Intracranial Procedures Notes PDF Fall 2022

NA 741 Principles of Anesthesia II Fall 2022 Intracranial Procedures Anatomy & Physiology Review CNS Cells Cerebrospinal Fluid Cushions brain, provides buoyancy, & provides ideal conditions for neurologic function Loc...

NA 741 Principles of Anesthesia II Fall 2022 Intracranial Procedures Anatomy & Physiology Review CNS Cells Cerebrospinal Fluid Cushions brain, provides buoyancy, & provides ideal conditions for neurologic function Locations o Ventricles (L/R lateral, 3rd, 4th) o Around brain o Subarachnoid space in the brain and spinal cord Production o Choroid plexi in ventricles @ 20 mL/hr o Volume ~ 150 mL at any given time o ICP = 5 – 15 mmHg Reabsorption o Arachnoid villi at superior sagittal sinus into venous circulation via pressure gradient CSF Plasma Osmolarity 295 295 (mOsm/L) Na+ (mEq/L) 138 138 K+ (mEq/L) 2.8 4.5 Cl- (mEq/L) 119 102 HCO3- (mEq/L) 22 24 PaCO2 (mmHg) 47 40 pH 7.33 7.40 Glucose (mg/dL) 60 90 Protein (mg/dL) 35 7000 M. Lane 1 NA 741 Principles of Anesthesia II Fall 2022 Blood Brain Barrier Areas of the brain that are NOT Separates CSF from plasma inside the BBB: Endothelial cell tight junctions restrict passage of large molecules & ions 1. CRTZ o Substances with molecular weight > 500 daltons 2. Area Postrema o Polar molecules (amino acids, glucose, mannitol) 3. Posterior pituitary o Water soluble drugs 4. Pineal gland o Proteins 5. Choroid plexus Permeable to lipid-soluble molecules 6. Hypothalamus o Anesthetics, CO2, ETOH, O2, nicotine Cerebral Blood Flow Arterial Venous o Anterior o Cortex/cerebellum § Internal carotid arteries à Circle of § Superior sagittal sinus Willis à hemispheres § Dural sinus § 80% of CBF o Basal brain o Posterior § Inferior sagittal sinus § Vertebral arteries (via subclavian) à § Vein of Galen Basilar artery à Posterior brain and § Straight sinuses cervical spinal cord o All blood exits brain into jugular veins § 20% of CBF Cerebral blood flow is regulated by “flow-metabolism coupling” Normal CBF is 50 mL/100g tissue/min (15% CO) o 750 mL/min (15% of CO) Ischemia occurs at 20 mL/100g tissue/min Cell death occurs at 10 mL/100g tissue/min Five Key Determinants of Cerebral Blood Flow 1. Cerebral Metabolic Rate (CMRO2) 2. Cerebral Perfusion Pressure (CPP) 3. PaCO2 4. PaO2 5. Venous Pressure CMRO2 CBF has direct correlation with CMRO2 (↑ demand = ↑ supply) o ↑ CMRO2 = ↑ CBF o ↓CMRO2 = ↓ CBF Oxygen consumption o 20% of total body oxygen consumption o 60% for electrical activity o 40% for cellular integrity o Takeaway: can only ↓ CMRO2 up to 60% Increase CMRO2: o Seizures o Ketamine o N2O o Hyperthermia Decrease CMRO2: o Halogenated anesthetics o IV anesthetics (Propofol, Etomidate, Barbiturates) o Hypothermia: ↓ 7% per 1o C body temperature (suppression @ 18-20o C) M. Lane 2 NA 741 Principles of Anesthesia II Fall 2022 Cerebral Perfusion Pressure (CPP) CPP = MAP – ICP (or CVP); whichever is higher CBF autoregulation is maintained when CPP is between 50-150 mmHg CPP effect on CBF CPP = MAP – ICP (or CVP) < 50 mmHg cerebral vessels are maximally vasodilated in effort to ↑ CBF 50 - 250 mmHg constant and consistent CBF CBF = CPP/CVR cerebral vessels are maximally vasoconstricted in effort to ↓ > 150 mmHg CBF o Note: do NOT confuse CPP with MAP When is autoregulation impaired? o Intracranial Tumor o Volatile anesthetics o Head Trauma o Chronic HTN (right shift in CPP curve) PaCO2 PaCO2 has a direct correlation with CBF: ↑ PaCO2 = ↑ CBF o CSF pH alters cerebral arteriolar diameter PaCO2 effect on CBF 80 – 100 mmHg cerebral vessels are maximally vasodilated in effort to ↑ CBF for each 1 mmHg change in PaCO2, there is a 1-2 mL/100g/min 26 – 80 mmHg change in CBF cerebral vessels are maximally vasoconstricted in effort to ↓ < 25 mmHg CBF Think about how respiratory acidosis/alkalosis affect CBF Metabolic acidosis does NOT affect CBF à H+ can’t cross BBB PaO2 & Venous Pressure PaO2 PaO2 effect on CBF < 50 – 60 mmHg cerebral vessels are