Expansion of TPA window to 4.5 hours by AHA (Stroke 2009;40:)
(Stroke. 2007;38:1655.)
5. Multimodal CT and MRI may provide additional information
that will improve diagnosis of ischemic
stroke (Class I, Level of Evidence A).
This recommendation
has been added since the previous guideline.
Class II Recommendations
1. Nevertheless, data are insufficient to state that, with the
exception of hemorrhage, any specific CT finding (including
evidence of ischemia affecting more than one
third of a cerebral hemisphere) should preclude treatment
with rtPA within 3 hours of onset of stroke (Class
IIb, Level of Evidence A).
This recommendation has not
changed from the previous guideline.
TABLE 10. Approach to Arterial Hypertension in Acute Ischemic Stroke
|
TABLE 9. Immediate Diagnostic Studies: Evaluation of a Patient With Suspected Acute Ischemic Stroke
|
TABLE 8. National Institutes of Health Stroke Scale
|
Class I Recommendations
185 mm
Hg and their diastolic blood pressure is
110 mm Hg (Class
I, Level of Evidence B) before lytic therapy is started.
This recommendation has not changed from previous
statements. If medications are given to lower
blood pressure, the clinician should be sure that the
blood pressure is stabilized at the lower level before
treating with rtPA and maintained below 180/105 mm Hg for at
least the first 24 hours after intravenous rtPA treatment.
Because the maximum interval from stroke onset until
treatment with rtPA is short, many patients with sustained
hypertension above recommended levels cannot be
treated with intravenous rtPA.
15% during
the first 24 hours after onset of stroke. The level of
blood pressure that would mandate such treatment is
not known, but consensus exists that medications
should be withheld unless the systolic blood pressure is >220
mm Hg or the mean blood pressure is >120 mm Hg (Class I,
Level of Evidence C). This recommendation has changed
from previous statements in that a potential goal for
lowering blood pressure is now included. Research testing
the effects of early treatment of arterial hypertension on
outcomes after stroke is under way. The panel looks
forward to any data that will clarify this management
decision. Class II Recommendations
24 hours for patients
who have preexisting hypertension and are
neurologically stable unless a specific
contraindication to restarting treatment is known (Class IIa,
Level of Evidence B). This recommendation was not
included in previous statements. Class III Recommendations
|
Class I Recommendations
Class II Recommendations
Class III Recommendations
80-85% of strokes
majority are thrombotic vs. embolic (Mitral Stenosis, MI, A-Fib)
Hallmark of stroke is sudden onset of focal neurological derangement in a vascular area
| Hemorrhage | Migraine | Hyperglycemia | Carotid Dissection |
| Todd's Paralysis | Bell's | Encephalitis/Abscess | Temporal Arteritis |
| Hypoglycemia | Hyponatremia | Hypertensive Encephalopathy | Air Embolism |
| Multiple Sclerosis | Dementia |
Anterior Circulation
Frontoparietal Lobes
Anterior Aspect of Temporal Lobes
Optic Nerve and Retina
Deep Gray Matter Structures
Posterior Circulation
Medial Aspect of Temporal Lobes
Visual Occipital Cortex
Thalamus
Brainstem
Upper Spinal Cord
Cerebellum
Auditory and Vestibular Aspects of the Ear
Paralysis mainly of opposite leg and mild arm involvement
Sensory deficits paralleling paralysis
Altered mentation, confusion, judgment, and impaired insight
Gait apraxia (clumsiness)
Bowel and bladder incontinence
Paralysis of opposite side of body; arm and face worse than leg
Sensory deficits paralleling paralysis
Blindness in half of visual field (hemianopsia)
Aphasia (if dominant hemisphere involved, usually left)
Hemineglect (If non-dominant hemisphere, usually right)
Inability to recognize known objects (agnosia)
If Gaze preference, patients look towards the lesion
Blindness in one half of visual field (hemianopsia)
Third nerve paralysis
Lack of visual recognition (visual agnosia)
Altered mental status with impaired memory
Cortical blindness
Crossed Signs-face one side, body the other
Hemiparesis or quadriparesis (or worse yet locked in syndrome)
