Chapter 13 Diseases Affecting the Brain PDF

Diseases Affecting the Brain • Cerebral Physiology o Cerebral Blood Flow, Blood Volume, and Metabolism ▪ CBF is modulated by: cerebral metabolic rate, cerebral perfusion pressure (CPP, the difference btw MAP and ICP), & PaCO2 and PaO2 tensions ▪ CPP = MAP – ICP ▪ Various drugs and intracranial patho...

Diseases Affecting the Brain • Cerebral Physiology o Cerebral Blood Flow, Blood Volume, and Metabolism ▪ CBF is modulated by: cerebral metabolic rate, cerebral perfusion pressure (CPP, the difference btw MAP and ICP), & PaCO2 and PaO2 tensions ▪ CPP = MAP – ICP ▪ Various drugs and intracranial pathologies → impact CBF ▪ Normal physiologic conditions, CBF is → autoregulated over a range of CPPs ▪ With intact autoregulation, normal CBF in an awake person is 50 mL/100g brain tissue per min ▪ In the past, CBF was thought to be autoregulated over a range of CPPs of 50 to 150 mm Hg in chronically normotensive pts • However, more recent data suggest that the lower limit of autoregulation may be >50 mm Hg in normotensive individuals • Also, the autoregulatory range may be dynamic, changing in response to physiologic factors (e.g., sleepwake cycles) and likely varies among individuals • Normal adult brain weighs approx 1500 g and normal CO is 5 L/min → CBF is 750 mL/min or 15% of CO during the awake state ▪ Autoregulatory range: MAP 50-150 to maintain blood flow • BP outside of this range? pressure-dependent (depends on pt’s BP) ▪ know: • calculate MAP • calculate CPP • 120/80 MAP: 93 o MAP formula: (SBP + 2xDBP) / 3 ▪ If CVP > CPP, • ICP 5, CVP 12 which do you use to calculate CPP? The higher one, CVP. ▪ Cerebral metabolic rate: the rate of oxygen consumption by the brain (CMRO2) ▪ Normal cerebral metabolic rate is measured as rate of O2 consumption (CMRO2): 3-3.8 mL O2/100g brain tissue per min • During awake resting conditions, total body O2 consumption → 250 mL O2/min • Therefore total brain O2 consumption → 18-23% of total body O2 consumption • CMRO2 decreased by temperature reductions and various anesthetic drugs o CMRO2 is increased by temperature increases and seizures • calculate the amount of O2 in mL that would be required for a pt per min. o brain wt: 1,500 g o 45-57 mL ▪ Anesthetic and intensive care management of neurologically impaired pts relies heavily on manipulation of intracranial volume and pressure ▪ These in turn are influenced by cerebral blood volume (CBV) and CBF ▪ CBF and CBV → do not always change in parallel • Ex: vasodilatory anesthetics and hypercapnia → produce parallel increases in CBF and CBV • Conversely, moderate systemic hypotension still within the brain’s autoregulatory capacity produce minimal change inCBF but, as a result of compensatory vessel dilation, an increase in CBV • Similarly, partial occlusion of an intracranial artery (embolic stroke) → reduce regional CBF o However, vessel dilation distal to the occlusion, which is an attempt to restore circulation, can produce an increase in CBV o Arterial CO2 Partial Pressure ▪ Variations in PaCO2 produce corresponding changes in CBF via vasodilation and vasoconstriction ▪ CBF increases by 1 mL/100 g/min (or ~15 mL/min for a 1500-g brain) for every 1 mm Hg increase in PaCO2 • If PaCO2 goes up by 1 mmHg, CBF will increase by 1 mL/100g brain tissue/min → be able to calculate • A similar decrease occurs during hypocapnia when PaCO2 is acutely decreased • The impact of PaCO2 on CBF → mediated by variations in the pH of the CSF o Decreased CSF pH causes → cerebral vasodilation o Increased CSF pH → vasoconstriction • CBF is decreased ~50% when the PaCO2 is acutely lowered to 20 mmHg ▪ PaCO2 can also modulate CBV • The extent of CBV reduction is dependent on the anesthetic being used • In general, vasoconstricting anesthetics tend to attenuate the effects of Paco2 on CBV • o o o The ability of hypocapnia to acutely decrease CBF, CBV, and ICP → fundamental to the practice of clinical neuroanesthesia • Significant acute hypocapnia → increase risk for cerebral ischemia d/t excessive vasoconstriction • The ability of hypocapnia to decrease CBV, and thus ICP → attenuated by the return of CSF pH to normal after approx 6 hrs of hypocapnia • This reduces the effectiveness of induced hypocapnia as a means of long-term control of intracranial HTN Arterial Oxygen Partial Pressure ▪ Decreased PaO2 does not significantly affect CBF until a threshold value of approximately 50 mmHg is reached • Below this threshold, there is abrupt cerebral vasodilation, and CBF increases • Arterial hypoxemia PLUS hypercapnia exerts a synergistic effect—increases in CBF exceed the increase that would be produced by either factor alone • Hyperoxia has minimal, if any, effect on CBF Cerebral Perfusion Pressure and Cerebral Autoregulation ▪ The ability of the brain to maintain CBF at constant levels despite changes in CPP → autoregulation ▪ Autoregulation → active vascular response characterized by: • (1) arterial constriction when CPP is increased • (2) arterial dilation in response to decreases in CPP ▪ When CPP is below the lower limit of autoregulation → cerebral blood vessels are maximally dilated, and CBF decreases • CBF becomes directly related to CPP • In normotensive patients, the lower limit of CPP is ~ 50 mm Hg. Below that pressure, cerebral blood vessels are maximally vasodilated, and as the pressure drops further, CBF decreases (flow becomes pressuredependent) • As CPP is further decreased, cerebral ischemia may ensue, causing → nausea, dizziness, and altered consciousness. ▪ When CPP is increased above the upper limit of autoregulation → cerebral arterioles are maximally constricted, and CBF varies proportionally with CPP • If CPP increases further, fluid may be forced across blood vessel walls into the brain parenchyma → producing cerebral edema • The risk of cerebral hemorrhage increases • In normotensive patients, the upper limit of autoregulation is believed to be a MAP of ~150 mm Hg. Above this pressure, cerebral vessels are maximally constricted and CBF increases (pressure-dependent flow) ▪ **increased BP → vessels constrict ▪ **decreased BP → vessels dilate ▪ not normotensive → lost the ability to autoregulate ▪ In the setting of chronic HTN, autoregulation curve is displaced to the right so that pressure dependence of CBF occurs at a higher CPP at both the lower and upper limits of autoregulation • In those with chronic HTN, risk for cerebral ischemia can occur at SBP that would be tolerated by normotensive individuals • Autoregulation of CBF is shifted to the RIGHT (pressure dependence occurs at higher MAPs at both the upper and lower limits of autoregulation) in chronic HTN, but not acute hypertension. • Decreases in systemic blood pressure are not as well tolerated in patients with chronic HTN (cerebral ischemia can occur at higher pressures than in normal subjects). • Loss or impairment of autoregulation include intracranial tumors, head trauma, and volatile anesthetic agent administration. ▪ Gradual tx of HTN can restore the autoregulation curve to normal ▪ Acute HTN → produce signs of central nervous system dysfunction at MAP values that are well tolerated in chronically hypertensive patients • Similarly, an acute hypertensive response a/w direct laryngoscopy or surgery may exceed the upper limit of autoregulation in chronically