vasodilated in effort to ↑ CBF > 60 mmHg NO EFFECT on CBF Venous Pressure o ↑ CVP = ↓ cerebral drainage = ↑ cerebral volume o Impairing venous drainage § Jugular compression (positioning: tucking the chin can impair venous drainage) § ↑ intrathoracic pressure (cough, PEEP) § Thrombosis § Vena cava syndrome Intracranial Pressure (ICP) Cushing’s Triad Normal ICP: 5 – 15 mmHg 1. HTN (body’s attempt to maintain Intracranial HTN: ICP > 20 mmHg perfusion) o S/S: HA, N/V, papilledema, ↓LOC, seizure, coma 2. Bradycardia (baroreceptor reflex) Initial rise in volume is compensated by shunting CSF into spinal cord, once 3. Irregular respirations (medullary exhausted then CPP (and therefore CBF) begins to suffer compression) Monro-Kellie Hypothesis o Cranium = rigid box with 3 volumes: 1. Brain = 80% 2. Blood = 12% 3. CSF = 8% o ↑ in one requires a ↓ in others to maintain the same pressure o Causes of increased volume for each component § Brain à swelling, tumor, etc. § Blood à increased CBF (volatile anesthetics, vasodilators, etc) and bleeding § CSF à increased CSF production, decreased CSF reabsorption, impaired BBB, CSF flow obstruction o Points 1 – 2 are compensated o Points 2 – 3 is where compensation begins to fail and you start having s/s of intracranial HTN and focal ischemia o Points 3-4 is where you start having risk of global ischemia & intracranial herniation M. Lane 3 NA 741 Principles of Anesthesia II Fall 2022 Ways to Lower ICP o Hyperventilate (effect lasts 4-6 hours) o Mannitol 0.25-1 g/kg o Furosemide 0.5-1 mg/kg o Corticosteroids o Restrict Fluids o Elevate HOB o Hypothermia (not recommended for CHI) o Normotensive to slightly hypertensive Cerebral Blood Flow Summary Graph o Below autoregulation limit à vessels are maximally dilated à pressure dependent o Above autoregulation limit à vessels are maximally constricted à pressure dependent o The vessel diameter is only blue because the graph had MAP as blue. Cerebral Protection Ischemic & Reperfusion Brain is susceptible to rapid ischemic injury o High rate of oxygen & glucose consumption o Unable to store oxygen and glucose à very dependent on adequate blood flow o Unable to dispose of toxic metabolites quickly Global ischemia 2/2 severe hypotension or anemia o Treated with interventions aimed to restore total cerebral perfusion Focal ischemia is a regional insult o Treatment focused on the region in question o A “penumbra” of salvageable tissue usually surrounds the necrotic core o Augment CPP while decreasing reperfusion injury § Restoration of flow = ↑ free radicals & inflammatory mediators = exacerbation of injury Ventilation Management Vt 6-8 mL/kg Peak pressure < 40 cmH2O No PEEP unless needed for oxygen requirement o PEEP ↓ cerebral venous drainage & ↓ CO PPV to control ventilation & PaCO2 o Also ↓ risk for VAE when in sitting position Fluids & Electrolytes Euvolemia with isotonic or slightly hypertonic solutions Avoid glucose containing solutions o Glucose is quickly metabolized and is not osmotically active à cerebral edema o Ideal BG: 90-280 mg/dL § Hypoglycemia: no glucose for ATP § Hyperglycemia: more glucose is converted to lactic acid if ischemia is present Diabetes Insipidus is a loss of intravascular water à hypotonic solutions acceptable Excessive NaCL: hyperchloremic metabolic acidosis Tumor Resections Preoperative Evaluation Identify problems to plan appropriately o Intracranial mass lesion & ↑ ICP § Most important information is presence/extent of intracranial hypertension (H&P, MRI, CT, etc.) § HA, dizziness, visual/gait disturbances, N/V, seizures, altered LOC, confusion, papilledema, loss of strength/sensation, cranial nerve dysfunction, etc. Premedication limited or avoided completely o Be extremely careful with drugs that depress respiration (↑PaCO2) Continue steroids & anticonvulsant therapy Induction & Airway Management Goal is limit changes in ICP & CPP Consider preinduction A-line, osmotic diuresis, or CSF drainage Hypotension & hypoventilation must be avoided Strict BP control during intubation (↑ r/f herniation) Propofol as induction agent M. Lane 4 NA 741 Principles of Anesthesia II Fall 2022 Blunt SNS from laryngoscopy: Fentanyl (1-2 μg/kg), Lidocaine (1-1.5 mg/kg), or esmolol 10-20 mg Adequate vascular access is mandatory o 2 large bore IVs + arterial line (possible CVL) Mayfield pins after induction & vascular access o Adm propofol, opioids, or esmolol to blunt Excessive neck flexion/extension/rotation can compress IJ and impair cerebral venous drainage ICP control is paramount until dura is opened HD instability must be minimized d/t impaired autoregulation o Hypotension = ischemia o Hypertension = ↑ r/f bleeding and edema Decreasing ICP & Increasing Exposure: manipulating the variables of the Monro-Kellie hypothesis Vascular Compartment CSF Compartment Cellular Compartment (reducing cerebral blood volume) (reducing CSF volume) (reducing cellular edema) o No PEEP o Ventriculostomy o Mannitol (0.25-1 g/kg) or o Hyperventilation Lasix (0.5-1 mg/kg) o Limit Volatile Anesthetic o Hypertonic saline (3% @ 50- o HOB elevated 100 mL/hr) o Limit IVF to euvolemia o Steroids Maintenance of Anesthesia Avoid increases in ICP (at least until dura is opened) Maintaining CPP Neuromonitoring requirements Fluid maintenance with dextrose-free-iso-osmolar crystalloid or colloids to achieve euvolemia Rapid Emergence is the goal (Short-acting, easily titratable drugs) o Propofol, remifentanil, sevoflurane, desflurane, possibly N2O Maintenance of Anesthesia: Drugs Volatile Gas < 0.5 MAC (cerebral vasodilation) Propofol gtt 50-300 μg/kg/min (depends on VA use) Remifentanil 0.05-2 μg/kg/min (IBW) o Beware of opioid-induced hyperalgesia o Low-dose ketamine or magnesium sulfate can help attenuate this Emergence from Anesthesia Patients with normal GCS (13-15) are usually extubated HD control is paramount (HTN can lead to worsening cerebral edema) o Labetalol, esmolol, nicardipine, etc. on hand o Coughing or vomiting can be deleterious § Careful titration of opioids and antiemetics o Control pain without obtunding patient § Short-acting opioids, IV acetaminophen, LA infiltration by surgeon, dexmedetomidine, etc. Types of Tumors Intracranial Tumors In adults, supratentorial lesions are more common from CNS support cells (gliomas, astrocytomas, oligodendrogliomas, etc.) Most common metastatic tumor to the brain includes melanoma or those that originate in the lung, breast, or kidney Primary concern is usually elevated ICP Infratentorial & Posterior Fossa Tumors Close proximity to brainstem o More HD distress, changes in respiratory control, and arousal changes o Altered respiratory patterns, cardiac dysrhythmias, or CN dysfunction More frequently require postoperative intubation and mechanical ventilation Positioning can be prone, lateral, or sitting o Particular risk for VAE: especially if patient is spontaneously ventilating Cerebral Aneurysms Saccular aneurysm: most common cause of subarachnoid bleeding o Arterial bleeding à subarachnoid space o Venous bleeding à subdural space Essential causes of rupture = ↑ aneurysmal distention pressure o ↑ MAP = ↑ distention = ↑ aneurysm radius = ↑ wall tension o ↓ ICP = ↓ distention = ↓ aneurysm radius = ↓ wall tension Most common sign of SAH is “worst headache of my life” o Syncope, N/V, photophobia, fever, obstructive hydrocephalus, etc. Aneurysm and Transmural Pressure o MAP = pressure pushing outwards (making rupture more likely) M. Lane 5 NA 741 Principles of Anesthesia II Fall 2022 o ICP = pressure pushing inwards (making rupture less likely; like a tamponade effect) Rupture more likely with: HTN, drop in ICP Most common aneurysm locations in Circle of Willis o ACA = 40% o MCA = 25% o PCA = 25% o BA = 10% Rupture Risk o ↑ transmural pressure (TMP = MAP – ICP) o Diameter > 2.5 cm (Laplace) o Smoking o Excessive EtOH o Recreational drugs o Age > 40 o Female o Systemic HTN Surgical options: aneurysm clipping or endovascular