Sensory loss, hemi or all 4 extremities
Diplopia
Dysconjugate Gaze
Nystagmus
Dysarthria/Dysphagia
Vertigo
Decreased LOC or syncope
Ataxia
Vomitting
Patients presenting with pontine infarction may describe a preceding
transient pain radiating from the unilateral eye to the nose, following which
they developed numbness or ataxic hemiparesis on the side contralateral to the
pain.4 The “beauty parlor syndrome” has been described in elderly patrons
receiving shampoo treatments. Mechanical impingement by neck rotation and
hyperextension decreases vertebral artery flow and produces hypoperfusion at the
atlanto-occipital-distal vertebral artery junction. Patients may present with
vertigo and ataxia.5
Stroke notification
Check Glucose
Consider Aortic Dissection or if neck pain in the absence of trauma, consider arterial dissection of neck vessels
Obtain a BP in both arms
NIH Stroke Scale (FERNE) , but remember it leaves out some CN, gait, and nystagmus
EKG
Draw Labs-CBC, PT/PTT, Lytes, C-XR, Consider ABG, C-Spine, LFTs
Get a stat CT Minus Head
multimodal MRI including gradient echo is at least as and probably more sensitive for bleeds than CT (J Neuro Neurosurg Psych 2001 Apr;70 suppl 1:I7-11)

Keep MAP<130
Hob flat may increase CPP (Neurology 2005;64:1354)
Elevate head of bed to 30º
Hyperventilation or Mannitol only if acute deterioration
Only to prevent recurrent seizures
ASA well proven (huge Chinese study)
No harm if you give it in hemorrhagic stroke, but still not advised (Stroke, 2000;31:1240-1249)
No benefit to other anticoagulants unless
concerns over pt with current A.Fib (Stroke 33:856, 2002)
lytics up to 4.5 hours (NEJM 2008;359(13):1317)
Must be read by neuroradiologist (Neurologists, general radiologists, and certainly ER docs are not qualified)
Symptomatic intracerebral hemorrhage occurred in 6.4% of tPA recipients but only
0.6% of placebo recipients (P < 0.001). Mortality at three months was 17% in the
tPA group and 21% in the placebo group (P = 0.30).
A number-needed-to-treat analysis of the NINDS trial indicates that for every
eight acute stroke patients treated, one will benefit. One patient in 17 will
suffer an intracranial hemorrhage, and one in 40 will die. These numbers may be
helpful in explaining risks and benefits to patients who are eligible for
thrombolytic treatment.
Meta-analysis of current thrombolytic for stroke data
Symptomatic ICH 6.2% Absolute Risk Increase
Fatal ICH 2.5% Absolute Risk Increase
(Stroke. 2003 Jun;34(6):1437-42.)
The major risk of t-PA is symptomatic intracerebral
hemorrhage, which occurred in 6.4 percent of patients who received t-PA, as
compared with 0.6 percent of patients who received placebo.1 These figures
represent an absolute difference in the risk of symptomatic intracerebral
hemorrhage of 6 percent. Seventy-five percent of the patients with a symptomatic
intracerebral hemorrhage were dead at three months. Yet despite the risk of
intracerebral hemorrhage, the mortality at three months was insignificantly
lower in patients treated with t-PA (17 percent) than in placebo-treated
patients (21 percent). Two reasons may underlie the similar mortality of t-PAtreated
and placebo-treated patients despite a higher risk of symptomatic intracerebral
hemorrhage among patients treated with t-PA. First, most patients who had an
intracerebral hemorrhage had large strokes and were likely to do poorly
regardless of the presence of intracerebral hemorrhage within the damaged brain.
Secondly, t-PA probably makes some "big" strokes much smaller. The patients with
small strokes are less likely to die.
Patients treated with t-PA who have very large strokes (very severe neurologic
deficits, meaning an NIH stroke scale score greater than 20) and who already
have evidence of a large acute ischemic stroke on baseline CT have an increased
risk of symptomatic intracerebral hemorrhage. 17 However, patients in these two
subgroups who receive t-PA are more likely to return to normal than patients who
are treated with placebo. The decision to use t-PA in these patients should be
made only after frank discussion of the potential risks and benefits with both
the patient and the family.