normotensive patients ▪ Autoregulation of CBF may be lost or impaired during a variety of conditions, including the presence of intracranial tumors or head trauma and the admin of volatile anesthetics ▪ Increased impairment of autoregulation →leads to greater dependence of CBF on systemic blood pressure such that the autoregulation curve is no longer flat Cerebral Venous Blood Pressure ▪ Increases in intracranial venous blood pressure → impede venous drainage from the brain and may predispose the pt to cerebral edema and cerebral ischemia, the latter d/t increases in ICP, which in turn reduces CPP ▪ Impaired venous drainage can increase brain bulk and complicate intracranial surgery ▪ Examples of situations that can cause impaired venous drainage include SVC syndrome, cerebral venous thrombosis, or jugular vein compression, as can occur with improper neck positioning during sx ▪ With coughing against a partially closed glottic opening → increases in intrathoracic pressure result in transient increases in cerebral venous pressure ▪ However, if a coughing or bucking pt is tracheally intubated → the glottis is stented open by the ETT, and the effects of a cough or buck on CVP will be decreased compared to those encountered in nonintubated pts ▪ Venous blood pressure has little effect on CPP or CBF but may profoundly affect CBV. In order for blood to flow out of the cranial vault, ICP must be greater than CVP. Increases in CVP at a steady ICP lead to increases in CBV. Other causes of increased intracranial venous pressure include sinus venous thrombosis, jugular compression (extreme head flexion or rotation), and superior vena cava syndrome (seen in metastatic dz). • Effects of General Anesthesia on CBF and O2 Consumption o Volatile agents increase CBF and decrease cerebral metabolism. With prior hyperventilation, a decrease in CBF might occur with isoflurane. o Nitrous oxide by itself increases CBF and cerebral metabolism (this is d/t the sympathomimetic actions of nitrous oxide) o With the exception of ketamine, the IV general anesthetics (propofol, etomidate, thiopental) decrease both CBF and cerebral metabolism. ▪ Ketamine is a cerebral vasodilator and causes CBF and cerebral metabolism to increase. o **test question: list of what increases and decreases CBF and CMRO2 o Anesthetic Drugs • Increased Intracranial Pressure o Intracranial vault contains neural tissue, blood, and CSF. o During normal conditions, brain tissue, intracranial CSF, and intracranial blood have a combined volume of ~ 1200 to 1500 mL, and o Normal ICP = 5-15 mmHg o Any increase in one component of intracranial volume must be offset by a decrease in the volume of another intracranial component to present an increase in ICP ▪ If there’s a tumor, something must shift/compensate to decrease ICP ▪ Usually, CSF is shunted down into spinal cord—most common ▪ If not compensated → increased ICP → herniation…etc. o Signs and symptoms of increased ICP: ▪ headache ▪ nausea ▪ vomiting ▪ papilledema ▪ decreased LOC ▪ coma o Diagnosis: increased ICP is diagnosed based on the s/s and radiologic evidence (mass, herniation, midline shift) and by directly measuring ICP o Monitoring: a pressure transducer can be placed into the subdural space (known as subdural bolt), brain parenchyma, or ventricle (ventriculostomy). Ventriculostomy also allows the withdrawal of CSF in order to analyze CSF and regulate ICP. A lumbar drain will also allow this, but there is a risk of herniation in certain clinical settings. o Case study question: ▪ What is normal ICP? 5-15 mmHg ▪ Your patient has been diagnosed with a subdural hematoma. His heart rate is 50 bpm and his BP is 190/115. Explain the hemodynamic data? • Cushing’s triad o HTN, bradycardia, irregular respirations o Cushing’s triad: a reflex increase in mean arterial BP, a reflex decrease in HR, irregular respirations o Hyperglycemia is detrimental in cerebral ischemia because it can exacerbate the damage to the brain caused by the lack of blood flow and oxygen. ▪ 1. increases inflammation in the brain. ▪ 2. increase oxidative stress ▪ 3. impair blood flow ▪ **know these o Hyperglycemia increases metabolism. o Hypocarbia is a good, but transient way to lower ICP. o Propofol decreases CBF and decreases CMRO2 o Methods to Decrease Intracranial Pressure o Specific Causes of Increased Intracranial Pressure • o o o Normal pressure hydrocephalus: impaired CSF reabsorption lumbar puncture shows normal or low CSF pressure CT, MRI shows large ventricles treatment: drain CSF via shunt or acetazolamide/Diamox (carbonic anhydrase inhibitor) • Cerebrospinal Fluid CSF is produced by ultrafiltration and secretion by the cells of the choroid plexus and via the passage of water, electrolytes, and other substances across the blood-brain barrier o CSF is constantly produced at a rate of 500-600 mL/day in adults o CSF is absorbed by arachnoid villi and granulations within the dura mater bordering venous sinusoids and sinuses o The intracranial vault is compartmentalized by meningeal barriers, and increases in the contents of one region of the brain may cause regional increases in ICP and potential herniation of the contents of that compartment into a different compartment. o PRODUCED IN: CHOROID PLEXUS o ABSORBED FROM: ARACHNOID VILLI o lateral ventricles, 3rd vent, 4th vent--all these areas have a choroid plexus, which contributes to the formation of CSF (all of these generate CSF) o foramina vs. foramen: ▪ foramina—dual pathway (foramina of Luschka—out of lateral side of 4th ventricle) ▪ foramen—one (foramen of Magendie is midline) o CSF reabsorbed in arachnoid villi. • A patient has a defect in the arachnoid villi. What finding would the healthcare professional expect to note? a. Production of excess cerebrospinal fluid (CSF) b. Ischemia in the choroid plexuses c. Cloudy cerebral spinal fluid on analysis d. Absorption of too little cerebrospinal fluid o ANS: D CSF is reabsorbed by means of a pressure gradient between the arachnoid villi and the cerebral venous sinuses. CSF is produced in the choroid plexuses in the lateral, third, and fourth ventricles. The arachnoid villi do not provide perfusion to the choroid plexuses. Cloudy CSF can indicate infection (meningitis). • Spontaneous Intracranial Hypotension (SIH) o Pts with SIH present with an abrupt-onset orthostatic headache when assuming the upright position o Symptoms frequently increase during the second half of the day and may be a/w tinnitus, muffled hearing, or other cranial nerve deficits o Headache is relieved by assuming a horizontal position o SIH is caused by → leaking of CSF from the spine though meningeal diverticula, dural tears, or CSF-venous fistulas o MRI → normal, but findings suggestive of SIH include → meningeal enhancement, engorgement of venous sinuses, or herniation of the cerebellar tonsil though the foramen magnum o A CSF opening pressure of <6 cmH2O may or may not be present in pts with SIH as symptoms are thought to be related to low CSF volume rather than low CSF pressure o CT myelography → gold standard to identify spinal CSF leaks o Dynamic imaging studies using CT or fluoroscopy can also be used with or without digital subtraction, which can be helpful in localizing leaks o Tx of SIH → supportive measures, epidural blood patch, and sx ▪ Surgical procedures to repair the