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You have just encountered a possible stroke patient. You ask yourself, what should I do first? How do I know it is a stroke? Is it too late to reverse the damage? How do I do the right things in the right order? This book will help you answer these critical questions. It provides practical advice on the care of stroke patients in a range of acute settings. As new and effective treatments become available, and designated stroke centers are created, this guidebook will help inform the healthcare professionals responsible for delivering care. The content is arranged in chronological order, covering the things to consider in assessing and treating the patient in the emergency department, the stroke unit, and then on transfer to a rehabilitation facility. All types of stroke are covered. A comprehensive set of appendices contain useful reference information including dosing algorithms, conversion factors and stroke scales.
Cambridge University Press
9780521674942 - Acute Stroke Care - A Manual from the University of Texas-Houston Stroke Team - by Ken Uchino, M.D., Jennifer K. Pary, M.D. and James C. Grotta, M.D.
Stroke is the most common neurological emergency, and, because effective treatment is available that must be started within minutes, most acute neurological presentations should be assumed to be a stroke until proven otherwise by history, exam, or radiographic testing. Unfortunately, there is not a quick and easy laboratory or clinical test to determine for sure that the patient lying in front of you is having a stroke, so an accurate history and exam are essential.
The term “stroke” usually refers either to a cerebral infarction or to non-traumatic cerebral hemorrhage. Depending on the population you are seeing (ethnicity, age, comorbidities) the ratio of infarcts to hemorrhages is about 4:1.
As will be described in more detail in Chapter 3, cerebral infarcts can be caused by a number of pathological processes, but all end with an occlusion of a cerebral artery or vein. If the arterial occlusion results in a reduction of blood flow insufficient to cause death of tissue (infarction), it is termed “ischemia.”
As will be described in more detail in Chapter 8, non-traumatic cerebral hemorrhages are caused by a number of pathological processes which all lead to bleeding into the brainparenchyma and ventricles. Bleeding into the subarachnoid space (Chapter 9) is usually caused by a ruptured aneurysm or vascular malformation. Other types of brain bleeding, for example into the subdural or epidural space, are usually traumatic and are not considered in this book.
When taking the history, the most characteristic aspect of a cerebral infarct or hemorrhage is the abrupt onset, so be sure to get the exact flavor of the onset. It is also imperative to determine as precisely as possible the time of onset. The symptoms most often stay the same or improve somewhat over the next hours, but may worsen in a smooth or stuttering course. Ischemic strokes (but not hemorrhages) may rapidly resolve, but even if they resolve completely, they may recur after minutes to hours.
The second characteristic historical aspect of cerebral infarcts is that the symptoms will usually fit the distribution of a single vascular territory. This is also the most important characteristic of the neurological exam in a patient with an infarct. Therefore, patients with an infarct will present with symptoms and signs in the middle, anterior, or posterior cerebral arteries, a penetrating artery (producing a “lacunar” syndrome), or the vertebral or basilar artery (see below).
Parenchymal hemorrhages also occur in characteristic locations, and usually share the same symptom complex and signs as cerebral infarcts except that early decrease in level of consciousness, nausea and vomiting, headache, and accelerated hypertension are more common with hemorrhages.
Subarachnoid hemorrhages classically present as a bursting very severe headache (“the worst headache of my life”), and are often accompanied by stiff neck, decreased consciousness, nausea and vomiting. Focal neurological signs are often absent; if present, they usually signify associated bleeding into the parenchyma.
There is currently no 100% sensitive and specific test for cerebral infarction in the emergency department, so that the diagnosis is usually made on the basis of a characteristic history, exam, presence of comorbidities, and the absence of seizures or other stroke mimics. CT scanning is usually negative in the first three hours, or shows only subtle signs that have low inter-observer reliability. If available, MR imaging, or detection of an occluded artery by transcranial Doppler or arteriography (by CT, MRI or intra-arterial catheterization), can be confirmatory. Parenchymal or subarachnoid hemorrhage, on the other hand, can be reliably detected by emergent CT scanning.
All of the following may present similarly to a stroke. In all cases, the distinction can be made by an emergent MRI scan, which will show abnormal diffusion-weighted signal in most stroke cases, but not in mimics.
As discussed previously, there are two main types of stroke: ischemic and hemorrhagic. The majority of this book describes the approach to either type of stroke, but there are specific chapters on ischemic stroke, TIA, ICH, and SAH:
The following initial measures apply to all stroke patients. They are necessary to stabilize and assess the patient, and prepare for definitive therapy. All current and, probably, future stroke therapies for both ischemic and hemorrhagic stroke are best implemented as fast as possible, so these things need to be done quickly. This is the general order to do things, but in reality, in order to speed the process, these measures are usually dealt with simultaneously. They are best addressed in the ED, where urgent care pathways for stroke should be established and part of the routine (see Chapter 10).
© Cambridge University Press
Preface; List of abbreviations; 1. Stroke in the emergency department; 2. What to do first; 3. Ischemic stroke; 4. TPA protocol; 5. Neurological deterioration in acute ischemic stroke; 6. Ischemic stroke prevention: why we do the things we do; 7. Transient ischemic attack (TIA); 8. Intracerebral hemorrhage (ICH); 9. Subarachnoid hemorrhage (SAH); 10. Organization of stroke care; 11. Rehabilitation; Appendices 1-14.