1. Description of the problem

By definition stroke refers to the sudden onset of neurologic deficits, not associated with trauma. This broad definition does not distinguish between hemorrhage into the brain or ischemia to a given brain region. However, only about 10% of strokes in the US are hemorrhagic, and as a result, the term “stroke” is often used interchangeably with ischemic stroke.

In this section the basic acute management of both forms of stroke will be covered. While technically subarachnoid hemorrhage is a form of hemorrhagic stroke, the management of this disease has become quite specialized over the past decade and the reader is referred to recently published guidelines from the Neurocritical Care Society. Prompt recognition and referral to a high-volume neurosurgical center that deals with aneurysm repair is recommended.

Ischemic stroke presents as a sudden loss of neurologic function, often manifest as a deficit in one side of the body with sparing of function on the contralateral side. Stroke rarely presents as a bilateral phenomenon in the absence of severe reduction in the level of consciousness. In contrast, variation in the degree of involvement of the given side of the body is common, and often can provide insight into the location and vascular distribution of the stroke.

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Despite some characteristic, though subtle, aspects to the presentation of ischemic stroke in comparison to hemorrhagic stroke, a CT scan is required to definitively distinguish between these two categories of stroke. The use of CT is mandatory due to the opposite management approaches for ischemic vs. hemorrhagic stroke.

Key management points

Any patient who is suspected of having had a recent stroke, even if more than a day old, should get an emergent CT. This is to allow for rapid initiation of appropriate management of blood pressure and to determine the need for additional imaging studies within the first few hours of admission. In general, ischemic stroke patients are allowed to have any systolic blood pressure below 220 mmHg, while hemorrhagic stroke patients should have their systolic blood pressures lowered to under 160 mmHg urgently for 4-6 hours, then under 140 for the duration of their stay. The highest risk for re-bleeding and worsening of outcome is within the first 24-48 hours, making differentiation between these two forms of stroke the top priority for initial evaluation.

2. Emergency Management

Stroke is a neurologic emergency, much the same as myocardial infarction. The first step is to consider stroke as a possible cause for a patient’s presenting symptoms. The core element of stroke care is determination of eligibility for tissue plasminogen activator (t-PA). There are well-established guidelines for the administration of t-PA, which are provided here for reference. Critical to determining the appropriateness of t-PA is ensuring the patient does not have an intracranial hemorrhage (ICH).

Therefore, once the diagnosis of stroke is considered, a CT scan should be rapidly obtained to establish ischemia as the cause. It is important to note that a negative CT is common in the acute phase of ischemic stroke presentation. Occasionally more subtle evidence can be found for large strokes, such as hyperdense middle cerebral artery (MCA) sign, insular ribbon sign or subtle asymmetry in the gray–white junctions. A normal CT should be expected for early stroke presentations, and once bleeding has been excluded as a cause for the deficits, if the patient has presented in under 4.5 hours, he or she should strongly be considered for t-PA administration.

In addition to rapidly obtaining a CT, establishing a detailed history and a definitive time of onset is critical to subsequent management decisions. All other medical problems should be determined, particularly the presence of diabetes and any recent surgical procedures, even if thought to be minor. These factors can also alter the decision on thrombolytic therapy and should be obtained quickly and completely upon presentation. Finally, performance of the NIH stroke scale assessment exam is very useful in documenting the severity of stroke, estimating risk of bleeding, and tracking stroke recovery and/or progression, and it facilitates communication with neurology subspecialists.

Management points not to be missed

Adult presents with signs/symptoms consistent with acute stroke:

Do emergently for All Stroke Patients

Note vitals and evaluate airway.

Obtain stat Head CT without contrast.

Send basic labs, though treatment does not need to be delayed for labs unless there is a suspected coagulopathy or other blood dyscrasia.

Ischemic Stroke

Patient is a candidate for intravenous t-PA if:

1. You can conclusively establish the time of onset and obtain a history

2. t-PA can be given in under 4.5 hours from above onset time

3. Ischemic stroke in any territory based on CT negative for hemorrhage

Consider withholding t-PA therapy if:

1. Systolic blood pressure >185 mmHg, or diastolic >110 mmHg

2. Patient has a known coagulopathy

3. Patient is on blood thinners (need INR before t-PA can be given, OK if <1.7)

4. Patient has had a prior stroke or head trauma in the past 3 months

5. Patient has had a prior intracranial hemorrhage

6. Patient has had gastrointestinal bleeding within the past 3 weeks

7. Patient has had major surgery in the past 14 days

8. Patient has had arterial puncture at a non-compressible site within the last week

9. Patient has active bleeding or signs of trauma

10. Platelet count is <100,000 mm3

11. Blood glucose is <50 mg/dL

12. Patient has had preceding seizure

13. CT scan shows clear evidence for infarct >1/3 the hemisphere

Additional considerations:

If between 3 and 4.5 hours, t-PA should not be used if:

1. Patient is >80 years old

2. NIH stroke scale score is >25

3. History of both prior stroke and diabetes

4. Patient is on anticoagulants

Hemorrhagic Stroke

Patient is not a candidate for t-PA.