site of leak can be performed ▪ Pts may experience rebound intracranial HTN following surgical repair and may require therapeutic lumbar puncture • Intracranial Tumor ▪ Intracranial tumors classified as primary (those arising from the brain and its coverings) or metastatic • Primary brain tumors, also called gliomas → originate from virtually any cell type within the CNS • The classification of gliomas depends on histologic cell type, but these tumors are frequently subclassified based on specific oncogenic mutations that can influence choice of treatment and prognosis ▪ Supratentorial tumors → more common in adults • Present with headache, seizures, or new neurologic deficits • Supratentorium → above tentorium (75% of tumors develop here) ▪ Infratentorial tumors → more common in children o o • Present with obstructive hydrocephalus and ataxia • Infratentorium → below tentorium ▪ Tx → surgical resection or debulking, chemo radiation • Gamma knife irradiation differs from traditional radiation therapy in that multiple radiation sources are used, and because the tumor is addressed from multiple angles, radiation to the tumor can be maximized while the radiation dose to any single area of surrounding brain tissue can be diminished • Such treatment can also be accomplished with the use of XR and particle-based modalities such as proton beam • Emerging therapies → immunotherapy and oncolytic virotherapy, the latter employing viruses specifically programmed to kill neoplastic cells ▪ In anatomy, the infratentorial region of the brain is the area located below the tentorium cerebelli. The area of the brain above the tentorium cerebelli is the supratentorial region. The infratentorial region contains the cerebellum, while the supratentorial region contains the cerebrum. ▪ Which cerebral vascular hemorrhage causes meningeal irritation, photophobia, and positive Kernig and Brudzinski signs? a. Intracranial b. Subarachnoid c. Epidural d. Subdural o ANS: B Assessment findings related to only a subarachnoid hemorrhage include meningeal irritation and inflammation, causing neck stiffness (nuchal rigidity), photophobia, blurred vision, irritability, restlessness, and low-grade fever. A positive Kernig sign, in which straightening the knee with the hip and knee in a flexed position produces pain in the back and neck regions, and a positive Brudzinski sign, in which passive flexion of the neck produces neck pain and increased rigidity, may appear. • In adults, how are most intracranial tumors located? a. Infratentorially b. Supratentorially c. Laterally d. Posterolaterally o ANS: B Approximately 70% to 75% of all intracranial tumors diagnosed in adults are located supratentorially (above the tentorium cerebella). The other options are not primary locations for intracranial tumors in adults. Specific Brain Tumor Classes ▪ Astrocytomas • well-differentiated (low grade) gliomas—often manifest in young adults w new-onset seizures. Surgery or radiation results in symptom-free long-term survival • pilocytic astrocytomas—affect children and young adults. If resection possible, prognosis is very good • anaplastic astrocytomas—are poorly differentiated tumors that usually evolve into glioblastoma multiforme tumors. Prognosis is intermediate • glioblastoma multiforme (grade IV glioma)—lesions often appear with central necrosis and surrounding edema. Treatment involves surgical debulking combined with radiation and chemo and is aimed at palliation, not cure. Life expectancy is usually on the order of weeks. ▪ Meningiomas • Usually slow-growing, well-circumscribed, benign tumors. • They arise from the arachnoid cap cells, not the dura mater. • Surgical resection is the mainstay of treatment. Prognosis is usually excellent. • Malignant meningiomas are rare. ▪ Pituitary Tumor **know functional vs. nonfunctional tumors • Usually arise from cells from the anterior pituitary gland and may occur with tumors of the parathyroid and pancreatic islet cells as part of multiple endocrine neoplasia (MEN) type 1 . These tumors can be functional or nonfunctional. • Functional tumors—(ie hormone-secreting tumors) usually occur as a result of an endocrinologic disturbance r/t the hormones secreted by the tumor and are usually smaller (<1 cm in diameter) at the time of diagnosis • ▪ o • Nonfunctional tumors—usually more than 1 cm in diameter when diagnosed and cause symptoms related to their mass (headache, visual changes resulting from compression of the optic chiasm) o larger; diagnosed when symptoms get worse • Anterior pituitary gland hormones: ACTH, growth hormone, LH, FSH, TSH • Posterior pituitary gland hormones: vasopressin, oxytocin Acoustic Neuroma • Usually a benign schwannoma involving the vestibular component of cranial nerve VIII within the internal auditory canal. • Symptoms: hearing loss, tinnitus, and disequilibrium. Larger tumors may cause symptoms r/t compression of cranial nerves, most commonly the facial nerve (CN 7), as well as the brainstem • Treatment: is surgical resection w or w/o radiation therapy. Surgery usually involves intraoperative cranial nerve monitoring with electromyography or brainstem evoked potentials. • Prognosis: usually very good; however, tumor reoccurrence is common • Schwannoma is a type of nerve sheath tumor that develops from the myelin sheath covering peripheral nerve cells. • CN VIII—vestibulocochlear n. has 2 parts (vestibular part, cochlear part) o Acoustic neuroma involves the vestibular component Management of Anesthesia Disorders Related to Vegetative Brain Function o Coma: a state of profound unconsciousness produced by drugs, disease, or injury affecting the central nervous system. The causes of coma include structural lesions (tumor, stroke, abscess, or intracranial bleeding) or diffuse disorders (hypothermia, hypoglycemia, hepatic or uremic encephalopathy, postictal state, or drug effects). The most common means used to classify the overall severity of coma is the Glasgow Coma Scale o Glasgow Coma Scale Response Score EYE OPENING spontaneous 4 to speech 3 to pain 2 Nil 1 BEST MOTOR RESPONSE obeys 6 localizes 5 withdraws (flexion) 4 abnormal flexion 3 extensor response 2 nil 1 VERBAL RESPONSES o oriented 5 Confused conversation 4 inappropriate words 3 Incomprehensible sounds 2 nil 1 Determining causes of coma ▪ Vital signs (could point to hypothermia) ▪ Respiratory patterns—irregular breathing patterns may reflect an abnormality at a specific site in the CNS ▪ Neurological patterns ▪ Pupillary responses ▪ Motor responses to painful stimuli ▪ Lab evaluation and other tests o o o Abnormal patterns of breathing Ataxic (Biot’s breathing) unpredictable sequence of breaths varying in rate and tidal volume medulla apneustic breathing gasps and prolonged pauses at full inspiration (long inspiration followed by brief expiration) pons/pontine Cheyne-Stokes breathing cyclic crescendodecrescendo tidal volume pattern interrupted by apnea (deep rapid breaths followed by long pause) cerebral hemispheres congestive heart failure central neurogenic hyperventilation marked hyperventilation central thrombosis or embolism posthyperventilation apnea awake apnea following moderate decreases in Paco2 frontal lobes Pupillary responses ▪ Compression of the diencephalon or thalamic structures leads to small (2 mm) but reactive pupils ▪ Unresponsive