Ebook Warlow’s stroke (4/E): Part 2
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Ebook Warlow’s stroke (4/E): Part 2
9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2.1Basic overview of subarachnoid hemorrhage, 4379.2Mechanisms of subarachnoid bleeding. 4389.3Neuroimaging patterns and findings. 4439.4Personal and genetic influences on subarachnoid hemorrhage, 4479.5Examination features in patients with subarachnoid hemorrhage. 4499.6Investigative course. 4509.1B Ebook Warlow’s stroke (4/E): Part 2asic overview of subarachnoid hemorrhage9.1.1Anatomic overviewA basic grasp of the anatomy of the brain and its vascular supply is crucial to understaEbook Warlow’s stroke (4/E): Part 2
nding the pathophysiology of bleeding in different intracranial compartments. The brain surface and skull are separated by three layers of membranes, 9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2 the inner surface of the dura. Although the space between the pia and brain, the dura and skull, and the arachnoid and dura are only potential spaces with no separation under normal circumstances, the subarachnoid space that lies between the arachnoid and pia is filled with cerebrospinal fluid. In Ebook Warlow’s stroke (4/E): Part 2addition, the major cerebral arteries and their large branches travel in the subarachnoid space, only entering the brain tissue in the form of small pEbook Warlow’s stroke (4/E): Part 2
enetrating arterioles. Thus, subarachnoid hemorrhage (SAH) occurs either from a source vessel traveling in the subarachnoid space, or when a hemorrhag9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2may cause intraparenchyma] extension with development of an intracerebral hemorrhage simultaneously with SAH,again because the pia provides little mechanical barrier support. In the second section of this chapter, we will review the multiple specific conditions and mechanisms that lead to SAH.Subara Ebook Warlow’s stroke (4/E): Part 2chnoid hemorrhage occurs either from a source vessel traveling in the subarachnoid space, or when a hemorrhage that originates in brain tissue dissectEbook Warlow’s stroke (4/E): Part 2
s through the thin pia membrane and into the subarachnoid space.Several additional anatomic peculiarities are worth noting. First, the arteries in the9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2 the brain. As a consequence, rupture of these arteries can quickly extravasate a large volume of blood with devastating consequences. Second, because the subarachnoid space is an open, fluid-filled space, in contrast to the epidural and subdural potential spaces, there may be less tamponade effect Ebook Warlow’s stroke (4/E): Part 2as there is no threshold of pressure required to dissect open a space to be filled with blood. Third, whereas the anatomic structure of the epidural aEbook Warlow’s stroke (4/E): Part 2
nd subdural spaces inherently work to contain hemorrhages within those compartments and anatomically isolate them from other intracranial structures, 9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2prio and Heinrich Mattle.» 2019 John Wiley & Sons Ltd. Published 2019 by John Wiley & Sons Ltd.438 I 9 What (aưt^ưHíiubtuactMoid hemorrhage?subarachnoid space is a fairly large container of cerebrospinal fluid, continuous over the outer surface of the brain and spinal cord. This fact may be exploite Ebook Warlow’s stroke (4/E): Part 2d when seeking to confirm a diagnosis of SAH by lumbar puncture, but can also be deleterious as the proinflammatory blood products spread to intracranEbook Warlow’s stroke (4/E): Part 2
ial, ophthalmic, and spinal structures distant from the site of hemorrhage. Finally, because multiple important structures traverse (cerebral arteries9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2ent inflammation can provoke a wide variety of secondary injuries such as cerebral vasospasm, cranial neuropathies, hydrocephalus, and diabetes insipidus. Injury from SAH is a combination of harm caused by local effects at the site of bleeding, concurrent intraparenchymal injury, disruptions of cere Ebook Warlow’s stroke (4/E): Part 2brospinal fluid dynamics with hydrocephalus and elevated intracranial pressures, and harm to other structures in the subarachnoid space.9.1.2EpidemiolEbook Warlow’s stroke (4/E): Part 2
