CNS Brain A Review PDF

Cerebral Blood Flow is normally autoregulated. Governed by: Cerebral Metabolic Rate (Rate of Oxygen Consumption) – CMRO2 Cerebral Perfusion Pressure (CPP) PaCO2 & PaO2 Influence of drugs Intracranial abnormalities CPP=MAP-ICP and CBF=CPP/CVR Parameter...

Cerebral Blood Flow is normally autoregulated. Governed by: Cerebral Metabolic Rate (Rate of Oxygen Consumption) – CMRO2 Cerebral Perfusion Pressure (CPP) PaCO2 & PaO2 Influence of drugs Intracranial abnormalities CPP=MAP-ICP and CBF=CPP/CVR Parameter Normal Value CBF 50 mL / 100 g brain tissue / min CPP 80-100 mmHg CVR 1.6 – 2 mmHg / mL 100 g brain tissue / min MAP 70 – 110 mmHg ICP 5 – 15 mmHg CMRO₂ 3.0-3.8 mL O₂ / 100 g brain tissue / min PaCO₂ 35 – 45 mmHg PaO₂ 80-100 mmHg Anesthetic & intensive care management of neurologically impaired patients relies heavily on manipulation of intracranial blood volume (CBV) and CBF. Vasodilatory anesthetics & hypercapnia ➔ ⇧ CBF & ⇧CBV CBF and CBV do not always change in parallel Moderate systemic hypotension decreases CBF and increases CBV Partial occlusion of an intracranial artery (embolic stroke) decreases CBF and increases CBV Arterial Partial Pressures CO2 Variations in PACO2 ➔ CBF + CBV. Impact on CBF is mediated by variations in CSF pH around arterial walls. Vasoconstriction anesthetics tend to attenuate PaCO2 effects on CBV. Hypocapnia decreases CBF, CBV, and ICP. Attenuated by Adaptive Change: return to CSF pH to normal after prolonged periods of hypocapnia reduces the effectiveness of induced hypocapnia as a means of long-term control of intracranial hypertension. Active transport of HCO3- into the OR from CSF requires 6hrs to return CSF pH to normal.  PaO₂ (Partial Pressure of Oxygen): As PaO₂ increases, cerebral blood flow decreases. PaCO₂ (Partial Pressure of Carbon Dioxide): As PaCO₂ increases, cerebral blood flow increases. MAP (Mean Arterial Pressure): Cerebral blood flow remains relatively constant over a range of MAP values but increases sharply at higher pressures. ICP (Intracranial Pressure): As ICP increases, cerebral blood flow decreases. A drop in PaO2 does not significantly affect CBF until a threshold value of 50mmHg, below this threshold there is vasodilation (CBF increases). Hypoxia and hypercapnia have a synergistic effect. Cerebral Autoregulation Active vascular response is characterized by arterial constriction in response to increase in BP or dilation in response to decreased BP. Autoregulation of CBF range is 50-150mmHg. In chronic hypertension there is a RIGHT shift to the autoregulation curve, higher thresholds. Rapid decrease in BP (vasodilating drugs) in patients with chronic hypertension can precipitate a stroke. Lost or impaired autoregulation under a variety of conditions including presence of intracranial trauma, head trauma, or administration of volatile anesthetics. Increased Venous BP Changes in CBF Decrease A/V pressures Increases in CBV and ICP decreases CPP Origin CVP VP in neck and base of the skull Contribute to: Increased brain bulk during intracranial surgery Impede the surgeons access to the target brain areas Causes: venous sinus thrombosis, jugular compression, superior vena cava syndrome, increased intrathoracic pressure (transient effect) Intracranial Pressure Factors leading to alterations in CSF flow or its absorption into the vasculature can often lead to increased ICP. Increased Intracranial Elastance Normally changes in one component are well compensated for by other components (homeostasis) A point can be reached at which even a small change in intracranial content results in a large change in ICP Cerebrospinal Fluid (CSF) CSF is formed by the choroid plexus/brain parenchyma (500-600mL/day). CSF circulates through the ventricles and into the subarachnoid space. CSF is absorbed into the venous circulation by arachnoid villi/granulations. CSF has unidirectional flow 1. Lateral ventricles 2. Foramen of monro (interventriculas) 3. Third ventricle 4. Cerebral aqueduct 5. Fourth ventricle 6. Foramina of Magendie and Luschka 7. Subarachnoid space (1st cisterna magna) 8. Arachnoid villi/granulations 9. Venous sinuses Herniation Syndromes 1. Subfalcine herniation is a herniation of the cingulate gyrus under the falx cerebri. There is a compression of the Anterior Cerebral Artery. 