinant factor VIIa, or vitamin K.
- If the patient is on clopidogrel or aspirin, consider a platelet transfusion (possibly recombinant factor VIIa).
Skull Base Fracture
- Signs and symptoms of a skull base fracture include:
- Raccoon eyes (periorbital ecchymosis).
- Battle's sign (bruising behind one or both ears).
Traumatic Brain Injury: Managing CPP and ICP
- Maintain cerebral perfusion pressure (CPP) while decreasing ICP.
- Excessive hyperventilation can increase cerebral ischemia.
- Use methods to decrease ICP as discussed previously, except:
- Do NOT administer mannitol or hypertonic saline after the first 24 hours of injury.
- Do NOT administer furosemide to patients with a traumatic brain injury who are already receiving mannitol.
- Do NOT administer hypertonic saline in the presence of significant pre-existing hyponatremia.
- Avoid rapid or excessive fluid administration, as this can increase ICP.
- Consider using a ventriculostomy to drain CSF and reduce ICP.
- Monitor intracranial pressure continuously.
Area Postrema
- The area postrema (AP) found in the medulla oblongata is a circumventricular organ (CVO) with a unique characteristic of being permeable to lipid-soluble molecules like anesthetics, CO2, ETOH, O2, and nicotine.
- The AP is also permeable to water-soluble molecules such as amino acids, glucose, mannitol, and proteins.
- It plays a role in triggering vomiting reflexes, which is vital for eliminating toxins from the body.
Cerebral Blood Flow
- Cerebral blood flow (CBF) is the volume of blood flowing through the brain per unit time.
- Normal CBF is 50 mL/100g tissue/min (15% of total cardiac output), resulting in approximately 750 mL/min.
- Ischemia occurs when CBF drops below 20 mL/100g tissue/min, while cell death ensues at 10 mL/100g tissue/min.
- CBF is regulated by an intrinsic mechanism called "flow-metabolism coupling."
- Cerebral blood flow is regulated by five key determinants:
- Cerebral Metabolic Rate of Oxygen (CMRO2)
- Cerebral Perfusion Pressure (CPP)
- Partial Pressure of Carbon Dioxide in Arterial Blood (PaCO2)
- Partial Pressure of Oxygen in Arterial Blood (PaO2)
- Venous Pressure
- The brain utilizes approximately 20% of the body's total oxygen consumption. Of this, 60% aids in electrical activity, and the remaining 40% contributes to maintaining cellular integrity.
Cerebral Metabolic Rate of Oxygen (CMRO2)
- CBF directly correlates with CMRO2, meaning increased demand requires an increased supply of oxygen.
- An increase in CMRO2 leads to an increase in CBF.
- A decrease in CMRO2 results in a decrease in CBF.
- Factors that increase CMRO2 include seizures, ketamine, nitrous oxide (N2O), and hyperthermia.
- Factors that decrease CMRO2 include halogenated anesthetics, intravenous anesthetics (propofol, etomidate, barbiturates), and hypothermia.
- Note that hypothermia decreases CMRO2 by 7% per 1°C decrease in body temperature.
- Suppression of CMRO2 can be achieved at temperatures between 18-20°C.
Cerebral Perfusion Pressure (CPP)
- CPP is the driving force of blood flow to the brain.
- Computed as CPP= (MAP – ICP or CVP), whichever value is higher.
- Autoregulation of CBF is maintained when CPP is between 50-150 mmHg.
- Autoregulation can become impaired by factors such as irregular respirations leading to medullary exhaustion.
- Below 50 mmHg, the cerebral vessels are maximally vasodilated in an attempt to increase CBF, while above 150 mmHg, vascular constriction occurs to limit CBF.
Monro-Kellie Hypothesis
- The Monro-Kellie hypothesis explains the interplay of volume changes within the rigid skull.
- The skull is considered a rigid box containing three compartments:
- The brain (80%)
- Blood (12%)
- Cerebrospinal fluid (CSF) (8%)
- An increase in one compartment's volume necessitates a decrease in another to maintain constant intracranial pressure.
