Книги по МРТ КТ на английском языке / Neurosurgery Fundamentals Agarval 1 ed 2019

Type I: Normal perfusion and blood flow with 60% increase after Diamox challenge.

Type II: Decreased CBF with less than 10% increase after challenge.

Type III: Decreased CBF with steal phenomenon resulting in decreased local perfusion.

12.1.6  Ischemic S troke Therapeutic Management

Acute Treatment

Initial definitive management aims at recanalization of the occluded vessel thus providing the required oxygen and nutrients to tissue at risk.

•IV tPA: Patients who receive therapy are 30% more likely to have no disability at 3 months.

Eligiblity: Age more than 18 years, within 4.5 hours of last seen well (European Cooperative Acute Stroke Study III [ECASS III]), wake up stroke. If IV tPA cannot be given, aspirin 300 mg PR or 325 mg PO can be given.

◦◦ Contraindications: ICH, subarachnoid hemorrhage (SAH), aneurysm or arteriovenous malformation (AVM), active bleeding, anticoagulants or heparin within 48 hours, platelet count less than 100,000, head trauma or cranial surgery within 3 months,

SBP more than 185 mmHg, DBP more than 110 mmHg, caution if major surgery within 14 days.

◦◦ Outcomes: Almost 33% patients benefit, 7.9% rate of ICH (vs. 3.5% in controls), but no increased risk of death.

•Mechanical thrombectomy: By stent retriever, suction aspiration, or other devices.

◦◦ Eligibility: within 8 hours of symptom onset.

◦◦ Outcomes: 48–82% recanalization with 3–7% risk of adverse events, about 1/4th of patients improve to mRS less than 2 at 3 months. The

Highly Effective Reperfusion Evalu- ated in Multiple Endovascular Stroke Trials (HERMES) showed earlier treatment with endovascular and medical therapy resulted in lower disability compared to medical therapy alone.9 However, the treatment window from onset of symptoms was found to be 7.3 hours. After that time period, there was no benefit from combina- tion therapy.

Subacute Treatment

Subacute treatment focuses on optimization of hemodynamic parameters, electrolytes, and management of potential complications until the patient can be safely started on anticoagulation for secondary stroke prevention.

•Permissive hypertension:

◦◦ Hypertension in acute ischemic stroke or TIA should not be aggressively treated unless SBP > 220 mmHg. Typi- cal SBP floor for patients with no prior history of hypertension should be set at 160 mmHg and in those with such history at 180 mmHg.

-If tPA was given, SBP captured < 185/110 mmHgs.

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-If mechanical thrombectomy, BP cap < 140 mmHg at our institution (guidelines unclear).

-Indications to treat include malignant hypertension (DBP > 140 mmHg), acute renal failure, aortic dissection, acute left ventricular failure.

•Other management parameters:

◦◦ Eunatremia, serum glucose 140–180 mg/dL.

◦◦ Immediate deep vein thrombosis prophylaxis unless tPA given, if so, defer until 24 h.

◦◦ Patient should be evaluated by speech therapy for dysphagia.

•Complications: Malignant edema

◦◦ Treat with hypertonic saline 23.4% 30 mL bolus q4 hours.

◦◦ Mannitol at 0.5–1.25 g/kg, need to monitor serum osmolarity.

◦◦ May need decompressive hemicraniectomy.

Secondary Prevention

Once the acute risks have passed, patients should be anticoagulated to prevent secondary strokes. In addition, a full stroke workup to determine the cause and minimize risk factors should be obtained including:

•Glycosylated hemoglobin, lipid panel, transthoracic echocardiogram.

•Holter monitor if cardioembolic cause suspected.

•Dual therapy with aspirin 81 mg and clopidogrel 75 mg daily if intracranial atherosclerosis is present and thought to be the cause of stroke (Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events [CHANCE] trial).10,​11

•Lipid-lowering therapy with statins such as atorvastatin 40 mg if low density lipoprotein (LDL) > 70 or 80 mg if LDL> 100.12

•Anticoagulation with warfarin or new oral anticoagulants if atrial fibrillation present.

12.1.7  Intraparenchymal Hemorrhage Management

Hemorrhagic stroke is the cause of 15% of all strokes with vast etiology including hypertension, amyloid angiopathy, coagulopathy, vascular malformations, and hemorrhagic conversion of ischemic stroke.