2. Transtentorial Herniation is a herniation of supratentorial contents, there is brainstem compression. Patient has altered consciousness, defects in gaze and afferent ocular reflexes, hemodynamics and respiratory compromise leading to death.  o Uncal Herniation is a subtype of transtetorial herniation, there is ipsilateral CN III dysfunction: pupillary dilation, ptosis, and lateral deviation of the affected eye, brainstem compression leading to death. 3. Herniation of cerebral tonsils is herniation of the tonsils through the foramen magnum due to increased infratentorial pressure. This could lead to medullary dysfunction, cardiorespiratory instability and subsequent death. 4. Herniation through traumatic cranial defect is a herniation of brain contents out of the cranial cavity Increased ICP Diagnosis: symptoms, radiography and direct measurement of ICP Non-specific signs and symptoms: headache, nausea, vomiting, papilledema, spontaneous hyperventilation, changes in mental status, decreased consciousness and coma Radiography aids in the diagnosis: CT and MRI help diagnose the presence of tumor, hematoma or obstruction of CSF flow. Anxiety and painful stimulation can initiate abrupt increases in ICP Methods for measuring and monitoring ICP Ventriculostomy allows for pressure monitoring and withdrawal of CSF for decreasing ICP or lab analysis. Lumbar subarachnoid catheter is less accurate compared to the ventriculostomy Methods to decrease ICP Elevation of the Head: 30o above heart level and avoid head-down positions Hyperventilation: lowers PaCO2 CSF drainage: lumbar or ventricular Administration of hyperosmotic drugs: mannitol, avoid hypovolemia or hypokalemia, careful with limited cardiac reserve or CHF Loop diuretics: furosemide, system dehydration and improve oxygenation Corticosteroids: dexamethasone or methylprednisolone, effective in localized vasogenic cerebral edema around brain tumors or pseudo motor cerebri. Not effective in decreasing ICP in some other forms of intracranial hypertension (closed head injury)  Cerebral vasoconstricting anesthetics: acute head injury at high doses, barbiturates and propofol Surgical decompression Treat any sustained increase of ICP >20mmHg Mannitol has maximum beneficial effects with an intact blood-brain barrier. It initially increases intravascular blood volume and has vasodilation properties. Etiology of increased ICP Tumors: size, edema at surrounding brain tissue, obstruction of CSF flow Intracranial Hematomas: mass lesions, obstruction of CSF reabsorption Infections: edema, obstruction of CSF reabsorption Aqueductal Stenosis is a more common cause of obstructive hydrocephalus. There is congenital narrowing of cerebral aqueducts as confirmed by CT. Symptoms include intracranial hypertension and seizures. Treatment is ventricular shunting. Anesthesia management includes intracranial hypertension. Pseudomotor Cerebri Benign Intracranial Hypertension. ICP > 20mmHg, normal CSF composition, normal sensorium and absence of local intracranial lesion. Symptoms include headaches and bilateral visual disturbances, increased during pregnancy Treatment includes removal of 20-40mL of CSF (lumbar), acetazolamide (decreases CSF formation), corticosteroids, lumbar peritoneal shunt. Anesthesia Management for lumbar peritoneal shunt General anesthesia is the most logical choice. Avoid exacerbation of intracranial hypertension and ensure adequate CPP. Avoid hypoxia and hypercarbia. Use spinal anesthesia to parturient women. Normal Pressure Hydrocephalus Triad of dementia, gait changes, and urinary incontinence (develops over a period of weeks to month). Mechanism involves compensated but impaired CSF absorption from a previous insult (subarachnoid hemorrhage, meningitis, or head trauma). Lumbar puncture to lower CSF pressure with