midsize pupils (5 mm) may indicate midbrain compression ▪ Fixed and dilated pupils (>7 mm) usually indicates oculomotor nerve compression (herniation) →possible drug intoxication/overdose ▪ Pinpoint pupils (1 mm) may indicate opioid or organophosphate intoxication (herbicides, pesticides, insecticides), focal pontine lesions, or neurosyphilis ▪ **know Motor responses to painful stimulus ▪ decorticate response—(flexion of the elbow, adduction of the shoulder, extension of the knee and ankle) are usually indicative of diencephalic dysfunction. Damage above cerebellum and brainstem → supratentorial ▪ decerebrate response—(extension of the elbow, internal rotation of the forearm, leg extension) implies a more severe brain dysfunction. Damage to brainstem or cerebral lesions that compress the thalamus and brainstem. ▪ Patients with pontine or medullary lesions often exhibit no response to painful stimuli ▪ Regarding cranial fossas, where would cerebellum or brainstem be? a. anterior b. lateral c. mid d. posterior e. temporal ▪ ANS: posterior decerebrate • • decorticate Lab evaluation and other tests o electrolytes o blood glucose (hypoglycemic) o liver and renal function tests o tells us about encephalopathies o drug and toxicology screening o CBC and coag studies might suggest intracranial bleeding, thrombocytopenia, or coagulopathy o CT or MRI-may identify a structural cause (stroke or tumor) o lumbar puncture—may be performed if meningitis or subarachnoid hemorrhage is suspected Cerebrovascular Disease ▪ Stroke characterized by sudden neurologic deficits resulting from ischemia (88% of cases) or hemorrhage (12% of cases) • Ischemic stroke is described by the area of the brain affected and the etiologic mechanisms. Hemorrhagic strokes are classified as intracerebral (15%) or subarachnoid (85%) ▪ Stroke → leading cause of death and disability ▪ In developed countries, stroke-related mortality has decreased over the past several decades, probably because of better control of coexisting diseases such as HTN and DM, smoking cessation, and greater awareness of stroke RFs and clinical cues of stroke onset (allowing faster initiation of tx) ▪ Other stroke-related disorders of the cerebrovascular system → atherosclerotic disease of the carotid artery, cerebral aneurysm, arteriovenous malformation, and moyamoya disease Hyperdensity indicates the presence of substance that absorb x ray, while hypodensity indicates the presence of substances that block x ray. Atrial fibrillation, rheumatic heart disease, and valvular prosthetics are risk factors for which type of stroke? a. Hemorrhagic b. Thrombotic c. Embolic d. Lacunar ANS: C. Embolic ▪ o High-risk sources for the onset of embolic stroke are atrial fibrillation (15% to 25% of strokes), left ventricular aneurysm or thrombus, left atrial thrombus, recent myocardial infarction, rheumatic valvular disease, mechanical prosthetic valve, nonbacterial thrombotic endocarditis, bacterial endocarditis, patent foramen ovale, and primary intracardiac tumors. Hemorrhagic stroke is often the result of hypertension. Thrombotic CVAs develop most often from atherosclerosis and inflammatory disease processes that damage vessel walls. Lacunar strokes are usually caused by perivascular edema. ▪ Thrombotic strokes are caused by a blood clot that develops in the arteries supplying blood to the brain, usually due to atherosclerosis or high cholesterol. ▪ Embolic strokes are caused by a blood clot or plaque debris that develops elsewhere in the body and then travels to one of the blood vessels. Cerebrovascular Anatomy ▪ Blood supply to the brain via 2 pairs of vessels → internal carotid arteries and the vertebral arteries • These vessels join on the inferior surface of the brain → to form the circle of Willis, which, during ideal circumstances, provides collateral circulation to multiple areas of the brain • Unfortunately, all the elements of an intact circle of Willis are present and functional in only about 1/3 of people as some segments may be hypoplastic or absent • Each internal carotid artery gives rise to → an anterior cerebral artery and continues on to become → a middle cerebral artery • These vessels arising from the carotid arteries comprise the → anterior circulation and ultimately supply the frontal, parietal, and lateral temporal lobes; the basal ganglia; and most of the internal capsule • The vertebral arteries each give rise to a posterior-inferior cerebellar artery before converging at the level of the pons to form the basilar artery • The basilar artery generally gives rise to 2 anterior-inferior and 2 superior cerebellar arteries before dividing to become the paired posterior cerebral arteries • Vessels that receive their predominant blood supply from this vertebral-basilar system comprise → the posterior circulation and typically supply the brainstem, occipital lobes, cerebellum, medial portions of the temporal lobes, and most of the thalamus • The anterior and posterior circulations communicate via → the posterior communicating artery, and the left and right anterior cerebral arteries communicate via the anterior communicating artery • Occlusion of specific arteries distal to the circle of Willis results in → predictable clinical neurologic deficits    o The circle of Willis is supplied by the R and L internal carotids and the basilar artery. The circle of Willis permits collateral blood flow in the event that a major vessel (R or L internal carotid or basilar artery becomes occluded. All vessels in the circle of Willis are paired except for the basilar and anterior communicating artery Acute Ischemic Stroke ▪ Pts who experience sudden onset of neurologic dysfunction or describe neuro S&S evolving over mins-hrs → most likely experiencing a stroke ▪ An ischemic stroke → result of an occlusion of a vessel that supplies a region of brain resulting in cellular ischemia and subsequent cellular death ▪ A transient ischemic attack → sudden vascular-related focal neuro deficit that resolves within 24 hrs w/o intervention • Transient ischemic attack (TIA) is a sudden vascular-related focal neurological deficit that resolves within 24 hours and may represent an impending ischemic stroke. ▪ Approx 1/3 of pts who suffer a TIA will subsequently suffer a stroke ▪ o Stroke represents → a medical emergency, and prognosis depends on the time elapsed from the onset of symptoms to thrombolytic intervention if thrombosis is the cause of the symptoms ▪ Pts who receive early tx to restore cerebral perfusion → better outcomes ▪ Systemic HTN → most significant risk factor for acute ischemic stroke, and long-term tx of systolic or diastolic HTN dramatically reduces the risk of a 1st stroke • Cigarette smoking, hyperlipidemia, DM, excessive alcohol consumption, and increased serum homocysteine concentrations are also associated with increased risk of acute ischemic stroke. ▪ In pts with suspected stroke → noncontract CT distinguishes acute intracerebral hemorrhage from ischemia • This distinction is important because tx of hemorrhagic stroke is substantially different from treatment of ischemic stroke • CT is relatively insensitive to ischemic changes during the first few hrs after a stroke but is very sensitive for detection of intracranial bleeding ▪ Diagnosis: • CT reliably distinguishes acute intracerebral hemorrhage