- Increased volume in each compartment can be caused by:
- Brain: Swelling, tumors
- Blood: Increased CBF (volatile anesthetics, vasodilators), bleeding
- CSF: Increased production, decreased reabsorption, impaired blood-brain barrier (BBB), CSF flow obstruction
- The body attempts to compensate for increased volume in the first two compartments.
- Compensation failure begins when both the second and third compartments are affected, leading to symptoms of intracranial hypertension (ICH) and focal ischemia.
- Global ischemia and intracranial herniation become potential risks when the third and fourth compartments are affected.
Ways to Lower ICP
- Hyperventilation: This can decrease ICP, but the effect is temporary (4-6 hours).
- Mannitol: Used as an osmotic diuretic (0.25-1 g/kg).
- Furosemide: Another diuretic (0.5-1 mg/kg).
- Corticosteroids: Can reduce brain swelling.
- Fluid Restriction: Limits fluid buildup in the brain.
- Elevating the Head of Bed: Promotes drainage of CSF.
- Hypothermia: Not recommended for traumatic brain injury.
- Maintaining Normotensive to Slightly Hypertensive Blood Pressure: Increases CPP and improves CBF.
Anatomy & Physiology Review
- The CNS is composed of neurons and glial cells, with neurons functioning as the functional unit
- Glial cells provide support and protection for neurons, including astrocytes for metabolic regulation and the blood-brain barrier, oligodendrocytes for myelin sheath production in the CNS, ependymal cells for CSF production, and microglia for phagocytosis of debris
Cerebrospinal Fluid
- CSF cushions the brain and spinal cord, provides buoyancy, and maintains ideal conditions for neurological function
- CSF is produced by the choroid plexus in the ventricles at a rate of ~20 mL/hr with a total volume of ~150 mL
- Normal ICP is 5-15 mmHg and elevated ICP > 20 mmHg can cause various symptoms including headache, nausea, vomiting, papilledema, decreased level of consciousness, seizures, coma etc.
- The Monro-Kellie hypothesis states that the cranium is a rigid box with three volumes: brain (80%), blood (12%), and CSF (8%). An increase in one volume requires a decrease in others to maintain the same pressure.
Blood Brain Barrier
- Separates the CSF from the plasma
- Restricts passage of large molecules and ions greater than 500 daltons, polar molecules (amino acids, glucose, mannitol), water-soluble drugs, and proteins
- Permeable to lipid-soluble molecules (anesthetics, CO2, ethanol, O2, nicotine)
- Not present in intracranial tumors, head trauma, areas exposed to volatile anesthetics, and chronic hypertension
PaCO2
- Directly correlates with CBF: an increase in PaCO2 increases CBF
- A 1 mmHg increase in PaCO2 leads to a 1-2 mL/100g brain tissue/min increase in CBF and vice versa
- Maximum vasodilation occurs at 80-100 mmHg PaCO2 and maximum vasoconstriction occurs at 25 mmHg
PaO2 & Venous Pressure
- PaO2 < 50-60 mmHg leads to cerebral vasodilation and increased CBF, but PaO2 > 60 mmHg does not affect CBF
- Increased CVP decreases cerebral drainage and increases cerebral volume, impairing venous drainage
- Jugular compression, increased intrathoracic pressure, thrombosis and vena cava syndrome can also impair venous drainage
Intracranial Pressure
- Cushing's triad includes hypertension, bradycardia, and irregular respiration as a result of increased ICP
- The body attempts to maintain perfusion with hypertension, bradycardia is caused by baroreceptor reflex, and irregular respirations are a result of medullary compression
Ways to Lower ICP
- Hyperventilation can lower ICP but its effect lasts only 4-6 hours
- Mannitol (0.25-1 g/kg), furosemide (0.5-1 mg/kg), corticosteroids, fluid restriction, elevating the head of bed (HOB), hypothermia, and maintaining normotensive to slightly hypertensive blood pressure are other treatment options for managing ICP.