large ventricles in imaging. Treatment involves drainage of CSF via ventriculoperitoneal or ventriculoartrial shunt. Intracranial Tumors They can be primary or metastatic and originate from virtually any CNS cell type Supratentorial tumors Infratentorial tumors  Common in adults Common in children Headaches, seizures, or neurologic deficits Obstructive, hydrocephalus and ataxia Treatment is surgical resection or debulking, chemotherapy (does not penetrate BBB well) and radiation. Low-grade Gliomas are the least aggressive class and are well differentiated. Usually seen in young adults with new onset of seizures. Treatment is surgical or radiation treatment, if maintained symptom from there is long-term survival. Pilocytic Astrocytoma is benign and typically seen in children and young adults. Origins in the cerebellum, cerebral hemispheres, hypothalamus or optic pathways (optic glioma). Seen as a well demarcated lesion with NO or minimal edema. Very good prognosis after surgical resection. Anaplastic Astrocytoma is poorly differentiated and disrupts the BBB. Generally, evolves to glioblastoma multiforme. Treatment is resection, radiation, or chemotherapy. Has an intermediate prognosis. Glioblastoma Multiforme (grade IV glioma) makes up 30% of all primary brain tumors in adults. It is highly aggressive and the deadliest form of brain tumor. Surgical debulking and chemotherapy are palliative care and not a cure. Life expectancy is weeks. Oligodendroglioma is a mixture of oligodendrocytes and astrocytes. Makes up 6% of primary intracranial tumors. Seizures predate the appearance of tumor in imaging. There are calcifications within the tumor. Treatment initially is resection and NOT radiation, later treatment is resection with chemotherapy and radiation. Ependymoma is commonly seen in childhood and young adults. The most common location is on the floor of the 4th ventricle. Symptoms include obstructive hydrocephalus, headache, nausea, vomiting, and ataxia. Treatment involves resection and radiation. Prognosis typically depends on the completeness of resection. Primitive Neuroectodermal Tumor (retinoblastoma, medulloblastoma, pineoblastoma, and neuroblastoma) Medulloblastoma is the most common pediatric primary malignant brain tumor. It may disseminate via CSF to SC. Symptoms are like in ependymoma. Treatment is resection and radiation. Prognosis is very good if treatment leads to tumor disappearance on both brain MRI and tumor cells within the CSF. Meningioma are slow growing, well circumscribed, benign tumors arising from arachnoid cap cells, NOT the dura mater. They are most common near the sagittal sinus, falx cerebri, and cerebral convexity. Usually apparent on plain radiographs and CT scans because of calcifications. Often blood supply comes from the external carotid artery. Treatment is surgical resection, and prognosis is excellent (maybe recurrent). Pituitary Tumors Pituitary Adenomas (anterior pituitary gland) are functional and non-functional tumors. Functional tumors are microadenomas and hormone secreting. Non-functional tumors are macroadenomas and symptoms are related to their mass. May cause panhypopituitarism, which is a rare condition where the pituitary gland fails to produce most or all its hormones. Pituitary apoplexy is a medical emergency that occurs when there is sudden bleeding into or impaired blood supply of the pituitary gland. Symptoms include abrupt onset of headache, visual changes, ophthalmoplegia, altered mental status secondary to hemorrhage, necrosis or infarction within the tumor. Treatment is surgical resection through open craniotomy or transsphenoidal approach. A prolactinoma is a noncancerous tumor of the pituitary gland that produces an excessive amount of prolactin, a hormone responsible for milk production in the breasts. This condition can lead to various symptoms due to the elevated levels of prolactin and the pressure exerted by the tumor on surrounding tissues. Treatment is bromocriptine which is used to treat hyperprolactinemia. Acoustic Neuroma is a benign