Intracranial Procedures PDF

Intracranial Procedures Hunter Speeg, DNP, CRNA Outline Anatomy & Physiology Review Basic Management of intracranial procedures Tumors Aneurysms Traumatic Brain Injury VP Shunt CNS Cells BRAI Functional...

Intracranial Procedures Hunter Speeg, DNP, CRNA Outline Anatomy & Physiology Review Basic Management of intracranial procedures Tumors Aneurysms Traumatic Brain Injury VP Shunt CNS Cells BRAI Functional N Nerve Unit “glue” Neuron Glial Ependym Oligodendrocyt Pseudounipola al es r Astrocyt -Choroid plexus -Myelin Sheath for CNS Microglia Multipola - Dorsal Root Ganglion Bipolar es -CSF production **Don’t confuse with r - -Most abundant Schwann cells** -Macrophages - Most abundant Retina - -Metabolic -Phagocytize Ear regulation debris - Blood brain Barrier -Neuronal injury repair - Secrete & absorb Glutamate, GABA, & ATP Cerebrospinal Fluid L/R Ventricles Cushions brain, provides buoyancy, & Foramen of provides ideal conditions for neurologic Monro function 3rd Ventricle Locations Ventricles (L/R lateral, 3rd, 4th) Aqueduct of Sylvius Around brain 4th Ventricle SA space in brain/spinal cord Production Foramen of Foramen of Choroid plexi in ventricles @ 20 mL/hr Luschka Magendie Volume ~ 150 mL at any given time (paired) ICP = 5 – 15 mmHg Subarachnoid Space + Reabsorption Central Canal Arachnoid villi at superior sagittal sinus Superior into venous circulation via pressure Sagittal gradient Sinus Cerebrospinal Fluid Cerebrospinal Fluid 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 Blood Brain Barrier Separates CSF from plasma Endothelial cell tight junctions restrict passage of large molecules & ions Substances with molecular weight > 500 daltons Polar molecules (amino acids, glucose, mannitol) Water soluble drugs Proteins Permeable to lipid-soluble molecules Anesthetics, CO2, ETOH, O2, nicotine Blood Brain Barrier Areas not present: 1. CRTZ 2. Area Prostrema 3. Posterior pituitary 4. Pineal gland 5. Choroid plexus 6. Hypothalamus Cerebral Blood Flow Arterial Venous Anterior Cortex/cerebellum Internal carotid arteries  Superior sagittal sinus Circle of Willis  hemispheres Dural sinus 80% of CBF Basal brain Posterior Inferior sagittal sinus Vertebral arteries (via Vein of Galen subclavian)  Basilar artery  Straight sinuses Posterior brain and cervical spinal cord All blood exits brain into jugular 20% of CBF veins Cerebral Circulation Arterial Venous A Bigger Picture Cerebral Blood Flow Regulated by “flow-metabolism coupling” Normal = 50mL/100g tissue/min (15% CO) 750 mL/min (15% of CO) Ischemia = 20 mL/100g tissue/min Cell death = 10 mL/100g tissue/min CBF CPP = CVR Five Key Determinants 1. Cerebral Metabolic Rate (CMRO2) 2. Cerebral Perfusion Pressure 3. PaCO2 4. PaO2 5. Venous Pressure  CMRO2 CBF has direct correlation with Increasing CMRO2 (↑ demand = ↑ supply) Seizures ↑ CMRO2 = ↑ CBF Ketamine ↓CMRO2 = ↓ CBF N2O Hyperthermia Oxygen consumption 20% of total body oxygen Decreasing consumption Halogenated anesthetics 60% for electrical activity IV anesthetics (Propofol, Etomidate, 40% for cellular integrity Barbiturates) Takeaway: can only ↓ CMRO2 up to Hypothermia 60% - ↓ 7% per 1o C body temperature (suppression @ 18-20o C) Cerebral Perfusion Pressure CPP = MAP – ICP (or CVP); whichever is higher CPP = MAP – ICP (or CBF autoregulation  CPP b/w 50-150 mmHg CVP) < 50 mmHg = max vasodilation 50-150 mmHg = constant/consistent CBF > 150 mmHg = max vasoconstriction CBF CPP Note: do NOT confuse CPP with MAP = CVR When is autoregulation impaired? Intracranial Tumor Head Trauma Volatile anesthetics Chronic HTN (right shift in CPP curve) PaCO2 Direct correlation with CBF ↑ PaCO2 = ↑ CBF CSF pH alters cerebral arteriolar diameter ↑ 1 mmHg PaCO2 = ↑ 1-2 mL/100g brain tissue/min ↓ 1 mmHg PaCO2 = ↓ 1-2 mL/100g brain tissue/min Max vasodilation = 80-100 mmHg Max vasoconstriction = 25 mmHg Think about how respiratory acidosis/alkalosis affect CBF Metabolic acidosis does NOT affect CBF  H+ can’t cross BBB PaO2 & Venous Pressure PaO2 Venous Pressure PaO2 < 50-60 mmHg = ↑ CVP = ↓ cerebral cerebral vasodilation = drainage = ↑ cerebral ↑CBF volume PaO2 > 60 mmHg does NOT Impairing venous drainage affect CBF Jugular compression (positioning) ↑ intrathoracic pressure (cough, PEEP) Thrombosis Vena cava syndrome Intracranial Pressure Normal = 5 – 15 mmHg Cushing’s Triad Intracranial HTN 1. HTN (body’s attempt to ICP > 20 mmHg maintain perfusion) S/S = HA, N/V, papilledema, 2. Bradycardia (baroreceptor ↓LOC, seizure, coma reflex) Initial rise in volume is 3. Irregular respirations compensated by shunting (medullary compression) CSF into spinal cord, once exhausted then CPP (and therefore CBF) begins to suffer Intracranial Pressure Monro-Kellie Hypothesis Cranium = rigid box with 3 volumes: Brain = 80% Blood = 12% CSF = 8% Cerebr al ↑ in one requires a ↓ in others ischem ia to maintain the same pressure ↓ CBF Edema ↓ CPP ↑ ICP Ways to Lower ICP Hyperventilate (effect lasts 4-6 hours) Mannitol 0.25-1 g/kg Furosemide 0.5-1 mg/kg Corticosteroids Restrict Fluids Elevate HOB Hypothermia (not recommended for CHI) Normotensive to slightly hypertensive Cerebral Blood Flow Summary Graph Arterial Vessel Diameter r/t MAP ICP Cerebral Protection: Ischemic & Reperfusion Brain is susceptible to rapid ischemic injury High rate of oxygen & glucose consumption Unable to store substrate Unable to dispose of toxic metabolites quickly Global ischemia s/t severe hypotension or anemia Treated with interventions aimed to restore total cerebral perfusion Focal ischemia is a regional insult Treatment focused on the region in question A “penumbra” of salvageable tissue usually surrounds the necrotic core Augment CPP while decreasing reperfusion injury Restoration of flow = ↑ free radicals & inflammatory mediators = exacerbation of injury Cerebral Protection: Ventilation Management Vt 6-8 mL/kg Peak pressure < 40 cmH2O No PEEP unless needed for oxygen requirement PEEP ↓ cerebral venous drainage & ↓ CO PPV to control ventilation & PaCO2 Also ↓ risk for VAE when in sitting position Cerebral Protection: Fluids & Electrolytes Euvolemia with isotonic or slightly hypertonic solutions Avoid glucose containing solutions Glucose is quickly metabolized and is not osmotically active  cerebral edema Ideal BG = 90-280 mg/dL Hypoglycemia = no glucose for ATP Hyperglycemia = more glucose converted to LA if ischemia is present If DI  hypotonic solutions acceptable Excessive NaCL = hyperchloremic metabolic acidosis Tumor Resection Preoperative Evaluation Identify problems to plan appropriately 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 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 Blunt SNS from laryngoscopy: Fentanyl (1-2 μg/kg), Lidocaine (1-1.5 mg/kg), or esmolol Induction & Airway Management Adequate vascular access is mandatory 2 large bore IVs + arterial line (possible CVL) Mayfield pins after induction & vascular access 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 Hypotension = ischemia Hypertension = ↑ r/f bleeding and edema Decreasing ICP & Increasing Exposure No PEEP Hyperventilation Limit Volatile Anesthetic Vascular Compartment: Cerebral Blood HOB elevated Volume Reduction Limit IVF to euvolemia CSF Compartment: CSF Reduction Ventriculostomy Mannitol (0.25-1 g/kg) or Lasix (0.5-1 mg/kg) Hypertonic saline (3% @ 50-100 Cellular Compartment: Edema Reduction mL/hr) 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) 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) Beware of opioid-induced hyperalgesia 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) Labetalol, esmolol, nicardipine, etc. on hand Coughing or vomiting can be deleterious Careful titration of opioids and antiemetics Control pain without obtunding patient Short-acting opioids, IV acetaminophen, LA infiltration by surgeon, dexmedetomidine, etc. 