from ischemia, which have very different treatments. Conventional angiography is useful in demonstrating arterial occlusion. ▪ Acute ischemic strokes are caused by embolism occurring from a cardiac source, large-vessel atherothromboembolism (often from the carotid bifurcation), or from small-vessel occlusive disease. • Echo is useful for evaluating the patient’s cardiac status and looking for cardiac or aortic sources of embolism • Management of acute ischemic stroke includes aspirin. Intravenous recombinant tissue plasminogen activator (tPA) is used in patients who meet specific eligibility requirements if treatment can be initiated w/in 3 hours of onset of symptoms. ▪ DVT prophylaxis—5,000 units of SQ heparin q12h → most common tx • pts who can’t be anticoagulated → need compression stockings ▪ Conventional angio → useful for demonstrating arterial occlusion • The vasculature can also be visualized noninvasively using CT or magnetic resonance angio • Alternatively, transcranial Doppler ultrasonography → provide indirect evidence of major vascular occlusion and offers the advantage of realtime bedside monitoring in pts undergoing thrombolytic therapy ▪ The etiologies of acute ischemic stroke are categorized according to the TOAST classification into 5 groups: • 1. Large artery atherosclerosis (e.g., carotid stenosis) • 2. Small vessel occlusion (e.g., lacunar stroke) • 3. Cardioaortic embolic (e.g., emboli from atrial fibrillation) • 4. Other etiology (e.g., stroke due to hypercoagulable states or • vasculopathies) • 5. Undetermined etiology ▪ Management of Acute Ischemic Stoke ▪ Management of Anesthesia for Ischemic Stroke Revasc Perioperative and Periprocedural Stroke ▪ Most periop strokes → ischemic, and pts undergoing cardiac, neuro, and major vascular surgery → greatest risk for stroke ▪ IR procedures performed on the heart and major arteries → risk for periprocedural stroke ▪ The higher incidence of stroke in these pt populations is r/t: • (1) a higher incidence of baseline stroke risk factors (HTN, atherosclerosis, DM) • (2) risks of periop emboli (open cardiac procedures, invasive radiologic procedures to the cerebrovasculature) • (3) acute alterations in systemic physiology, including systemic or regional hypotension resulting in impairment of blood flow ▪ Pts having noncardiovascular and nonneuro sx → still at risk for periop stroke ▪ Overall, the risk for periop symptomatic stroke in adults having noncardiovascular and nonneuro procedures → 0.1%, w/ pts having amputations, abdominal exploration, and small bowel resection at greatest risk ▪ RFs for symptomatic periop stroke: • Increasing age, MI within 6 months, renal dysfunction, hx of stroke or TIA, HTN, COPD, smoking, and preop or intraop metoprolol use • B blockers, especially metop → caution in the periop period and titrated with care to avoid hypotension ▪ Pts who suffer a periop stroke have an eightfold increased risk for death w/i 30 days of sx compared to those who did not suffer a stroke ▪ Elective sx delayed following a stroke → for up to 9 mons to allow for return of cerebral autoregulation, risk factor reduction, and tx of underlying stroke etiology, if one can be identified ▪ o If periop stroke occurs → should be recognized early • Difficult in the periop period b/c pts may have residual effects from GA or sedatives • One should have an index of suspicion for stroke in the postop period if a pt’s mental status does not improve as expected, a relationship btw opioid admin and fluctuations in consciousness can be ruled out, or evidence of a focal neuro deficit • If one has a high suspicion for stroke → a gross neuro exam should be conducted and documented to establish a baseline and note deficits ▪ Downstream, the pt should undergo a noncontrast CT of the head to rule out other causes such as intracranial hemorrhage ▪ If suspicions for stroke are confirmed → neurologist should be consulted to determine if the patient is a candidate for thrombolytics despite recent sx ▪ Meanwhile, O2 delivery to the brain should be optimized by avoiding hypoxia and hypotension. ▪ Periop covert stroke → new focal region of cerebral ischemic injury following surgery and anesthesia that is without clinical manifestations and is only evident on brain MRI • Covert stroke occurs in about 7% of pts > 65 yrs having elective, noncardiac surgery • RFs for covert stroke appear to only be increasing age • Sex, prior hx of stroke or TIA, hx of vascular disease, type of sx, and anesthetic technique → do not influence risk of covert stroke • Pts who have covert stroke → have increased risk of periop delirium as well as overt stroke & cognitive decline 1 year following sx Acute Hemorrhagic Stroke ▪ Acute hemorrhagic strokes result from either intracerebral or subarachnoid hemorrhage • Intracranial hemorrhage—is 4 Xs more likely than ischemic stroke to cause death. Diagnosis requires a CT. IV administration of recombinant activated factor VII within 4 hours of onset has been shown to decrease hematoma volume and improved clinical outcome ▪ Results from extravasation of blood in the cranial vault that in turn impairs perfusion of normal brain ▪ Hemorrhagic stroke 4xs more likely to cause death than is ischemic stroke ▪ Acute hemorrhagic stroke cannot be reliably distinguished from ischemic stroke based on clinical criteria alone • A noncontrast CT needed to detect the presence of bleeding • The estimated volume of extravasated blood and the level of consciousness → 2 most reliable predictors of outcome ▪ Subarachnoid hemorrhage—spontaneous SAH most commonly results form rupture of intracranial aneurysms. ▪ Risk factors for aneurysm rupture: aneurysm size (>25 mm), systemic HTN, cigarette smoking, cocaine abuse, female gender, and use of oral contraceptives ▪ S/Sx: photophobia, neck stiffness, decreased LOC, and focal neurologic changes, + Brudzinski and + Kernig • Brudzinski: pain when putting chin to chest • Kernig: straightening leg results in back/neck pain ▪ Diagnosis: based on clinical symptoms (“worst headache of my life”) and CT demonstration of subarachnoid blood. ▪ Treatment: involves localizing the aneurysm with conventional or magnetic resonance angiography and excluding the aneurysmal sac from the intracranial circulation while preserving the parent artery. Outcomes are optimal when treatment is performed within 72 hours of bleeding. Supportive treatment includes anticonvulsants, control of systemic blood pressure, and ventricular drainage ▪ Vasospasm: the incidence and severity of vasospasm correlate with the amount of subarachnoid blood on CT. Vasospasm typically occurs 3 to 15 days after SAH. Triple H therapy—HTN, Hypervolemia, passive Hemodilution) is initiated if vasospasm occurs. Nimodipine, a CCB, improves outcomes when initiated on the first day and continued for 21 days after SAH ▪ Which cerebral vascular hemorrhage causes meningeal irritation, photophobia, and positive Kernig and Brudzinski signs? a. Intracranial b. Subarachnoid c. Epidural d. Subdural ANS: B Assessment findings related to only a subarachnoid hemorrhage include meningeal irritation and inflammation, causing neck stiffness (nuchal rigidity), photophobia, blurred vision, irritability, restlessness, and low-grade fever. A positive Kernig sign, in which straightening the knee with the hip and knee in a flexed