coiling o Intervention should take place within 48 hours of initial bleeding Induction of Anesthesia Limit preoperative sedation to avoid hypercapnia A-line for induction 2 large bore IV’s Type and Cross 2-4 units PRBCs; have them in the room Smooth induction with tight BP control o Propofol, Lidocaine o Fentanyl, Esmolol Maintenance of Anesthesia TIVA vs. Volatiles BP 15-20% below baseline o Prevent vasospasm o ↓ EBL Limit excess crystalloids Clipping: may ↑ MAP Clamping: when the parent vessel is clamped, increase MAP ~ 80-100 mmHg to ensure adequate collateral blood flow Emergence from Anesthesia Need rapid wake up for neuro assessment Similar considerations as intracranial mass Keep BP within 20% of baseline Cerebral Aneurysm: Intraoperative Rupture Most likely during: o Dural Incision (↓ ICP) o Excessive brain retraction o Aneurysm dissection o Clipping or clip release Treatment o Volume: Immediate, aggressive volume replacement (PRBC) o Pressure: ↓ MAP to 40-50 mmHg o Visualization: Surgeon will attempt to clip feeder vessel à may need adenosine 0.3-0.4 mg/kg à transient cardiac arrest to halt blood flow and improve visualization Cerebral Aneurysm Clipping and Endovascular Coil Clipping Endovascular Coil Involves placing a clip at the base of aneurysm involves transarterial catheterization to thread coil into Removes aneurysm from MAP so it can’t rupture aneurysm sac. anymore A neuro-interventional radiology procedure Treated the same as an open craniotomy aneurysm clip with the addition of heparin (necessary when a foreign metal material is being implanted into the body) o Heparin 70 units/kg bolus o Protamine at end of case: 1mg for every 100 units of heparin M. Lane 6 NA 741 Principles of Anesthesia II Fall 2022 Cerebral Vasospasm Linked to morbidity/mortality after SAH (1:4 patients w/I 4-9 days) Free Hgb irritate vasculature à hyperactive vasculature à cerebral vasoconstriction à cerebral infarction Most common presentation: new neurologic deficit or altered LOC Gold standard for diagnosis: cerebral angiography Prevention/detection: frequent neuro checks and/or daily transcranial doppler exam Cerebral Vasospasm: Treatment Maintain CPP (MAP-ICP or CVP) Perfusion to ischemic areas is pressure dependent because the blood vessels supplying ischemic areas are already maximally vasodilated; therefore, MAP will need to be increased 20 – 30 mmHg above baseline to maintain CPP Triple H Therapy = Hypervolemia + Hemodilution + Hypertension o Liberal hydration (↓ viscosity) + ↑ BP = ↑ CBF o Goal Hct = 27-32% Nimodipine is the only CCB associated with ↓ morbidity/mortality o Does NOT relieve vasospasm, but instead it increases collateral flow Traumatic Brain Injury 15-20% of mortality in ages 5-35 50% of all deaths related to trauma o Hypotension, hypoxemia, intracranial HTN, hematoma, etc. Ensure stable C-spine, protected airway, HD stability, & cerebral protection Stat non-contrast head CT to assess for bleeding Key considerations o Unstable C-spine o Bloody airway or skull-base fracture o Full stomach o Intracranial HTN Blood thinners? o Warfarin reversal with FFP, recombinant factor 7a, or vitamin K o Clopidogrel or aspirin reversed with plt transfusion (possibly recombinant VII) Skull Base Fracture o Raccoon Eyes: Periorbital ecchymosis o Battle’s sign: bruise behind one or both ears Traumatic Brain Injury Anesthetic Implications Maintain CPP while decreasing ICP o Too much hyperventilation can ↑ ischemia o Use methods to ↓ ICP previous discussed, EXCEPT: DO NOT GIVE…. STEROIDS or possibly mannitol o Hypertonic saline ideal o Avoid N2O because you don’t know what other injuries are present o Avoid colloids and hypotonic solutions Ventriculoperitoneal Shunt VP shunt allows excess CSF to drain into peritoneal cavity 3 key parts o Burr hole access through dura o Abdominal incision o Subcutaneous tunneling from head to abd (connect the sites) o Catheter passed through Most stimulating portion is usually tunneling M. Lane 7