Systolic blood pressure goal is <140 mmHg.

Control blood pressure quickly using fast-acting calcium channel blocker:

    Nicardipine: start 5 mg/hr IV and increase 2.5 mg/hr every 5-15 min until systolic is at goal

    Clevidipine: start 1-2 mg/hr IV and double rate every 90 seconds until near goal, then smaller incremental changes every 5-15 min until at goal

Follow exam closely and consider repeat imaging if changes are seen.

3. Diagnosis

Diagnostic approach

While there are some subtle clinical features that can distinguish ischemic from hemorrhagic stroke, CT is the cornerstone of diagnosis. That said, one should have a strong clinical suspicion for stroke prior to ordering any imaging. This must be the case as the most common CT finding in the acute ischemic stroke setting is a normal CT. Thus, the clinical exam that suggests a common vascular region of the brain, such as hemiplegia or aphasia, should prompt rapid CT evaluation to determine the next most appropriate step.

In the setting of severe stroke symptoms, a CT angiogram may be appropriate. Extensive MCA or carotid occlusion is unlikely to respond IV t-PA, and patients should be referred quickly to an interventionalist for evaluation.

Other important tests to consider are CBC and coagulation assays. These are of relative importance since low platelets or high INR would be contraindications to t-PA administration. However, in the absence of a coagulation abnormality history, active anticoagulation therapy or evidence for bleeding, t-PA administration is not delayed for results on these labs.

Normal lab values

By far the most common imaging finding in acute stroke is a normal imaging study. After that, any subtle hypodensity should be carefully considered and evaluated for correlation to presenting deficits. A few special patterns can be seen and are important to recognize as they suggest the need for more aggressive intervention.

As shown in Figure 1, the hyperdense MCA sign is a bright MCA on scan due to the presence of static blood in the form of an acute clot within the vessel. Patients with this finding will demonstrate significant impairment, such as hemiplegia and neglect, and may benefit from mechanical thrombectomy if available.

Figure 1.

CT scan showing Hyperdense MCA sign.

Figure 2 demonstrates an insular ribbon sign. This finding can be very subtle and is often seen early in large MCA strokes. These findings portend a large stroke and significant deficits if nothing is done.

Figure 2.

CT showing the insular ribbon sign on the right (blue arrow).

When CT confirms a large-volume stroke (Figure 3), future management of increased intracranial pressures must be considered. There are good data for the role of hemicraniectomy in acute stroke, demonstrating reduced mortality and improved functional outcomes regardless of hemisphere involved.

Figure 3.

This CT image shows a large left MCA distribution stroke with some left-to-right shift.

Differential diagnosis

There are only a few other clinical conditions that can mimic an acute stroke. These conditions include seizure, migraine, hypoglycemia and acute infection or febrile illness. As expected, a careful history can help in differentiating these mimics. In younger patients with fewer vascular risks, consideration of these alternatives is important. Seizures can cause a Todd’s paralysis or focal weakness, and this is why seizures are a relative contraindication to t-PA administration. In most cases the weakness is rapidly improving, though it can last for 24 hours or more. Complex migraines can also present as acute loss of vision or other focal deficits, and in older patients the deficits may occur as part of an aura and not be associated with a headache. While these kind of mimics provide a significant source of anxiety among non-subspecialty providers, recent studies have shown that bleeding complications from t-PA rarely occur in these patients.

As with the other mimics, infection and fever can cause old stroke symptoms to acutely worsen or, more rarely, unmask a stroke that was previously asymptomatic. This acute discovery of chronic disease can easily be mistaken for an acute event. However, often a history of similar presentations can be elicited, CT imaging is negative for new areas of injury or hemorrhage, and other evidence for evolving infection can be found, such as elevated white cell counts, lower-than-normal blood pressure or positive urinalysis. As with other mimics, these patients have a very low t-PA complication rate. However, given that fact that they do not need to be given t-PA, any complication that is encountered represents an avoidable complication. This highlights the importance of carefully probing for these conditions in the history and reviewing the appropriate labs prior to t-PA administration.

4. Specific Treatment

Ischemic Stroke

If the patient is considered a candidate for IV t-PA, then the following administration protocol is supported by the current literature:

Infuse 0.9 mg/kg (maximum dose of 90 mg). 10% of dose is given as a bolus over 1 minute; the rest is infused over a 60-min period.

A follow-up CT scan should be obtained at 24 hours post t-PA to determine extent of stroke and evaluate for hemorrhagic conversion.