position produces pain in the back and neck regions, and a positive Brudzinski sign, in which passive flexion of the neck produces neck pain and increased rigidity, may appear. ▪ ▪ ▪ ▪ In adults, how are most intracranial tumors located? a. Infratentorially b. Supratentorially c. Laterally d. Posterolaterally ANS: B Approximately 70% to 75% of all intracranial tumors diagnosed in adults are located supratentorially (above the tentorium cerebella). The other options are not primary locations for intracranial tumors in adults. Subtypes of hemorrhagic strokes →defined based on the location of blood • Blood located within the brain proper → intraparenchymal hemorrhage • Blood located in the epidural, subdural, or subarachnoid spaces → epidural hematoma, subdural hematoma, and subarachnoid hemorrhage • Blood located in the ventricular system → intraventricular hemorrhage, and it is usually not an isolated event but instead occurs in the setting of other types of hemorrhagic stroke • 4 major types of intracranial hematomas: o epidural hematoma o traumatic subarachnoid hematoma o subdural hematoma Intraparenchymal Hemorrhage • intraparenchymal hematoma—an abnormal collection of blood within the brain tissue proper. Treatment can be difficult. • Also known as intracerebral hemorrhage • A collection of blood in the brain parenchyma • A primary intraparenchymal hemorrhage → occur in the absence of a gross anatomic source (arteriovenous malformation) for the hemorrhage o Occurs more in blacks and those with poorly controlled HTN • Secondary causes of intraparenchymal hemorrhage → rupture of arteriovenous malformation, trauma, or bleeding from a brain tumor • Pts with intracerebral hemorrhage often deteriorate clinically as a result of hematoma expansion or cerebral edema that worsens during the 1st 24-48 hrs following the acute bleed • Late hematoma evac → ineffective at decreasing mortality • The efficacy of earlier surgical evac of a hematoma to decrease ischemic injury and edema to the surrounding tissue remains unclear • More recently, the stereotactic intracerebral hemorrhage underwater blood aspiration (SCUBA) technique → described as a treatment for intraparenchymal hemorrhage o SCUBA technique involves stereotactic implantation of a small catheter into the hematoma allowing for aspiration of blood and a decrease in hematoma size • IV admin of recombinant activated factor VII has been tried and has minimal effect on hematoma expansion rate, no significant effect on overall outcome, and may increase risk for arterial thrombosis • Intraventricular hemorrhage is a particularly ominous form of intracranial hemorrhage because the blood will occlude CSF drainage • Prompt ventricular drainage should be performed to treat any signs of hydrocephalus • Sedation, with or without drug-induced skeletal muscle paralysis → helpful in managing pts who require prolonged tracheal intubation to protect the airway and manage ventilation and oxygenation • The goal of BP management involves balancing the need to maintain cerebral perfusion while decreasing risk for rebleeding or hematoma expansion o The American Heart Association and American Stroke Association recommend the following: ▪ In pts with an initial SBP btw 150-220 mmHg → SBP should be decreased to a goal of 140 mmHg • Further decreases in BP do not improve neuro outcome and may predispose to renal injury ▪ In pts with an initial SBP > 220 mm Hg → SBP should aggressively be decreased to 140160 mmHg o The choice of antihypertensive drug used to decrease BP → depend on extent of desired BP reduction, titratability, pt comorbidities, and clinician experience Epidural Hematoma • epidural hematoma—results from arterial bleeding into the space between the skull and dura. The cause is usually a tear in a meningeal artery (may be a/w skull fracture). o ▪ ▪ Hemiparesis, mydriasis, and bradycardia then suddenly develop a few hours after the head injury, reflecting uncal herniation and brainstem compression. o Treatment is prompt drainage. • From skin to spinal cord: • Skin→SQ fat→muscle→supraspinous ligament→interspinous ligament→Ligamentum Flavum→ (epidural space)→dura mater→(subdural space)→arachnoid mater→(subarachnoid space)→pia mater—spinal cord 1. skin 2. SQ fat 3. muscle 4. supraspinous ligament 5. interspinous ligament 6. ligamentum flavum → thick, dense 7. epidural space (go here for epidural) 8. dura mater 9. subdural space 10. arachnoid mater 11. subarachnoid mater (go here for spinal) 12. pia mater 13. spinal cord • Most commonly occurs in trauma • The arteries that supply the dura mater → located btw the dura mater and the periostium of the cranial bones, and epidural hematoma is generally due to traumatic rupture of a meningeal artery • Generally, pts have a lucid interval following trauma but, as blood accumulates in the epidural space → hematoma volume can compress the brain and decrease perfusion o This results in progressive alterations in consciousness corresponding with ICP increases and CPP decreases • The prognosis following early hematoma evac is excellent Traumatic Subarachnoid Hematoma • traumatic subarachnoid hematoma—like SAH a/w aneurysmal rupture, subarachnoid hematomas are also associated with the development of cerebral vasospasm Subdural Hematoma • subdural hematoma—results from lacerated or torn bridging veins that bleed into the space between the dura and arachnoid. o Examination of the CSF reveals clear fluid, as subdural blood does not typically have access to the subarachnoid CSF. o Diagnosis is confirmed by CT. o Head trauma is the most common cause. ▪ Patients may view the head trauma as trivial, and it may have been forgotten. • Occurs when blood accumulates btw the dura mater and arachnoid layer • Most commonly occurs in the setting of trauma • This can occur following either major or minor trauma, with the latter often occurring in older pts w/ cerebral atrophy (a condition than lends itself to stretching and rupture of bridging veins that run in the subdural space) • Pts who take chronic anticoagulants and antiplatelet drugs → greatest risk • As with epidural hematomas, early evac → a/w better outcomes • S&S of SDH → evolve gradually over several days because the hematoma is due to slow venous bleeding o Headache → universal complaint o Drowsiness and obtundation → characteristic findings, but the magnitude of these changes may fluctuate from hour to hour o Lateralizing neuro signs eventually occur, manifesting as → hemiparesis, hemianopsia, or language disturbances o Elderly pts may have unexplained signs of progressive cognitive decline or dementia o s/sx—s/sx evolve gradually over several days (in contrast to epidural hematomas). ▪ Headache is a universal complaint. ▪ Drowsiness and obtundation are characteristic findings. ▪ Elderly patients may have unexplained progressive dementia o ▪ treatment: conservative medical management may be acceptable for patients whose conditions stabilize. Most often treatment consists of surgical evacuation of the clot, as the prognosis is poor if coma develops. • Conservative medical management of subdural hematomas → acceptable for pts whose condition stabilizes, but surgical evac of the clot is desirable in most pts • Most subdural hematomas → drained via burr holes; the procedure can be performed during GA, locals, or MAC • If the