Acute Stroke Care: A Manual from the University of Texas - Houston Stroke Team

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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.

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Editorial Reviews

From the Publisher
'… the authors reach their goal of guiding doctors through the vast amount of literature on stroke: the book is handy and very clearly written and will help general practitioners, residents and expert clinicians in their daily practice with stroke patients. We recommend the book to all doctors who are looking for a prompt access guide for diagnosis and treatment of stroke.' European Neurology
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Product Details

  • ISBN-13: 9780521674942
  • Publisher: Cambridge University Press
  • Publication date: 4/26/2007
  • Series: Cambridge Pocket Clinicians Series
  • Format: Mass Market Paperback
  • Pages: 230
  • Product dimensions: 4.25 (w) x 7.01 (h) x 0.67 (d)

Meet the Author

Ken Uchino is a Neurologist in the Department of Neurology at the University of Pittsburgh Medical School.

Jennifer Pary is a Vascular Neurologist at the Center for Neurosciences, Orthopedics and Spine, South Dakota.

James Grotta is Roy M. and Phyllis Gough Huffington Distinguished Professor and Chairman at the Department of Neurology, University of Texas Medical School.

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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 in the emergency department

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.

Is this a stroke?


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.

Signs and symptoms characteristic of the various arterial territories

  • Middle cerebral – contralateral loss of strength and sensation in the face, arm, and to a lesser extent leg. Aphasia if dominant hemisphere, neglect if non-dominant.
  • Anterior cerebral – contralateral loss of strength and sensation in the leg and to a lesser extent arm.
  • Posterior cerebral – contralateral visual field deficit. Possibly confusion and aphasia if dominant hemisphere.
  • Penetrating (lacunar syndrome) – contralateral weakness or sensory loss (usually not both) in face, arm, and leg. No aphasia, neglect, or visual loss. Possibly ataxia, dysarthria.
  • Vertebral (or posterior inferior cerebellar) – truncal ataxia, dysarthria, dysphagia, ipsilateral sensory loss on the face, and contralateral sensory loss below the neck.
  • Basilar – various combinations of limb ataxia, dysarthria, dysphagia, facial and limb weakness and sensory loss (may be bilateral), pupillary asymmetry, disconjugate gaze, visual field loss, decreased responsiveness.


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.

  • Seizures. If a seizure has a focal onset in the brain, the patient may be left with weakness, numbness, speech, or vision problems for a period of time (usually less than 24 hours) after the seizure. Unlike the typical cerebral infarct, focal deficits after a seizure are often accompanied by lethargy and have a resolving course, but if the patient has had a seizure accompanying a stroke it is impossible to know for sure how much of the deficit the patient displays is due to each. This is why patients with seizures at onset are usually excluded from clinical trials of new stroke therapies.
  • Migraine. Patients may have unilateral weakness or numbness, visual changes, or speech disturbances associated with a migraine headache (“complicated” or “complex” migraine). Also, patients with complicated migraine are at higher risk for stroke. In trying to make the distinction between complicated migraine and stroke, it is important to remember that because of the high prevalence of both migraine and stroke in the general population, it is dangerous to attribute the patient’s deficit to migraine just because the patient has a migraine history. The best rule of thumb is not to make the diagnosis of complicated migraine or migrainous stroke unless the patient has a history of previous complicated migraine events similar to the deficit displayed in the emergency department.
  • Syncope. This is usually due to hypotension or a cardiac arrhythmia. Stroke rarely presents with syncope alone. Patients with vertebrobasilar insufficiency may have syncope, but there are usually other brainstem or cerebellar findings if syncope is part of the stroke presentation.
  • Hypoglycemia. Patients with low blood sugar may have symptoms that exactly mimic a stroke. The important thing is to check the blood sugar and, if low, correct it. If the symptoms do not resolve with correction of the hypoglycemia, the symptoms are probably from a stroke.
  • Metabolic encephalopathy. Patients may have confusion, slurred speech, or rarely aphasia with this condition. They usually do not have other prominent focal findings.
  • Drug overdose. Similar to metabolic encephalopathy.
  • Central nervous system tumor. The location of the tumor would determine the type of signs and symptoms seen. A tumor, unlike a stroke, usually does not present with sudden focal findings, unless accompanied by a seizure (see above).
  • Herpes simplex encephalitis (HSE). This infection tends predominantly to affect the temporal lobes, so patients may have signs of aphasia, hemiparesis or visual-field cuts. Onset can be rapid and in its early stages may mimic a stroke, but fever, CSF pleocytosis, seizures and decreased level of consciousness are more prominent with HSE.
  • Subdural hematoma. Depending on the location, this may cause contralateral weakness or numbness that may mimic a stroke. A CT scan can make this diagnosis, but the subdural, if small, may be subtle.
  • Peripheral compression neuropathy. This may cause weakness or numbness in a particular peripheral nerve distribution and is usually not sudden in onset.
  • Bell’s palsy (peripheral seventh nerve palsy). The important point here is that the forehead and eye closure are weak on the same side. One can have a stroke involving the pons and produce a peripheral seventh nerve palsy, but usually there are other signs and symptoms such as weakness, a gaze palsy, or ipsilateral sixth nerve palsy.
  • Benign paroxysmal positional vertigo (BPPV). This may cause vertigo, nausea, vomiting, and a sense of imbalance, usually with turning of the head in one direction. This characteristic syndrome is due to labyrinthine dysfunction and not stroke. However, as with syncope, the presence of any brainstem or cerebellar signs should alert one to the possibility of a stroke.
  • Conversion disorder. Patients may develop neurological signs or symptoms of weakness, numbness, or trouble talking that are manifestations of stress or a psychiatric illness. Always assume that your patient has a true neurologic illness first.