Note: Some centers have considered lack of improvement at the end of infusion to be a treatment failure and in severely disabled patients will attempt intra-arterial clot removal in patients who are still under 6 hours of symptom onset. This is currently being studied as part of a large multicenter trial and is not recommended at this time due to high hemorrhagic risk.

Hemorrhagic Stroke

Systolic blood pressure goal is less than 140

Control blood pressure quickly using fast-acting calcium channel blocker:



Follow exam closely and consider repeat imaging if changes are seen.

Ischemic Stroke Non-t-PA candidates

In patients who are not candidates for t-PA or are beyond the window for t-PA but are still under 6 hours of symptom onset for anterior circulation infarcts, or under 12 hours for posterior circulation strokes, intra-arterial intervention should be considered.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

All stroke patients should be admitted to an ICU or step-down level of care to provide close neurologic monitoring. Early speech and swallow evaluations are important to document so that appropriate nutrition can be provided and complications of aspiration can be minimized. Serial exams every 2-4 hours for the first 24 hours are recommended. This is particularly true for patients who present with significant deficits that rapidly clear. Documentation of the normalization of the exam is critical as recurrence is common in this cohort and they could be candidates for t-PA or other interventions if symptom onset can be clearly defined. In many cases, a follow-up CT or MRI at 24-36 hours is appropriate to determine the extent of the stroke and risk for complications of elevated intracranial pressure.

In cases of ischemic stroke, a source for the stroke should be sought. Thus, an ECHO with microcavitation study, lipid profile, hemoglobin A1c and thyroid function tests should also be obtained. If a PFO is found on ECHO, bilateral lower extremity ultrasound should be considered to evaluate for a clot source for emboli. Antiplatelet therapy should be considered early as secondary stroke prevention. In cases of large stroke, this may be delayed for a few days. DVT prophylaxis should also be started early, within 48 hours, unless the stroke is very large or hemorrhagic.


Vascular imaging should always be performed in acute stroke patients. If MRI is used, an MRA of the head and neck should also be performed. While MRA can be overly sensitive, in those cases in which high-grade lesions or occlusion are suspected, evaluation with ultrasound or formal angiography can then be done in this small subpopulation. Ultrasound alone is of limited value in acute stroke since it does not provide any information on the status of the intracranial vasculature, thus requiring additional imaging to be performed anyway in cases in which carotid lesions are found.


Patients with negative follow-up imaging should raise concern for a stroke mimic or alternative underlying process. This is particularly true for patients with declining mental status. While stroke can commonly disturb language function and can make patients sleepy and lethargic, unresponsiveness is uncommon in acute stroke and should indicate a posterior circulation catastrophe or some non-vascular alternative diagnosis that needs urgent attention and management. In these cases, EEG, follow-up labs (with a toxicology screen if not done previously), and a lumbar puncture should be considered.


Ischemic strokes are caused by acute blockage of the flow of blood through a vessel supplying a particular brain region. The reduction of blood flow rapidly results in neuronal dysfunction within the vascular territory supplied by the vessel. The extent of neuronal death is dependent on the size of the vessel that is blocked, the duration of the blockage and the extent of collateral flow to the region. The cause for the blockage can vary. Local atherosclerotic disease, similar to cardiac disease, can occur intracranially and lead to local acute thrombosis.

In other cases, acute vascular injury, such as dissection, can cause obstruction of the vessel or embolic disease. Venous clot can also result in arterial blockage if a shunt pathway exists between the two circulations. Classically, patent foramen ovale (PFO) is considered the principal route; however, recent studies have found transcranial Doppler to have a higher sensitivity for shunt detection over traditional cardiac ultrasound microcavitary evaluation, suggesting that other shuts exist that could allow clots to migrate to the arterial circulation. Finally, clots in the heart from valve disease, wall motion defects or abnormal rhythms can also be seen.

Hemorrhage is less complicated in that often hypertension is the root cause. Cerebral hemorrhage results from rupture of the vessel wall. In some regions, Asia for example, ICH is more common and represents a higher percentage of strokes. There are some data to suggest that very low levels of lipids can contribute to ICH; however, this relationship does not affect care in the acute setting. The relationship to blood pressure accounts for the locations where ICH is commonly seen. The basal ganglia are most common, with rupture of the lenticulostriate vessels.

Lobar hemorrhage into the frontal lobes and temporal lobes are next most common, followed by cerebellar and posterior fossa bleeding. This lower propensity for hemorrhage in the posterior fossa accounts for the longer time allowed between symptom onset and intra-arterial intervention. In the elderly, amyloidosis results in recurrent lobar hemorrhages. Often these patents present with less symptomatic hemorrhages early on as the bleeds are commonly more superficial and small. Over time, cognitive impairment is common and progressive decline in function is seen with the recurrent bleeds.