ogy of subarachnoid hemorrhageAccording to recently compiled data, approximately 800000 people experience a new or recurrent stroke each year in the U9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2d Native American populations. A large prospective cohort study of stroke in Mexican Americans, for example, found that the age-adjusted risk ratio for SAH was 1.57 compared with non-Hispanic white populations, and double for black populations [2. 3]. The incidence appears to be greater yet among Na Ebook Warlow’s stroke (4/E): Part 2tive American and Pacific Islander populations, although among all race groups the proportion of SAH to all stroke types is typically near 3% [4-6]. NEbook Warlow’s stroke (4/E): Part 2
ot only are the rates of SAH greater in non-white racial groups, but mortality rates are uniformly higher as well [7]. Studies have not found a clear 9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2neurysm burden and location by race [8], Other risk factors for aneurysmal SAH include cigarette smoking, nicotine, caffeine and cocaine use, hypertension, low body mass index, and lower educational achievement (9).Approximately 3% of the 800000 strokes each year in the United States are subarachnoi Ebook Warlow’s stroke (4/E): Part 2d hemorrhages, with a higher incidence in black. Hispanic, and Native American populations. One-fifth of patients present stuporous with severe deficiEbook Warlow’s stroke (4/E): Part 2
ts, and around 15% have no identifiable cerebrovascular lesions on angiography.Describing the severity spectrum of SAH cases with precision is difficu9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2e interrater reliability and many studies indicate little statistical difference in outcome between grades [10], A reasonable approximation is that about 22% of patients with SAH due to ruptured aneurysms present stuporous and with severe deficits, or worse [11]. Approximately 15% of patients presen Ebook Warlow’s stroke (4/E): Part 2ting with subarachnoid bleeding have no identifiable cerebrovascular lesions on angiography [12, 13]. These patients are generally milder in severityEbook Warlow’s stroke (4/E): Part 2
and experience better outcomes [13, 14].An important caveat that must be kept in mind whenever interpreting literature on SAH is that most publication9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2is identified. This is primarily driven by the fact that a large preponderance of cases are caused by ruptured intracranial aneurysms, and because the course, management, and prognosis of secondary SAHs (e.g. bleeding from superficial melanoma metastases, subarachnoid extension of a primary intracer Ebook Warlow’s stroke (4/E): Part 2ebral hemorrhage) are primarily driven by the underlying primary disease process. For example, given that the incidence of intracerebral hemorrhage isEbook Warlow’s stroke (4/E): Part 2
more than three times greater than primary (aneurysmal or idiopathic) SAH. and that 40% of patients with intracerebral hemorrhage develop secondary S9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2use the significance and management of secondary SAH is poorly understood for most nonaneurysmal processes, the incidence is not clearly reported for most nonaneurysmal conditions and is difficult to estimate.Subarachnoid hemorrhage secondary to conditions such as subarachnoid extension of intracere Ebook Warlow’s stroke (4/E): Part 2bral hemorrhage, hemorrhagic metastases, and other processes are common.9.2 Mechanisms of subarachnoid bleedingIn this section, we will consider in grEbook Warlow’s stroke (4/E): Part 2
eater detail the various pathologic mechanisms that have been associated with subarachnoid bleeding, expanding upon the basic anatomic ideas already p9What caused this subarachnoid hemorrhage?Matthew B. Maoi and Andrew M. NaidechOipa-nw* o'Htwo'ogji. Sottweitem 0>»wsry, (Tivoja IL Iji*CHAPTER MENU9. Ebook Warlow’s stroke (4/E): Part 2ng themost common and lethal forms of primary hemorrhages in that intracranial compartment. Here we describe these vascular anomalies in greater detail.Saccular (berry) aneurysmHemorrhage from saccular aneurysm rupture is the best-studied cause of SAH. Saccular (or “berry") aneurysms are focal outpo Ebook Warlow’s stroke (4/E): Part 2uchings of a thinned and weakened artery wall. Although saccular aneurysms may form in any location of the arterial vascular system, in practice theyEbook Warlow’s stroke (4/E): Part 2
are overwhelmingly observed at or near vessel bifurcations on first- or second-order arterial branches of the vessels emanating from the circle of WilGọi ngay
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