Volume of hemorrhage can be calculated by using the approximation ABC/2. Where A, B, and C are measurements in each axis.

Acute Treatment

Initial management is focused on preventing expansion of the hematoma with reversal of any underlying causes of coagulopathy if present.

Blood pressure management: SBP less than 180 mmHg; no clear benefit with SBP less than 140 mmHg as shown by the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-2).13 Clevidipine or nicardipine drips are recommended. The primary difference is that clevidipine can be titrated quickly (within 90 s), whereas nicardipine can take up to 15 minutes.

•Diagnostic imaging: In the acute setting, CT head with interval scan at 6 hours is standard. Digital subtraction angiography (DSA) may be the next diagnostic modality of choice if aneurysmal rupture or AVM are suspected. MRI with and without contrast may be needed in the subacute setting if hemorrhage into tumor bed is suspected or if amyloid angiopathy is the culprit.

•Surgical intervention: The Surgical Trial in Lobar Intracerebral Hemor-

rhage (STITCH) I and II trials showed that there was no difference in patients receiving surgical versus conservative management in prophylactic supratentorial superficial hematoma evacuation. Those with deep-seated clots tend to do better with conservative management. External ventricular drain (EVD) placement and indications are discussed further in neurocritical care section. At the time of writing this text, the Minimally Invasive Surgery Plus Rt-PA for ICH Evacuation Phase

III (MISTIE III) trial to evaluate role of minimally invasive clot evacuation is ongoing.

•Coagulopathy: Reversal of coagulopathy, either iatrogenic or acquired, is paramount in preventing hematoma expansion. However, in patients where the bleed appears stable or, in patients with significant comorbidities in which anticoagulation is preferred, a balance needs to be struck. Recent data from the Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral hemorrhage associated with antiplatelet therapy (PATCH) trial suggests that patients randomized to receive platelet therapy in addition

to standard of care in a setting of spontaneous ICH had almost 25% more adverse events.14 More data is needed, however, this calls into question cavalier use of platelets in spontaneous ICH. Recommended reversal agents are outlined in Table 12.3.

12.1.8  Management of Carotid Atherosclerosis

Carotid atherosclerosis is a major cause of ischemic stroke. Intracranial carotid calcification is a significant predisposition in 75% of all strokes, with aortic arch calcification contributing to 45% of ischemic strokes as

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shown in the Rotterdam­ study.15 For patients with extracranial carotid calcification, the risk for stroke was much lower at 25%. Management of symptomatic carotid artery stenosis has to be expedited to prevent future ischemic events ( Fig. 12.2). Pressure control decreases risk of stroke in patients with carotid artery stenosis, but aggressive

management is contraindicated. The Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events (ACTIVE) trial suggests that addition of clopidogrel to aspirin in patients with carotid artery stenosis and atrial fibrillation who are not suitable for vitamin K antagonists may actually be beneficial.16 Surgical management of

carotid artery stenosis represents the definitive management. Current invasive modalities include carotid artery endarterectomy, balloon angioplasty, and stenting. Regarding carotid endarterectomy, patients should be kept on aspirin for at least 2–5 days, prior to surgery and on the day of surgery.

Carotid artery endarterectomy has:

•Clear benefit in symptomatic patients with more than 70% stenosis.17

•Marginal benefit in symptomatic patients with 50–69% stenosis.

•Some benefit in asymptomatic patients with more than 60% stenosis.

•No to minimal role in lesions with less than 30% (North American Symptomatic Carotid Endarterectomy

Trial [NASCENT]).17 or less than 40% stenosis (European Carotid Surgery Trial [ECST]),18 where intensive medical therapy is clearly preferred.

The procedure is generally contraindicated in patients with severe neurologic deficit, 100% occlusion, and other comorbidities that severely decrease the patient’s expectancy independent of current carotid atherosclerotic disease. According to the Carotid Revascularization Endarterectomy vs. Stenting Trial (CREST), there is no difference in overall mortality and morbidity in those with symptomatic or asymptomatic carotid atherosclerosis undergoing stenting or carotid endarterectomy.19 Most recent analysis of CREST data actually suggests that carotid endarterectomy is as safe as carotid artery stenting in terms of perioperative risk.20 There is controversy and lack of data to show whether stenting is superior to carotid endarterectomy in patients with average risk.7 CREST-2 and other trials are currently ongoing and aim to evaluate whether carotid endarterectomy or stenting plus modern medical therapy is superior to modern medical therapy alone in primary prevention of stroke in patients with high grade lesions.21 However, results are not expected to be available until early 2020s.