Currently stroke is the third leading cause of death and the most common cause for acquired disability. There are approximately 795,000 strokes a year and half that number of transient ischemic attacks (TIAs). Interestingly, there is an unequal distribution of strokes across the country with a significantly higher stroke rate in the Southeast. This region is referred to as the “stroke belt” as a result of this disparity, and the reasons for this difference in stroke distribution remain an area of research.

Disparities in the proportion of hemorrhagic strokes to ischemic strokes also exist worldwide, with a higher proportion of hemorrhage in Asian countries. The lower serum lipid profiles in these higher-hemorrhage regions, combined with the observation that induced ultra-low lipid levels appear to be associated with higher hemorrhage rates, suggest a potential role for diet and lipid profiles in this variation in distribution.

Over the years, primary and secondary stroke prevention have been the major focus of cardiovascular research. Much of what we know about the risk factors associated with stroke comes from cardiovascular studies looking at management of various cardiac conditions that happen to have stroke as one of the clinical endpoints for the trial. Atrial fibrillation is a good example. The appropriate management of atrial fibrillation was explored via large international trials comparing rhythm control to rate control with anticoagulation.

These studies were designed and run by cardiologists; however, stroke is a major complication of atrial fibrillation and was an important endpoint for the study. From this large study we learned that rate control and anticoagulation results in reduced stroke rates. This approach has led to our current preventive strategies to reduce overall cardiovascular event rates and includes daily aspirin, targets for cholesterol and low-density lipoprotein, tight blood sugar control in diabetics, and normalization of blood pressure.


While some data exist on the natural history of ischemic stroke patients, there are very few comprehensive studies. In general, most ischemic stroke patients will recover to some level of independence. Overall, about 70% of stroke patients will be able to perform most activities of daily living with no or minimal assistance. Only patients with very large strokes, complete MCA or carotid occlusions, have limited recovery.

Even in these cases, increases in lower extremity tone often allow these patients to weight bear and assist with transfers. Most can also recover to the point of taking food by mouth. These outcomes have driven neurologists to find ways of preventing subsequent strokes and physical therapists to find new ways to preserve and enhance function in stroke patients. Thus, while for some patients any loss of independence may be unacceptable, it is important to not be nihilistic about these patients on presentation.

Early prediction of outcome is easier in hemorrhagic stroke, where a scoring system has shown good correlation to outcomes. In general, hemorrhagic stroke patients do not do as well as ischemic stroke patients. Volume for volume, hemorrhage stroke patients will have greater disability at presentation and will recover less over time. The reasons for this are not entirely clear but are likely related to the mass effects and tissue disruption that occur as a result of the hematoma formation. That said, there is somewhat of a bimodal distribution within hemorrhagic stroke patients, with some presenting devastated and others presenting relatively minimally symptomatic.

What's the evidence?

Stroke Characteristics and Diagnosis

Fonarow. “Characteristics, performance measures, and in-hospital outcomes of the first one million stroke and transient ischemic attack admissions in Get with the Guidelines-stroke”. Circ Cardiovasc Qual Outcomes. vol. 3. 2010 May. pp. 291-302.

Alberts, MJ. “Diagnosis and treatment of ischemic stroke”. Am J Med. vol. 106. 1999 Feb. pp. 211-221.

Reed. “Inpatient costs, length of stay, and mortality for cerebrovascular events in community hospitals”. Neurology. vol. 57. 2001. pp. 305-314.

Ischemic stroke management


Wardlaw. “Thrombolysis for acute ischaemic stroke”. Cochrane Database Syst Rev. 2009 Oct 7. pp. CD000213

Ossi. “Hospital-based management of acute ischemic stroke following intravenous thrombolysis”. Expert Rev Cardiovasc Ther. vol. 9. 2011 Apr. pp. 463-72.

Hemorrhagic stroke management

Parker. “Management of spontaneous nontraumatic intracranial hemorrhage”. J Pharm Pract. vol. 23. 2010 Oct. pp. 398-407.

Morgenstern. “Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association”. Stroke. vol. 41. 2010 Sep. pp. 2108-29.

Subarachnoid hemorrhage management


Ischemic stroke

Hankey. “Rate, degree, and predictors of recovery from disability following ischemic stroke”. Neurology. vol. 68. 2007. pp. 1583-1587.

Hemorrhagic stroke

Hemphill. “The ICH score: a simple, reliable grading scale for intracerebral hemorrhage”. Stroke. vol. 32. 2001. pp. 891-897.

Manno. “Emerging medical and surgical management strategies in the evaluation and treatment of intracerebral hemorrhage”. Mayo Clinic Proc. vol. 80. 2005. pp. 420-433.

Mayer, SA, Rincon, F. “Treatment of intracerebral hemorrhage”. Lancet Neurol.. vol. 4. 2005. pp. 662-672.

Qureshi. “Spontaneous intracerebral hemorrhage”. N Engl J Med. vol. 344. 2001. pp. 1450-1460.