Figure 1 adapted from Marx J. Classification system for stroke patients.
Proceedings of the National Symposium on Rapid Identification and Treatment of
Acute Stroke, December 13, 1996. Washington, D.C.: National Institute of
Neurological Disorders and Stroke (NINDS), November 1997.
Contraindications to TPA
Get TEE, eval ekg for A-Fib. Carotid dopplers.
ASA or plavix
Site for NINDS Group Guidelines for TPA
editorial on why it has not been adopted more widely (Lancet 2006;5:722)
Neurosurgery consult
Elevated CK-MB after stroke are not necessarily
Giving ASA even to hemorrhagic stroke did not cause additional mortality or increased bleeds (Stroke 2000; 31:1240-9)
Strokes in Younger Patients (EMEDhome)
When evaluating a younger patient in the Emergency Department with a stroke, keep in mind the following:
As transesophageal echocardiography (TEE) is considered the most sensitive method to date to detect PFO (1), think to suggest a TEE as part of the evaluation.
"In the absence of other causative conditions, an ASD or PFO may be presumed
to be the underlying cause of cerebrovascular thromboembolism. The search for
these defects will be more cost-effective in younger stroke patients who, unlike
older patients, rarely have the cardiovascular conditions associated with
advanced age that commonly cause strokes in the elderly" (2).
References:
(1) Horton SC, Bunch TJ. Patent foramen ovale and stroke Mayo
Clin Proc 2004;79(1): 79-88.
(2) Jaber WA, et al. Suspect an atrial septal defect if a young patient
has a stroke Cleveland Clin J Med 2001; 68: 954-956.
(3) Cabanes L, et al. Atrial septal aneurysm and patent foramen ovale as
risk factors for cryptogenic stroke in patients less than 55 years of age. A
study using transesophageal echocardiography. Stroke 1993;
24:1865-1873.
(4) Jones J, Geninatti M. Cardiology Emerg Med Clin North Am
1997;15(2):341-63.
(Jama 2005;293(19):2391)
LR of the absence of facial paresis, arm drift, and abnormal speech is 0.39
|
||||||
Neurologists have described acute confusional states and acute agitated delirium with several sites of infarction [4, 5 and 6]. Some have been bilateral, others on the right (non-dominant) or the left (dominant) specifically. Restlessness, agitation and disorientation are common with posterior artery infarctions. Forced crying out, cursing and unintelligible speech often have been reported in these cases, as they were in our patient [2]. Hypertension and generalized slowing on EEG are described in some patients, whereas others have normal CT scans for some time before changes of density can be identified [2]. The course of delirium can last several weeks with varying outcomes. Older age, comorbidity, and extent of the infarction have significant impact. Our patient had a history that included diabetes mellitus, hypertension, adenocarcinoma, and psychiatric disorders, all of which could have produced some of the initial symptoms. It is unlikely that her fever was due to medications, because she had been taking them for weeks, or that it was due to infection, because an organism could not be cultured and the white blood cell count was persistently normal. The maximum outside temperature on that day was 76°C.
The Amitriptyline and Nortriptyline levels were less than 10 ng/ml. It is known that acute strokes can cause elevated temperature, agitation and hypothermia. Although total CK level was not obtained, it is unlikely that agitation caused the fever, as it persisted even after agitation resolved with sedation. The ultimate cause of her fever was puzzling, but the most likely etiology was the stroke. Whether or not the antibiotics prescribed at the onset eradicated an undetected infection was never resolved. The confirmed diagnosis of left posterior cerebral artery infarction certainly could have explained the majority of her signs and symptoms as well as the course.