Carotid angioplasty or stenting is indicated in the following populations7:

•Patients with significant cardiac comorbidities such as congestive heart failure (CHF) grade III or IV.

•History of myocardial infarction in the past month.

•Unstable angina.

•Complete occlusion of the contralateral carotid system.

•Severe scarring of the neck tissues due to surgery or radiation therapy.

•Damage or paralysis of contralateral laryngeal nerve.

12.1.9  Stroke Syndromes Internal Carotid Artery

Occlusion of the internal carotid artery (ICA) can result in strokes in up to 50% of patients depending on the collateral circulation. It results in contralateral hemiparesis, aphasia if the dominant lobe is involved, or hemineglect in nondominant hemisphere. It can also cause various degrees of hemianopia.

Anterior Cerebral Artery

Strokes in this artery distribution cause contralateral lower extremity weakness and loss of sensation. Occlusion of Huebner’s artery will result in upper extremity and facial weakness without increased rigidity.

Middle Cerebral Artery

Contralateral hemiplegia with hemianesthesia, and aphasia if dominant hemisphere involved. Upper division MCA strokes typically result in greater deficits of upper extremity and face than lower extremity. Lower division occlusion presents with Wernicke’s aphasia and hemianopia. Occlusion of lenticulostriate arteries arising from MCA results in varying degrees of contralateral hemiparesis.

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Gerstmann syndrome is a result of stroke in dominant hemisphere in angular and supramarginal gyrus. Patients present with agraphia, acalculia, finger agnosia, and left-right confusion.

•Foix-Chavany-Marie Syndrome is caused by bilateral anterior opercular strokes and presents with anarthria. It is also known as facio-labio-pharyngo- glosso-laryngo-brachial paralysis.

Posterior Cerebral Artery

Visual deficits are most often seen, including quadrantanopia, hemianopia, cortical blindness, or Gerstmann syndrome.

•Weber’s syndrome is caused by occlusion of midbrain perforators and results in ipsilateral oculomotor nerve palsy, palpebral palsy, mydriasis, diplopia, and contralateral hemiparesis.

•Benedict’s syndrome is a result of occlusion of paramedian perforators and is characterized by symptoms similar to Weber’s with addition of cerebellar ataxia.

Superior Cerebellar Artery

Primarily results in ipsilateral ataxia, dysmetria, and dysarthria. If occluded, proximally can result in contralateral sensory deficits.

Anterior Inferior Cerebellar Artery

Results in lateral pontine syndrome characterized by ipsilateral facial paralysis, loss of taste, deafness or tinnitus, extremity ataxia, and contralateral sensory loss.

Posterior Inferior Cerebellar Artery

Also known as lateral medullary syndrome, it is distinguished by absence of pyramidal tract findings.

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•Wallenberg’s syndrome results in hemianesthesia, specifically, ipsilateral facial sensory loss but contralateral body sensory loss, diplopia, Horner’s syndrome, pharyngeal and laryngeal paralysis, dysphagia, hoarseness, and ipsilateral ataxia.

•Dejarine’s syndrome results in thalamic hypergesic hemiparesis.

Basilar Artery

Can result in mesencephalothalamic syndrome, locked-in syndrome, Parinaud’s syndrome, or Weber’s syndrome.

Vertebral Artery

Depending on proximal-distal location of vertebral occlusion patients present with diplopia, vertigo, ataxia, and facial weakness.

Vertebrobasilar Insufficiency

Diagnosis requires two or more of the following: diplopia, drop attack, dysarthria, visual defect, or dizziness.

Thalamic Strokes

The thalamus primarily receives blood supply from the posterior cerebral artery and posterior communicating artery. Occlusion at distinct divisions of the posterior cerebral artery (PCA) can result in vastly different symptom presentation.

•Anterior thalamus is supplied by the tuberothalamic and polar arteries from the posterior communicating artery (Pcomm). Ischemia results in neglect, aphasia, and amnesia.