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 More HD distress, changes in respiratory control, & arousal changes Altered respiratory patterns, cardiac dysrhythmias, or CN dysfunction More frequently require postoperative intubation & mechanical ventilation Positioning can be prone, lateral, or sitting Particular risk for VAE Cerebral Aneurysm Cerebral Aneurysm Saccular aneurysm = most common cause of subarachnoid bleeding Arterial bleeding  subarachnoid space Venous bleeding  subdural space Essential causes of rupture = ↑ aneurysmal distention pressure ↑ MAP = ↑ distention = ↑ aneurysm radius = ↑ wall tension ↓ ICP = ↓ distention = ↓ aneurysm radius = ↓ wall tension Most common sign of SAH is “worst headache of my life” Syncope, N/V, photophobia, fever, obstructive hydrocephalus, Aneurysm and Transmural Pressure Transmural Pressure = MAP - ICP Dura Mater Arachnoid Mater CS Subarachnoid F Space ICP MAP ICP MAP Perfusion Pia Mater Brain Tissue Cerebral Aneurysm Aneurysm locations in Circle of Willis 40% ACA = 40% MCA = 25% PCA = 25% 25% BA = 10% Rupture Risk ↑ transmural pressure (TMP = MAP – ICP) Diameter > 2.5 cm (Laplace) Smoking Excessive EtOH 25% Recreational drugs Age > 40 Female 10% Systemic HTN Cerebral Aneurysm Surgical options = aneurysm clipping or endovascular coiling Intervention should take place within 48 hours of initial Preinduction Maintenance Emergence bleeding TIVA vs. Volatiles Limit sedation Need rapid wake up (hypercapnia) BP 15-20% below baseline for neuro A-line for induction Prevent vasospasm assessment ↓ EBL 2 large bore IV’s Similar Limit excess crystalloids considerations as T&C 2-4 units PRBCs (in Have PRBC in room intracranial mass room) May ↑ MAP during clipping BP within 20% of Smooth induction If clamp: MAP ~ 80-100 baseline Tight BP control mmHg Propofol, Lidocaine Fentanyl, Esmolol Cerebral Aneurysm: Intraoperative Rupture Most likely during: Dural Incision (↓ ICP) Excessive brain retraction Aneurysm dissection Clipping or clip release Treatment Volume Immediate, aggressive volume replacement (PRBC) Pressure ↓ MAP to 40-50 mmHg Visualization Surgeon will attempt to clip feeder vessel May need adenosine 0.3-0.4 mg/kg Cerebral Aneurysm Clipping Involves placing a clip at the base of aneurysm Removes aneurysm from MAP so it can’t rupture anymore Endovascular Coil involves transarterial catheterization to thread coil into aneurysm sac. A neuro-interventional radiology procedure Treated the same as an open craniotomy aneurysm clip, except you have to give heparin because a foreign metal material is being implanted into the body Heparin 70 units/kg bolus Protamine at end of case: 1mg for every 100 units of heparin Cerebral Vasospasm Linked to morbidity/mortality after SAH (1:4 patients w/I 4-9 days) Free Hgb irritate vasculature  hyperactive vasculature  cerebral vasoconstriction  cerebral infarction Most common presentation = new neurologic deficit or altered LOC Gold standard for diagnosis = cerebral angiography Prevention/detection Frequent neuro checks Daily transcranial Doppler exam Cerebral Vasospasm: Treatment Maintain CPP (MAP-ICP or CVP) Perfusion to ischemic areas is pressure dependent ↑ MAP 20-30 mmHg above baseline Triple H Therapy = Hypervolemia + Hemodilution + Hypertension Liberal hydration (↓ viscosity) + ↑ BP = ↑ CBF Goal Hct = 27-32% Nimodipine is the only CCB associated with ↓ morbidity/mortality 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 r/t trauma 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 Traumatic Brain Injury Key considerations Unstable C-spine Bloody airway or skull-base fracture Full stomach Intracranial HTN Blood thinners? Warfarin reversal with FFP, recombinant factor 7a, or vitamin K Clopidogrel or aspirin reversed with plt transfusion (possibly recombinant VII) Skull Base Fracture Raccoon Eyes = Periorbital Battle’s Sign = bruise behind one or both ecchymosis ears Traumatic Brain Injury Maintain CPP while decreasing ICP Too much hyperventilation can ↑ ischemia Use methods to ↓ ICP previous discussed, EXCEPT: DO NOT GIVE…. STEROIDS or possibly mannitol Hypertonic saline ideal Avoid N2O because you don’t know what other injuries are present Avoid colloids and hypotonic solutions Ventriculoperitoneal Shunt VP shunt allows excess CSF to drain into peritoneal cavity 3 key parts Burr hole access through dura Abdominal incision Subcutaneous tunneling from head to abd (connect the sites) Catheter passed through Most stimulating portion is usually tunneling References Barash, P., Cullen, B., Stoelting, R., Cahalan, M., Stock, M., Ortega, R., Sharar, S., & Holt, N. (2017), Clinical Anesthesia. 8th ed. Lippincott Williams & Wilkins Nagelhout JJ, & Elisha, S. (2018) Nurse Anesthesia. 6th ed. St. Louis, MO. Elsevier Saunders