It is quite important to consider this diagnosis early as it carries a high mortality, particularly in the elderly [2]. Rapid intervention with TPA is increasingly initiated to spare neuronal damage when it can be administered shortly after an event. It would not have been given to this patient 11 h post infarction. Because initial CT scans may not be diagnostic, an MRI or MRA is more definitive. Plan for workup depends on initial clinical evaluation, although in most hospitals the first imaging study would be a CT scan. A CT scan can exclude unexpected large lesions or the presence of bleeding but other investigations are necessary to identify the stenotic or occluded artery. Abnormal diffusion weighted imaging (DWI) is a very sensitive and specific identifier of ischemic stroke in patients presenting within 6 h of stroke. Although DWI can detect areas of ischemia within 15–30 min of onset after only 3 s of imaging, its availability is limited. CT scans are more available, easily obtained and cheaper than MRIs or DWIs, so they are usually ordered first. But when non-diagnostic and at the earliest suspicion of ischemic stroke, the alternatives should be considered. Once the delirium clears, post-stroke depression should be reassessed. Untreated depression has a negative impact on both rehabilitation and long-term prognosis, and a premorbid history for depression significantly increases the risk for recurrence. Post-stroke depression is a well-known phenomenon and consistent with our patient's symptoms [7]. When the anterior limbic system is disconnected from the destroyed posterior, the amygdala and anterior hippocampus can also induce confusion, fever, anger and amnesia. The infarct will also disrupt connections between the temporal neocortex and the limbic system, making it extremely difficult to use language-encoded memories. As time progresses to allow for collateral circulation, the symptoms may resolve if the infarction is not so large that it causes devastating destruction.
In conclusion, infarction of the posterior cerebral artery, whether unilateral or bilateral, may present first as delirium without many focal findings. When suspected, an MRI should be immediately obtained to help clarify a diagnosis. Intervention with TPA in all non-hemorrhagic strokes remains controversial but patients treated within 90 min definitely have improved outcomes. Early identification of the patients who may benefit from this approach is essential [8]. The affected limbic structures can produce early psychiatric symptoms involving delirium and altered affect and the later development of post-stroke depression.
ATLANTIS trial: Mild to moderate strokes 79% completely recover at 90 days vs. 56% for placebo. In moderate to severe, 33% TPA vs. 5% placebo. 22% change of intracranial hemorrhage. All symptomatic hemorrhages were fatal. (Stroke 2002, 33:493-496)
| NINDS study: inclusion criteria—ischemic stroke with clearly defined time of onset; measurable deficit on National Institutes of Health (NIH) stroke scale; no evidence of intracranial hemorrhage on computed tomography (CT) of brain; treatment—t- PA 0.9 mg/kg for maximum of 90 mg (10% given as bolus, 90% as constant infusion over 60 min [smaller than cardiac dose]); patient not to receive anticoagulants or antiplatelet drugs for 24 hr after treatment; strict protocol for blood pressure monitoring and control; exclusion criteria—prior stroke or head trauma within 3 mo; major surgery in previous 14 days; history of intracranial hemorrhage; hypertension; suspected transient ischemic attack (TIA); hypothesis—consistent and persuasive difference between t-PA and placebo in patients who recover with minimal or no deficit 3 mo after treatment; outcome—t-PA group had higher percentage of favorable outcomes; no increase in severe disability or death resulting from administration of t-PA; however, “you were ten times more likely to develop a symptomatic intracranial hemorrhage resulting from your stroke if you got t-PA than if you didn’t”; mortality from symptomatic intracranial hemorrhage 45% higher than mortality from disease process itself; t-PA patients 32% to 55% more likely to have complete recovery from stroke than placebo group (11%-13% more patients have complete recovery with t-PA than without it); must treat 8 to 9 patients to obtain one additional complete recovery; all patients with ischemic stroke benefited equally, regardless of size; these results held at 6 mo and 1 yr |
| Recommendations of Stroke Council of American Heart Association: published in 1996; t-PA should be given according to NINDS protocol by physicians with expertise in diagnosis of stroke and interpretation of CT; streptokinase should not be used; do not treat if CT signs suggest major infarct or treating facility cannot handle complications of intracranial hemorrhage (need neurosurgery backup plan); use caution in severe strokes (score >22 on NIH stroke scale); obtain informed consent |
| NIH stroke scale: fairly reliable and reproducible; primarily identifies lateralizing findings; evaluates 11 criteria; takes 5 to 8 min to perform; patient must have score >4 but <22 |
| CT criteria: must be done within 3 hr of symptom onset; parenchymal hypodensity indicates large stroke or long interval between time of stroke and patient’s arrival; study showed correct interpretation of CT by emergency physicians in 66% of cases, 83% for neurologists and radiologists; only 70% of emergency physicians interpreted CT correctly 100% of time, 40% of neurologists and 50% of radiologists |
Comparison of MRI and CT for Detection of Acute Intracerebral Hemorrhage
JAMA. 2004;292:1823-1830.