•Paramedian thalamus receives its blood supply from the thalamosubthalamic branches of P1. Strokes result in loss of consciousness.

•Inferolateral thalamus strokes cause pure hemisensory loss due to occlusion of P2 thalamogeniculate vessels.

•Posterior thalamus ischemia is a result of P2 posterior choroidal vessel

occlusion and causes poor memory and visual field cut.

Artery of Percheron is a rare variant in which a single artery arises from PCA to supply both thalami and the midbrain. Thrombosis can result in catastrophic bilateral stroke affecting consciousness and alertness.

imaging findings ( Table 12.5).23 It should only be used in aneurysmal subarachnoid hemorrhage ( Fig. 12.3).

Modified Fisher Scale

It is based on newer data and relies on simpler grading scheme ( Table 12.6).24

World Federation of Neurosurgical Societies (WFNS) Scale.

The WFNS scale is used to provide a quick reference for the level of consciousness and neurological deficit in patients with aneurysmal SAH ( Table 12.7).25

12.2  Subarachnoid Hemorrhage

12.2.1  Epidemiology

SAH represents a subset of ICH. Traumatic SAH is the most common cause of SAH. Cerebral aneurysm rupture is responsible for up to 80% of all spontaneous causes of SAH, with AVMs being responsible for another 5%. Other causes include arterial dissection, rupture of small arteries, hemorrhage into tumor bed, coagulation disorders, and others. The cause is unknown in one-fifth of all cases.

12.2.2  Risk and Prognosis Hunt-Hess Grading Scale

It is used to classify aneurysmal subarachnoid hemorrhage and predict mortality ( Table 12.4).22 Indirectly, the Hunt-Hess scale may be thought of as an indicator of hydrocephalus given that an EVD will often be placed with a grade 3 or higher.

Fisher Scale

Predicts the risk of vasospasm following aneurysmal bleed or rupture based on CT

12.2.3  Initial Management

During the acute period, neurological examination and head CT should be performed in any patient with suspected SAH. If head CT does not show overt findings of SAH, but it is still suspected, then diagnostic lumbar puncture should be performed to assess for number of red blood cells and xanthochromia. CT angiography (CTA) or DSA is the next step to assess for aneurysm if the presenting symptoms and tempo of clinical worsening allow.

•Blood pressure management: SBP should be kept less than 140 mmHg for unsecured aneurysms. Clevidipine or nicardipine drips are recommended.

•Other parameters: Maintain euvolemia with normal saline + 20 mEq KCl/L at 2 mL/kg/h. Maintain normal ICP values if able. Arterial and central venous line access needs to be established.

•Airway management: Comatose patients or those with concern for airway patency should be intubated.

•Diagnostic imaging: Initially CT and CTA, with DSA being the definitive imaging of choice.

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•Surgical intervention: EVD placement for initial stabilization if hydrocephalus is present or if significant intraventricular blood is present with concern for obstructive and/or communicating

Fig. 12.3  Subarachnoid hemorrhage. CT imaging showing

(a) Fisher grade 2 and (b) Fisher grade 3 subarachnoid hemorrhage. (Reproduced from Spetzler R, Kalani M, Nakaji P, Neurovascular Surgery, 2nd edition, ©2015, Thieme Publishers, New York.)

hydrocephalus. Additional indications are discussed further in neurocritical care section. Definitive surgical treatment of the underlying lesion (aneurysm, AVM, etc.) is dictated by patient presentation.

Table 12.6  Modified Fisher scale

Abbreviations: IVH, intraventricular hemorrhage; SAH, subarachnoid hemorrhage.

12.2.4  Vasospasm Prevention

Cerebral vasospasm, a narrowing of cerebral arteries, is a complication of SAH and is particularly dangerous in the subacute period.

Cerebral vasospasm typically peaks around day 7 post SAH, and usually manifests 3-14 days after hemorrhage. However, it can present as late as 21 days after the inciting event.

Other types of intracranial hemorrhage, trauma, surgery, and CSF diversion can all cause vasospasm to occur. It usually presents with confusion, altered sensorium, decreased consciousness, or focal deficits.

Table 12.7  World Federation of Neurosurgeons (WFNS) scale

Grade GCS score Focal Deficit

0

Abbreviation: GCS, Glasgow Coma Scale.