schwannoma involving CN VIII within the internal auditory canal. Symptoms include hearing loss, tinnitus, and disequilibrium. Large tumors at the cerebellum pontine angle can cause compression of CN V and VII as well as the brainstem. Treatment involves surgical resection with or without radiation therapy. Intraop CN monitoring and brainstem evoked potentials is necessary. Prognosis is very good, but recurrence is not uncommon. CNS Lymphoma (Microglioma) Primary CNS Lymphoma (Rare tumor) is commonly located supratentorial, especially deep gray matter or corpus callosum. It is associated with systemic lupus erythromatosus, Sjogren’s syndrome. Rheumatoid arthritis, immunosuppressed states, and infection with Epstein-Barr virus. Diagnosis is done with imaging and biopsy. It is reasonable to wait to administer corticosteroids until after pathologic specimens have been obtained since these tumors may be very sensitive to steroids. Treatment is chemotherapy (including intraventricular delivered drugs) and whole brain radiation. Prognosis is poor despite treatment. Metastatic brain tumor is most often originating in the lung or breast. Tumors that likely spread to the brain: Malignant melanoma Hypernephroma Carcinoma of colon Likely diagnosis when >1 intracranial lesion is present. Abnormal angiogenesis, these tumors tend to bleed more during resection than other CNS tumors.  Management of Anesthesia in Brain Tumor Resection Major Goals: 1. Maintaining adequate cerebral perfusion and oxygenation of normal brain. 2. Optimizing operative conditions to facilitate resection. 3. Ensuring a rapid emergence from anesthesia at the conclusion of the procedure to facilitate neurological assessment (post-operative period). 4. Accommodating intraoperative electrophysiologic monitoring if needed. Preoperative: Identify the presence of increased ICP. Symptoms include nausea, vomiting, altered level of consciousness, mydriasis, decreased reactivity of pupils with light, papilledema, bradycardia, systemic hypertension, and breathing disturbances. Imaging reveals midline shift (>0.5 cm). Preoperative administration of depressant (opioids, sedatives) should be AVOIDED in patients with diminished levels of consciousness. Benzodiazepines (small doses) for anxiety relief without meaningfully affecting ventilation. Induction of Anesthesia Thiopental, Etomidate, or Propofol for a rapid, reliable onset of unconsciousness without increasing ICP. Nondepolarizing muscle relaxants to facilitate tracheal intubation. Mechanical hyperventilation to decrease PaCO2 to ~35 mmHg. Abrupt sustained increases in BP may be accompanied by undesirable increases in CBF, CBV, and ICP and precipitate cerebral edema. Sustained hypotension should be AVOIDED to prevent brain ischemia. PEEP has a highly variable effect on ICP and is used with CAUTION by paying attention to ΔICP, MAP and CPP. Maintenance of Anesthesia Combining drugs of various classes, including nitric oxide, volatile anesthetics, opioids, barbiturates, and propofol. Spontaneous movement by patients undergoing surgery MUST BE PREVENTED. Movements could result in: increased intracranial volume and ICP, increased surgical bleeding (difficult surgical exposure). Direct injury to head and brain from pinions or surgical instrumentation. Skeletal muscle paralysis is typically maintained during intracranial surgery Monitoring: Intra-arterial catheter for BP and blood sampling Capnography to facilitate ventilation & PaCO2 management; detect venous air embolism. Central venous catheterization is useful for both intravenous access and monitoring fluid status Peripheral nerve stimulator to monitor persistence of drug-induced skeletal muscle paralysis.  