Results The study was stopped early, after 200 patients were enrolled, when it
became apparent at the time of an unplanned interim analysis that MRI was
detecting cases of hemorrhagic transformation not detected by CT. For the
diagnosis of any hemorrhage, MRI was positive in 71 patients with CT positive in
29 (P<.001). For the diagnosis of acute hemorrhage, MRI and CT were equivalent
(96% concordance). Acute hemorrhage was diagnosed in 25 patients on both MRI and
CT. In 4 other patients, acute hemorrhage was present on MRI but not on the
corresponding CT—each of these 4 cases was interpreted as hemorrhagic
transformation of an ischemic infarct. In 3 patients, regions interpreted as
acute hemorrhage on CT were interpreted as chronic hemorrhage on MRI. In 1
patient, subarachnoid hemorrhage was diagnosed on CT but not on MRI. In 49
patients, chronic hemorrhage, most often microbleeds, was visualized on MRI but
not on CT.
JAMA 2005;294(6):725
Our analysis suggests that EICs are prevalent within 3 hours of stroke onset
and correlate with stroke severity. However, EICs are not independently
associated with increased risk of adverse outcome after rt-PA treatment.
Patients treated with rt-PA did better whether or not they had EICs, suggesting
that EICs on CT scan are not critical to the decision to treat otherwise
eligible patients with rt-PA within 3 hours of stroke onset. (JAMA. 2001 Dec
12;286(22):2830-8.)
Optimal stroke scale to lyse 10-20
Stroke Among Patients With Dizziness, Vertigo, and Imbalance in the
Emergency Department: A Population-Based Study
Kerber KA, Brown DL, Lisabeth LD, et al. Stroke 2006;37:2484–7
Catherine Ambrose MDa
aDenver Health Medical Center, Denver, Colorado
Available online 30 March 2007.
As part of the Brain Attack Surveillance in Corpus Christi (BASIC)
project, this study sought to determine the percentage of stroke
patients who presented to the Emergency Department (ED) with the
complaints of dizziness, vertigo, or imbalance. This large
population-based study examined all patients over the age of 44 years
who presented to the ED or were directly admitted to the hospital
between January 2000 and June 2003 with the previously mentioned
isolated dizziness symptoms (DS) in Nueces County, Texas. The
association of age, sex, race/ethnicity, and isolated dizziness
symptoms with stroke or transient ischemic attack (TIA) was then
determined using multivariable logistic regression. A total of 1666
patients were included in the study, with 3.2% (53 of 1666) ultimately
diagnosed with stroke/TIA. Of those diagnosed, 23 presented with
dizziness as the chief complaint, 18 with vertigo, 11 with imbalance,
and 1 with more than one of the above symptoms. Isolated DS without
additional neurological findings was a strong negative predictor of
stroke/TIA (odds ratio [OR] 0.05; 95% confidence interval [CI]
0.02–0.11), whereas male sex was associated with an increased
association with stroke/TIA (OR 2.5; 95% CI 1.4–4.4). Patients
diagnosed with stroke/TIA were also found to be significantly older
(69.3 ± 11.7 vs. 65.3 ± 12.9, p = 0.02). No significant difference in
race/ethnicity was found between the stroke and non-stroke groups.