Radiographically, it becomes apparent in 30–70% of all patients who undergo repeat CTA or DSA.26 Only about 25% of all patients with SAH demonstrate clinical vasospasm. Clinical findings of vasospasm are not present in all cases of radiographic vasospasm. Transcranial dopplers (TCDs) or CTA can be used to detect vasospasm, but DSA is the gold standard as it also allows definitive management. TCDs are semiquantitative in their evaluation and rely on the Lindegaard ratio with values less than 3 being normal, 3–6 indicating mild vasospasm, and more than 6 showing moderate- to-severe vasospasm.

The Lindegaard ratio is simply the ratio of flow in the ipsilateral MCA to ICA. Values are highly operator dependent.

Prophylactic management of vasospasm is limited and typically relies on hydration, euvolemia, and avoidance of anemia. Prophylactically, triple H therapy is not indicated.27 Once vasospasm becomes a clinical possibility, immediate imaging of the brain with CT scan should be performed to rule out new-onset edema, expanding infarction, new hemorrhage, or hydrocephalus. Treatment options for confirmed vasospasm are discussed in more detail below.7

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•Pharmacological therapy: Nimodipine, and other calcium channel blockers dilate arteries, but in clinical practice, they have not been shown to prevent radiologic vasospasm.28 Effects of nimodipine are mediated through neuroprotection via its effects on blood rheology, anti-platelet effects, and dilation of collateral arteries rather than vasodilation. Statins have been shown to reduce vasospasm and mortality. Mannitol could be useful by improving blood rheology and microvascular perfusion. Of note, hypertonic saline may be preferable to mannitol for elevated ICP during the vasospasm window to allow for volume expansion.

•Hyperdynamic therapy: Places importance on CPP to maintain blood flow and prevent clinical vasospasm. It is named after its three major components:

◦◦ Hypertension (SBP < 220 mmHg in clipped aneurysms).

◦◦ Hemodilution with hematocrit 25–33%.

◦◦ Hypervolemia (CVP elevation to

8–12 cmH2O).

The hypertension component can be induced with dopamine at 2.5–20 μg/ kg/min, levophed 1–64 μg/min, phen- ylephrine 5–64 μg/min, or dobutamine up to 20 μg/kg/min. Hypervolemia can be induced with normal saline or plasmalyte at 150–250 mL/h or DDAVP (desmopressin).

•Endovascular therapy: Represents direct treatment for vasospasm but may have to be done multiple times for repeat vasospasm. Angioplasty is usually more effective than intra-arterial drug therapy with verapamil or nicardipine.

12.3  Aneurysms

12.3.1  Definitions

Cerebral aneurysms are local dilations of intracranial blood vessels and are

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thought to occur due to weakness in the vessel wall.

12.3.2  Epidemiology

Cerebral aneurysms occur in about 5% of the population29 and their rupture can result in devastating SAH. Ruptured cerebral aneurysm account for 5–15% of all stroke cases.30,​31 About 45% of ruptured patients never reach the hospital in time to receive proper treatment.29,​ 31 A third of the survivors reaching the hospital will develop moderate-to-se- vere lifetime disabilities. Modifiable risk factors for cerebral aneurysms include hypertension and smoking.32 Women make up two-thirds of all cerebral aneurysm cases with postmenopausal status being another risk factor.40,​29 Female sex is associated with increased risk of SAH and higher mortality.33 Pediatric cases are rare.

Almost 95% of all cerebral aneurysms are sporadically acquired defects.34,​35Less than 5% are thought to be congenital or due to genetic diseases. Saccular aneurysms, named after their balloon-like shape, make up 90% of all aneurysms with fusiform and blister aneurysms making up the remaining 10%.29,​31,​34 Fusiform aneurysms are more common in the vertebral system.7

Location within the circle of Willis appears to have an intricate relationship with aneurysm formation ( Fig. 12.4). Most of the cerebral aneurysms occur at bifurcations and are found in the carotid system (85–95%) rather than the posterior or vertebrobasilar system (5–15%). Aneurysms in the anterior communicating artery (ACoA) are the most common representing 30% of all cases. Pcomm and MCA are the second and third most common locations accounting for 25% and 20% of all cases, respectively. The basilar artery represents only 5–10% of all cases. Frequently, upon rupture or “sentinel-bleed”, the patients present