subdural hematoma is large, is chronic, or consists of clotted blood → removal may require craniotomy o Because a subdural hematoma is usually caused by venous bleeding → normocapnia is desirable following evac of the hematoma to allow for a larger brain volume, which may help to tamponade any sites of venous bleeding o Following hematoma evac, it may be best to avoid significant head elevation if the pt is able to tolerate a more horizontal position ▪ The horizontal position allows for a large brain volume due to increased venous blood volume that can tamponade further bleeding Subarachnoid Hemorrhage and Intracranial Aneurysms (part of this included above with Acute Hemorrhagic Stroke) • Spontaneous subarachnoid hemorrhage → most commonly results from rupture of an intracranial aneurysm • Various patho conditions → HTN, coarctation of the aorta, polycystic kidney disease, fibromuscular dysplasia, and the occurrence of cerebral aneurysms in first-degree relatives are a/w presence of cerebral aneurysms • Larger aneurysms → more likely to rupture • Other risk factors for rupture → HTN, cig smoking, cocaine abuse, female, and oral contraceptives • Pts may also present clinically with unruptured aneurysms o A common presentation of an unruptured aneurysm → development of a new focal neuro deficit o The cause of this new deficit → either a mass effect from an expanding aneurysm that compresses normal neuro structures or small emboli to the distal cerebral circulation from a thrombus contained within the aneurysm o Headache caused by mass effect can occur o New-onset seizures → indicate an unruptured aneurysm and result from the formation of a glial scar (gliosis) in brain parenchyma adjacent to the aneurysm o Unruptured aneurysms → identified incidentally on cerebral imaging performed for unrelated reasons • Aneurysm diameter is not static o Thus, although smaller aneurysms may be followed with serial imaging, larger aneurysms are often considered for tx b/c increased risk for spontaneous rupture • S&S of subarachnoid hemorrhage: o Severe headache, photophobia, nuchal rigidity, focal neurologic deficits, and decreased LOC • Dx confirmed by CT demonstration of subarachnoid blood o MRI is not as sensitive as CT for detecting acute hemorrhage o MRI useful for demonstrating subacute or chronic subarachnoid hemorrhage or infarction after CT findings have returned to normal o In pts where there is a strong suspicion for subarachnoid hemorrhage even with a negative head CT → lumbar puncture with CSF analysis (especially evaluating RBC count in successive collection tubes and xanthochromia) should be performed o Prompt establishment of the dx followed by tx of aneurysm → decrease M&M o 2 of the most common methods used to grade severity of subarachnoid hemorrhage → Hunt and Hess classification and the World Federation of Neurologic Surgeons grading system ▪ These grading systems useful because their stratification of severity helps prognosticate outcome and the efficacy of various therapies • A significant increase in serum catecholamine concentration is a/w acute subarachnoid hemorrhage, with greater concentration increases being a/w worsened severity of subarachnoid hemorrhage o This increase in serum catecholamines can impact the CV system o Manifestations include → changes in the ECG, such as ST-segment depression, T-wave inversion, and various arrhythmias o A mild increase in serum cardiac enzymes can also occur • On echo → decreased myocardial contractility, regional wall motion abnormalities that do not follow a distribution of a coronary artery, and Takotsubo cardiomyopathy → observed • o Apical cardiac function → preserved, a phenomenon attributed to the paucity of sympathetic innervation at the cardiac apex • Treatment of subarachnoid hemorrhage o Involves localizing the aneurysm with conventional or magnetic resonance angiography and operatively excluding the aneurysmal sac from the intracranial circulation while preserving its parent artery, if possible o Depending on location and characteristics of the aneurysm, and the volume and placement of associated bleeding → accomplished by craniotomy and surgery or via invasive radiologically guided techniques (aneurysm coiling) o Outcome is optimal when surgical tx is performed w/i first 72 hrs after bleeding o Operative surgical tx include → placement of a clip across the neck of the aneurysm with aneurysm wrapping or trapping reserved for very large aneurysms or those that lack a definitive neck ▪ In aneurysm trapping, a clip is placed on the artery both proximal and distal to the aneurysm after the artery distal to the aneurysm has been bypassed, usually by means of the superficial temporal artery o Endovascular techniques involve placing soft metallic coils in the dome of an aneurysm or placement of a stent in the parent artery so that the walls of the stent do not allow blood flow into the aneurysm. o Surgery delayed in pts with severe symptoms (coma) ▪ In these pts, other options, including interventional radiographic procedures, may be used o Anticonvulsants are admin should seizure activity occur o Systemic BP controlled, in recognition that HTN → increases the risk of rebleeding o Hydrocephalus → common after subarachnoid hemorrhage and is treated with ventricular drainage • Any change in mental status → promptly evaluated by CT to look for signs of rebleeding or hydrocephalus • Following subarachnoid hemorrhage with or without surgical or endovascular treatment of the aneurysm → important goal is prevention of vasospasm (intracranial arterial narrowing) and its consequences o Vasospasm triggered by many mechanisms → most important of which is the contact of free Hgb with the abluminal surface of cerebral arteries o Incidence and severity of vasospasm → correlate w/ amount of subarachnoid blood seen on CT o Vasospasm occurs 3-15 days after subarachnoid hemorrhage o For this reason, daily transcranial Doppler ultrasonographic exams may be performed to detect and follow the efficacy of tx of vasospasm o Nimodipine (CCB) → decrease risk of vasospasm and improve outcome in those who develop vasospasm when initiated on the first day of the bleed and continued for 21 days after subarachnoid hemorrhage o If vasospasm is identified → triple H therapy (HTN, hypervolemia, passive hemodilution) → traditionally initiated ▪ However, currently only HTN is generally employed with the goal of maintaining euvolemia, as complications such as pulmonary edema and other adverse complications related to hypervolemia and hemodilution, if they occur, can negatively impact outcome ▪ In addition to HTN, cerebral vasospasm → treated angiographically with either balloon dilatation or via directed instillation of vasodilators (papaverine, nicardipine, milrinone, or verapamil) → into the spastic vessels • Management of Anesthesia Arteriovenous Malformation (AVMs) ▪ Arteriovenous (AV) malformations: abnormal blood vessels with multiple direct arterial-to-venous connections without intervening capillaries. Rupture is not clinically associated with acute or chronic HTN episodes. Although often congenital, they commonly manifest in adulthood as either hemorrhage or new-onset seizures (stealing of blood away from normal brain toward the low-resistance AVM) • In other words, AVMs are vascular structures that contain