When compared to dizziness, patients with imbalance were found to have
an increased risk of stroke/TIA (OR 3.7; 95% CI 1.3–10.7), whereas no
increased risk was found between those with vertigo versus dizziness
(OR 0.9; 95% CI 0.4–2.0). The authors acknowledge several limitations
to this study, including lack of evaluation of the majority of study
patients in the ED by a neurologist, lack of magnetic resonance
imaging on most study patients leading to possible undiagnosed
strokes, and lack of comparison of symptom onset, duration,
aggravating/alleviating factors, headache, and auditory symptoms
between groups. The authors conclude that dizziness and vertigo are
not associated with stroke/TIA, whereas patients who present with
imbalance, those with additional neurologic findings, male gender, and
older age are at the highest risk for possible stroke/TIA.
The NIHSS as formulated by the National Institute of Neurological Disorders
and Stroke has been applied at our medical center as the SQS and is shown here
with maximal deficit scores clustered into 3 groups having a total of 7points
each (Fig.
1). The level of consciousness section to the NIHSS is grouped together in
the frontal regions with an aggregate deficit score totaling 7 for deficits in
alertness, ability to answer questions, and obey commands. A second cluster of 3
consisted of deficits in sensation, extinction, and language being clustered
along the motor strip and temporal-parietal regions; the extinction category
tests inattention with complete neglect scoring 2. In regards to sensory
deficits, this can be tested as withdrawal to noxious stimuli, with a severe
loss scoring 2 points. A third cluster was placed in the posterior regions and
included the maximal visual deficit score of 3 for bilateral hemianopia, and the
near to unintelligible deficit score of 2 for dysarthria was placed alongside
the maximal limb ataxia score of 2 in the cerebellar region; although speech
dysarthria can be a result of ischemic damage to the motor strip, an alternative
possibility would be dysarthria of a cerebellar origin and for convenience is
grouped here in the posterior fossa region. The maximal motor deficit score of 4
for each of 4 extremities is grouped together (green circle,
Fig. 1). Miscellaneous items that are not part of the 322 groupings are
separated by a line parallel to the catho-metal line: best gaze (forced
deviation of the eyes scores 2 points) and facial palsy (complete facial palsy
scores 3 points).
3. Discussion
Although not yet formally tested under controlled conditions, the SQS diagram
may accelerate the time factor in reaching an accurate score, but formal testing
of this hypothesis is needed. Although the NIHSS attempts to comprehensively
include all regions of the brain that could be affected by stroke, the weighting
factors for each functional item might need reassessment. The current equal
weighting for arms vs legs remains reasonable for now, because 1 study showed
very good reliability for these items with the 15-item NIHSS
[6]. However, the same study found the least reliable items to facial palsy
and dysarthria with low intraclass correlation coefficients being less than
0.40, and advocated a modified 11-item version of the NIHSS.
In summary, the presented SQS diagram shown in
Fig. 1, or similar versions, may facilitate training of examiners to
comprehend the overall structure of the NIHSS system. The SQS diagram is
intended only to serve as a supplement and not a replacement for current methods
of scoring. However, further testing of a single visual composite for the NIHSS
as an ancillary tool is needed to determine its actual usefulness. (AJEM
2008;26:189)
From EP Monthly:The year’s top stroke advances by Bobby Desai, MD
Less well-established is how many clinically evident lacunar infarcts ever cavitate to become "lacunes". It seems generally assumed that all lacunes start life as an infarct, even if the patient did not notice anything, and therefore share the same risk factors, etiology, prognosis, pathogenesis, etc, as clinically evident lacunar infarcts.3–5 However, suppose only a proportion of lacunar stroke lesions, perhaps as few as a third, ever cavitate, with the majority that fail to cavitate retaining the appearance of a WML?6 Counting lacunes could result in spurious risk factor and etiologic associations for lacunar stroke. We should not assume that the pathogenesis of clinically evident lacunar stroke is the same as for clinically silent lacunes. Equally, similarity in appearance between WMLs and clinically evident acute lacunar infarct could imply similar causation. However, surely the fact that one has caused symptoms (lacunar stroke/infarct) and the other not (WML/lacune) is important in itself and should lead to their careful distinction in any research at least until we know more.