ECG to detect responses related to intracranial tumors or surgery; reflect increases in ICP, surgical retraction or manipulation of the brainstem or CNs ICP continuously, NOT by routine. Coma State of profound unconsciousness produced by drug, disease, or injury affecting CNS. Dysfunction of brain regions responsible for maintaining consciousness is the pontine reticular activating system, midbrain, or cerebral hemispheres. Etiology is structural lesions and diffuse disorders. Prognosis is usually related to the cause and extent of injury to brain tissue. Glasgow Coma Scale asses the overall severity of coma. Initial Management is to establish a patent airway and ensure adequacy of oxygenation, ventilation and circulation. Determine the cause of the coma. Decreased BP and HR can lead to hypothermia. Irregular breathing patterns indicate an abnormality at a specific CNS site. Basic neurological examination is necessary. Abnormal patterns of breathing Abnormality Pattern Site of lesion/condition Ataxic (Biot's breathing) Unpredictable sequence of Medulla breaths varying in rate and tidal volume Apneustic breathing Gasps and prolonged pauses at Pons full inspiration Cheyne-Stokes breathing Cyclic crescendo-decrescendo Cerebral hemispheres, tidal volume pattern Congestive heart failure interrupted by apnea Central neurogenic Marked hyperventilation Cerebral thrombosis or hyperventilation embolism Posthyperventilation apnea Awake apnea following Frontal lobes moderate decreases in Paco₂ Basic neurological examination includes: Examination of the pupils and pupillary responses to light. Function of extraocular muscles via reflexes. Gross motor responses in the extremities. Neurological findings on compression of the brainstem during transtentorial herniation Region of Pupillary examination Response to Gross motor findings compression oculocephalic or cold caloric testing Diencephalon Small pupils (2 mm) Normal Purposeful, reactive to light semipurposeful, or decorticate (flexor) posturing Midbrain Midsize pupils (5 mm) May be impaired Decerebrate (extensor) unreactive to light posturing Pons or medulla Midsize pupils (5 mm) Absent No response oblongata unreactive to light In cases in which the cause of coma is unknown, discriminatory lab test looking for disorders of sodium or glucose, liver and renal function test looking for hepatic or uremic encephalopathy, drug and toxicology to identify exogenous intoxicants, complete blood count and coagulation studies looking for intracranial bleeding from thrombocytopenia or coagulopathy, CT or MRI to rule out tumor or stroke, lumbar puncture to test for meningitis or subarachnoid hemorrhage. 1ry Goal: Establish an airway, provide adequate cerebral perfusion and oxygenation, optimize operating procedures. Avoid increases in ICP during stimulating events like intracranial monitoring. Intraarterial catheterization for BP optimization & management of hyperventilation. Avoid anesthetic agents that increase ICP (halothane & ketamine). Nitric Oxide should be AVOIDED in a known or suspected pneumocephalus. Nondepolarizing muscle relaxants facilitate tracheal intubation and patient positioning. Avoid Succinylcholine, it can transiently increase ICP.  Stroke is the third leading cause of death in the US and the leading cause of major disability. Non-Hispanic whites are at risk of extracranial carotid artery disease and heart disease associated embolism. African Americans have higher risk of intracranial thromboembolic disease. Lower stroke rates in women. Highest stroke rates after the age of 75. Occlusion of specific arteries distal to the circle of Willis results in predictable clinical neurological deficits. Clinical features of cerebrovascular occlusive syndromes Occluded artery Clinical features Anterior cerebral artery Contralateral leg weakness Middle cerebral artery Contralateral hemiparesis and hemisensory deficit (face and arm more than leg) Middle cerebral artery (dominant hemisphere) Aphasia Middle cerebral artery Contralateral visual field defect Posterior cerebral artery Contralateral visual field defect Posterior cerebral artery Contralateral hemiparesis Penetrating arteries Contralateral hemiparesis Penetrating arteries Contralateral hemisensory deficits Basilar artery Oculomotor deficits and/or ataxia with crossed sensory and motor deficits Vertebral artery Lower cranial nerve deficits and/or ataxia with crossed