Cerebral Protection: Ischemic & Reperfusion
- The brain is susceptible to rapid ischemic injury due to its high rate of oxygen and glucose consumption, inability to store substrate, and its limited ability to dispose of toxic metabolites quickly
- Global ischemia due to severe hypotension or anemia requires interventions to restore total cerebral perfusion
- Focal ischemia is a regional insult treated by focusing on the affected region
- A “penumbra” of salvageable tissue usually surrounds the necrotic core, requiring augmentation of CPP while minimizing reperfusion injury
Cerebral Protection: Ventilation Management
- Mechanical ventilation should be managed with tidal volume (Vt) of 6-8 mL/kg, peak pressure less than 40 cmH2O and no PEEP unless needed for oxygenation
- Positive pressure ventilation (PPV) is used to control ventilation and PaCO2 and minimize the risk of venous air embolism (VAE) in sitting position
Cerebral Protection: Fluids & Electrolytes
- Euvolemia should be maintained with isotonic or slightly hypertonic solutions
- Avoid glucose-containing solutions as glucose is quickly metabolized and not osmotically active, potentially causing cerebral edema
- Ideal blood glucose levels are 90-280 mg/dL, with hypoglycemia leading to a lack of glucose for ATP production and hyperglycemia leading to increased lactic acid production
- If diabetes insipidus (DI) is present, hypotonic solutions are acceptable but excessive sodium chloride can cause hyperchloremic metabolic acidosis
Tumor Resection
- Preoperative evaluation should identify problems for appropriate planning, including intracranial mass lesion, elevated ICP, coughing, vomiting, and pain management
Intracranial Tumors
- In adults, supratentorial lesions are more common from CNS support cells
- The most common metastatic tumor to the brain include melanoma or those that originate in the lung, breast, or kidney
- The major concern with intracranial tumors is elevated ICP
Infratentorial & Posterior Fossa Tumors
- These tumors are located in close proximity to the brainstem which often leads to significant hemodynamic distress
- Often require postoperative intubation and mechanical ventilation
- May require prone, lateral, or sitting positioning
- Pose significant risk for venous air embolism (VAE)
Cerebral Aneurysm
- Saccular aneurysm is the most common cause of subarachnoid bleeding
- Arterial bleeding leads to subarachnoid space, venous bleeding leads to subdural space
- The most common sign of subarachnoid hemorrhage (SAH) is a "worst headache of my life"
- Transmural pressure (TMP) = MAP - ICP
-
Factors influencing aneurysm rupture:
- Increased Transmural pressure
- Diameter > 2.5 cm
- Smoking
- Excessive alcohol consumption
- Recreational drugs
- Age > 40
- Female
- Systemic hypertension
Cerebral Aneurysm: Surgical Options
- Surgical options include aneurysm clipping or endovascular coiling
- Intervention should take place within 48 hours of initial bleeding
- Preinduction: Limit sedation to avoid hypercapnia, obtain arterial line, 2 large bore IVs, transfuse 2-4 units of PRBCs, smooth induction
- Maintenance: Use TIVA vs. Volatile anesthetics, keep blood pressure 15-20% below baseline, minimize fluid administration
- Emergence: Rapid wake-up for neuro assessment, limit excess crystalloids, consider similar considerations as intracranial mass, keep blood pressure within 20% of baseline, use propofol, lidocaine, fentanyl, and esmolol
Cerebral Aneurysm: Intraoperative Rupture
- Most likely to occur during:
- Dural incision
- Excessive brain retraction
- Aneurysm dissection
- Clipping or clip release
-
Treatment includes:
- Immediate, aggressive volume replacement (PRBC)
- Lowering MAP to 40-50 mmHg
- Surgeon attempting to clip the feeder vessel
- Use of adenosine (0.3-0.4 mg/kg)
Cerebral Aneurysm: Clipping & Endovascular Coiling
- Clipping involves placing a clip at the base of the aneurysm to prevent rupture
- Endovascular coiling involves transarterial catheterization to thread a coil into the aneurysm sac
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Description
Test your knowledge on the effects of PaCO2 on cerebral blood flow and the various factors affecting intracranial pressure. This quiz covers conditions like subarachnoid hemorrhage and related clinical scenarios. Understand the key physiological responses and clinical implications in neurology.