What type of stroke?

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:

  • Ischemic stroke (Chapter 3).
  • Transient ischemic attack (Chapter 7).
  • Intracerebral hemorrhage (Chapter 8).
  • Subarachnoid hemorrhage (Chapter 9).

What to do first

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).

Airway – breathing – circulation (ABCs)

  • O2 via nasal cannula (routine oxygen delivery in ischemia might improve outcome).*
  • Intubation may be necessary if the patient shows arterial oxygen desaturation or cannot “protect” their airway from aspirating secretions. However, intubation means that the ability to monitor the neurological exam is lost. The best approach in such patients is to prepare to intubate immediately, but before doing so, take a moment to be sure the patient does not spontaneously improve or stabilize with good nursing care (suctioning, head position, etc.). Also, if needed, use sedating or paralyzing drugs with a short half-life, to allow for serial neurological exams.
  • Consider putting the head of the bed flat. This can significantly help cerebral perfusion. The head of the bed may need to be elevated if airway protection and continued nausea and vomiting are concerns for those with obtundation, nausea, severe dysphagia, or aspiration risk.
  • Consider normal saline bolus 250–500 cc if blood pressure is low.
  • If the blood pressure is high, antihypertensive treatment is discussed in subsequent chapters (Chapters 3, 4, 5, and 8).

What was the time of onset?

  • Determining the exact time of onset is critical for establishing eligibility for acute therapies, especially TPA (Chapter 4). It is very important to be a detective. You will usually be told a time by the paramedics or ED triage nurse, but be sure to recheck the information you receive from them. If possible, try to speak personally with first-hand witnesses, nursing home staff, etc. Often paramedic information is based on an inexact estimate given to the paramedic when they arrive on scene, and then gets handed down as fact. You can often help establish the time of onset by finding out the time that the emergency call arrived at the dispatch center, and work backwards with the person who called. Other useful questions are to remind bystanders of their daily routine, TV shows, etc. that might help them accurately establish the time they found the patient or called the emergency services.
  • In most cases, the onset is not observed – the patient is found with the deficit. In that case, or in patients who awaken with symptoms, the onset time is the time the patient was last seen normal. However, if the patient awoke with symptoms, be sure to ask if the patient was up in the middle of the night for any reason (often to go to the bathroom) – as sometimes this puts the patient in the time window for treatment.

How bad are the symptoms now?

  • Examine the patient and do the NIH stroke scale (NIHSS) (Appendix 14).
  • The initial stroke severity is the most important predictor of outcome.

Do a non-contrast head CT

  • This will immediately rule out hemorrhage (Chapters 8, 9) as blood is bright on a CT. The initial head CT should not show obvious acute ischemic changes in patients with ischemic infarcts who are eligible for acute interventions (Chapters 3–7), as acute ischemic changes become increasingly apparent between 3 and 24 hours.
  • The result will determine the first major branching point in therapeutic decision-making, to be covered in the subsequent chapters.
  • Obtaining the CT is often the major impediment in preparing for thrombolytic therapy, so efforts should be made to shorten “door to CT” time, which should be below 30 minutes. For instance, we allow the triage nurse to order the CT scan if a stroke is suspected, and stroke patients will get preference over any other patient for CT access. Another problem is prompt reading of CT scans, especially in small hospitals in

© Cambridge University Press

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Table of Contents

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.

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