sensory deficits Sudden neurological deficits result from ischemia, 88% of cases, described by area affected and etiology, 12% of cases are Hemorrhagic, 15% of which are intracerebral and 85% are subarachnoid. Characteristics of stroke subtypes Parameter Systemic Embolism Thrombosis Subarachnoid Intracerebral Hypoperfusion Hemorrhage Hemorrhage Risk Hypotension,Smoking, Smoking, Often none, Hypertension, factors Hemorrhage, Ischemic heart Ischemic Hypertension, Coagulopathy, Cardiac arrest disease, heart disease, Coagulopathy, Drugs, Peripheral Peripheral Drugs, Trauma vascular vascular Trauma disease, disease, Diabetes Diabetes mellitus, mellitus, White race White race and male and male gender gender Onset Parallels risk Sudden Often Sudden, often Gradually factors preceded by a during progressive transient exertion ischemic attack Signs and Pallor, Headache Headache Headache, Headache, symptoms Diaphoresis, Vomiting, Vomiting, Hypotension Transient loss Decreased of level of consciousness consciousness , Seizures Imaging CT CT CT CT CT (hypodensity), (hypodensity), (hypodensity (hyperdensity) (hyperdensity MRI MRI ), MRI , MRI ), MRI Transient Ischemic Attack (TIA) is a sudden vascular-related focal neurologic deficit that is resolved within 24hrs. Evidence of impending ischemic stroke. Most likely reflects embolism as a result of a cardiac cause. Prognosis of stroke depends on the time elapsed from the onset of symptoms to thrombolytic intervention (if thrombosis is the cause). Patients who receive early treatment to restore cerebral perfusion have better outcomes. Risk factors: systemic HTN (primary cause), cigarette smoking, hyperlipidemia, DM, excessive alcohol consumption, increased serum homocysteine. Imaging is a non-contrast CT; it is insensitive to ischemia changes in the first few hours after stroke, but it is very sensitive for detection of intracranial hemorrhage. Acute Ischemic Stroke Angiography (conventional, CT or MRI) or transcranial doppler US to demonstrate arterial occlusion. Echocardiography is used to evaluate the presence of anatomic or vascular abnormalities that could result in embolization. Patients with long standing diabetes mellitus or systemic hypertension are most likely to experience acute ischemic stroke resulting from small occlusive vessel disease. Management of Anesthesia Initial therapy is with Aspirin. Management of the airway, oxygenation, ventilation, systemic BP, blood glucose concentration, and body temperature. In most critically ill stroke patients, cerebral edema and increased ICP may complicate the clinical course. Malignant MCA (Middle Cerebral Artery) syndrome is characterized by significant brain swelling and increased intracranial pressure, presence of edematous infarcted tissue that cause compression of the ACA and PCA and cause secondary infarctions. Treatment would be a hemicraniectomy for decompression. Respiratory functions may be evaluated promptly in ALL stroke patients, maintain arterial oxygen saturation >95%. Maintenance of adequate BP, blood flow to ischemic regions is DEPENDENT on CPP. Hyperglycemia appears to parallel poor outcomes, normalization with insulin is recommended. Fever should be avoided, it increases CMRO2, with antipyretics or cooling blankets. Early in the treatment, prophylaxis to prevent deep vein thrombosis (heparin or pneumatic compression stockings) Intracerebral Hemorrhage 4x deadly than ischemic stroke. Most often in African Americans. Non-contrast CT to identify bleeding. The 2nd most reliable predictors of outcome are estimated volume of extravasated blood and level of consciousness. Clinical deterioration when cerebral edema worsens during first 24-48 hrs. AFTER acute bleeding. Treatment is to lower hematoma volume, administer IV recombinant activated factor VII within 4hrs of onset of symptoms. Treat any signs of hydrocephalus with ventricular drainage. For endotracheal intubation, sedation with or without drug-induced skeletal muscle paralysis. In patients with co-existing essential hypertension the goal is MAP