tangled arteries and veins which form connections and bypass normal tissues. ▪ Abnormal collections of blood vessels in which multiple direct arterial-to-venous connections exist w/o intervening capillaries • There is also no neural tissue within the nidus ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ AVMs typically represent high-flow, low-resistance shunts, with vascular intramural pressure being less than systemic arterial pressure Thus rupture does not appear to be clinically associated acute or chronic HTN These malformations are believed to be congenital S&Ss • Headache, new focal neurologic deficits d/t edema or compression of normal brain, acute hemorrhage, or seizure • The exact cause of AVM-associated seizures → unknown but has been attributed to either: o Steal (e.g., shunting of blood away from normal brain tissue toward the low-resistance AVM) o Gliosis due to hemosiderin deposits from previous hemorrhage Most AVMs are supratentorial An aneurysm can be found on the feeding artery in 4-10% of AVMs AVMs presenting in the neonatal or childhood period usually involve the vein of Galen, and presenting symptoms include hydrocephalus or macrocephaly and prominence of forehead veins, high output CO or HF Dx → MRI or angiography Before the advent of focused, high-dose radiation and selective cerebral angiography-based treatment regimens → primary surgical treatment of AVMs was a/w a high M&M Treatment • Combination of radiation, such as with gamma knife, angio-graphically guided embolization, and/or surgical resection • With smaller AVMs → pts may respond completely to radiation or embolization therapy • With larger AVMs → 2 techniques are typically used as adjunctive therapy before surgery to decrease the size of the AVM nidus and reduce both the complexity and risks of surgery Prognosis and periop outcome → estimated using the Spetzler-Martin AVM grading system, which classifies the AVM based on 3 features Other types of intracranial AVMs → venous angiomas, cavernous angiomas, capillary telangiectasias, and arteriovenous fistulas Venous Angioma • Venous angiomas or malformations consist of tufts of veins • Often they are occult lesions found during cerebral angio or MRI performed to evaluate other disease states • Rarely will a venous angioma present as either hemorrhage or new-onset seizures • These are low-flow, low-pressure lesions and usually contain intervening brain parenchyma within the nidus; they are therefore treated only if bleeding or intractable seizures occur Cavernous Angioma • Also known as cavernous hemangiomas or cavernomas • Typically benign lesions consisting of vascular channels without large feeding arteries or large veins • Brain parenchyma is not found within the nidus of the lesion • These low-flow, well-circumscribed lesions often present as new-onset seizures but occasionally manifest as hemorrhage • Seen on CT or MRI scans and typically appear as a flow void on cerebral angiograms • Treatment involves surgical resection of symptomatic lesions Capillary Telangiectasia • Low-flow, enlarged capillaries • One of the least understood vascular lesions in the CNS • Angiographically silent and difficult to diagnose antemortem • Risk of hemorrhage → low except for lesions occurring in the brainstem • Found incidentally at autopsy • A/w Osler-Weber-Rendu syndrome, Sturge-Weber syndrome Arteriovenous Fistula • Direct communications btw arteries and veins w/o an intervening nidus of smaller blood vessels • Commonly occur btw meningeal vessels w/i the dura mater or btw carotid artery and venous sinuses w/i the cavernous sinus • Some AV fistulas occur spontaneously o Many others are a/w → previous traumatic injury or, in the case of carotid-cavernous fistulas, w/ previous rupture of an intracavernous carotid artery aneurysm • Dural AV fistulas → present w/ tinnitus or headache • An occipital bruit can occur → since occipital artery is a common arterial feeder of an AV fistula • Treatment o Angio guided embolization or surgical ligation o Surgical tx a/w → risk of rapid and sig blood loss • Pts w/ carotid-cavernous AV fistulas → have orbital or retroorbital pain, arterialization of the conjunctiva, or visual changes o Dx → MRI or angio o Embolization effective tx ▪ Management of Anesthesia o Moyamoya Disease ▪ Progressive stenosis of intracranial vessels with secondary development of an anastomotic capillary network → hallmark ▪ Moyamoya → Japanese term for “puff of smoke” • Refers to angio finding of a cluster of small abnormal blood vessels ▪ Has familial tendency toward the development of this dz • May be seen following head trauma or other disorders such as neurofibromatosis, tuberous sclerosis, and fibromuscular dysplasia ▪ Affected arteries have a thickened intima and a thin media ▪ Since similar patho findings may be found in other organs → CNS abnormalities may be manifestations of a systemic disease ▪ Intracranial aneurysms occur with increased frequency in those w/ dz ▪ S&S of ischemia, such as TIAs & cerebral infarcts → common in peds • Hemorrhagic complications → common in adults ▪ Dx → MR angio → shows cluster of small abnormal blood vessels • MRI & CT → show a tissue void or hemmorhage ▪ Medical tx • Aimed at decreasing ischemic symptoms • Usually consists of a combination of vasodilators & anticoagulants • Surgical options divided into 2 categories: direct and indirect revascularization o Direct revascularization procedures → direct anastomosis of an extracranial artery, such as the superficial temporal artery or middle meningeal artery, with an intracranial artery, such as the middle cerebral artery ▪ A major advantage of extracranial-to-intracranial bypass procedures → blood flow is restored immediately following the procedure ▪ However, fewer pts w/ Moyamoya are candidates for direct approaches → b/c they do not have an adequately large intracranial vessel to allow for anastomosis o Indirect revascularization procedures → placement of an extracranial vessel onto the pia mater to allow for the growth of a new vascular network, derived from the extracranial vessel, to perfuse the ischemic brain ▪ Advantages → less procedural complications and a greater number pts are candidates ▪ Cons → less successful than direct procedures at restoring cerebral perfusion, and the beneficial effects take weeks to months to occur as success depends on the growth of a new vascular network ▪ Management of Anesthesia • Traumatic Brain Injury ▪ Traumatic brain injury is the leading cause of disability and death in young adults in the United States ▪ Diagnosis is made by CT scan. ▪ The Glasgow Coma Scale provides a method for assessing the seriousness of brain injury (scores below 8 indicate severe injury. Scores below 8 are by definition signify coma, and ~ 50% of these patients die or remain in vegetative states. ▪ Heterogenous dz ▪ Leading cause of death & disability in younger adults ▪ Categorized as penetrating or nonpenetrating → dependent on whether dura is breached ▪ Severity of TBI categorized by many metrics → usually GCS • Stratified into mild, moderate, or severe for GCS of 13 to 15, 9 to 12, and less than 9, respectively ▪ Nature of brain injury a/w TBI is categorized into → primary and secondary • Primary injuries o Occur at the time of trauma & d/t effect of external forces on intracranial content