And attack; Ischemic Stroke, Hemorrhagic Stroke, HI, SAH, Cerebral Ischemia (2023)

1. Description of the problem

By definition, stroke refers to the sudden onset of neurological deficits unrelated to trauma. This broad definition does not differentiate between hemorrhage in the brain or ischemia in a specific brain region. However, only about 10% of strokes in the US are hemorrhagic, which is why the term "stroke" is often used interchangeably with ischemic stroke.

This section covers basic acute management of both types of stroke. Although subarachnoid hemorrhage is technically a form of hemorrhagic stroke, treatment of this condition has become quite specialized over the past decade and the reader is referred to guidelines recently published by the Society for Neurocritical Care. Prompt identification and referral to a high-volume neurosurgical center that performs aneurysm repair is recommended.

Ischemic stroke presents as a sudden loss of neurological function, often manifesting as a deficit on one side of the body with preserved function on the contralateral side. Strokes rarely occur as a bilateral phenomenon unless there is severe impairment of consciousness. On the other hand, variation in the extent of involvement of a particular side of the body is common and can often provide information about the location and vascular distribution of the stroke.

Despite some distinctive, albeit subtle, features of ischemic stroke compared to hemorrhagic stroke, a CT scan is required to definitively differentiate between these two categories of stroke. The use of CT is mandatory due to the opposing treatment approaches for ischemic versus hemorrhagic stroke.

Important management points

Any patient with suspected recent stroke, even if it lasted more than a day, should undergo an emergency CT scan. This allows for the immediate initiation of appropriate blood pressure monitoring and determines the need for additional imaging studies in the first few hours after admission. In general, ischemic stroke patients can have any systolic blood pressure below 220 mmHg, while hemorrhagic stroke patients should urgently lower their systolic blood pressure to less than 160 mmHg for 4 to 6 hours and then to less than 140 during your stay. The greatest risk of rebleeding and deterioration in outcome occurs within the first 24 to 48 hours, making the distinction between these two types of stroke the highest priority for the initial assessment.

2. Emergency management

A stroke is a neurological emergency very similar to a myocardial infarction. The first step is to consider the stroke as a possible cause of the patient's symptoms. The core element of stroke treatment is the determination of tissue plasminogen activator (t-PA) eligibility. There are well established guidelines for the administration of t-PA which are provided here for reference. It is important to determine the suitability of t-PA to ensure that the patient does not have an intracranial hemorrhage (ICH).

Therefore, as soon as a diagnosis of stroke is considered, a CT scan should be performed immediately to determine ischemia as the cause. It is important to note that a negative CT scan is common in the acute phase of ischemic stroke. Occasionally, more subtle clues to severe stroke can be found, such as: B. the sign of hyperdense middle cerebral artery (MCA), the band-insula sign or a subtle asymmetry at the gray-white transitions. A normal CT should be expected at early signs of stroke, and once bleeding has been ruled out as a cause of deficits, t should be strongly considered if the patient presents in less than 4.5 hours.

In addition to the rapid creation of a CT, the creation of a detailed medical history and a definitive start time is crucial for subsequent management decisions. All other medical conditions should be determined, especially the presence of diabetes and any recent surgical procedures, even if considered minor. These factors can also influence the decision about thrombolytic therapy and should be assessed immediately and completely at the time of presentation. Finally, taking the NIH Stroke Scale Assessment Examination is very helpful in documenting stroke severity, estimating risk of bleeding, and monitoring stroke recovery and/or progression, as well as facilitating communication with neurologists.

Management points not to be missed

The adult exhibits signs/symptoms consistent with an acute stroke:

Conduct an emergency for all stroke patients

Note vital signs and assess the airway.

Get an instant CT scan of the head without contrast.

Undergo basic laboratory tests, although laboratory tests do not need to delay treatment unless coagulopathy or another blood dyscrasia is suspected.

ischemic stroke

The patient is a candidate for intravenous t-PA if:

1. You can finally set the start time and get a history

2. t-PA can be administered in less than 4.5 hours from the above start time

3. Ischemic stroke in any area based on negative CT for bleeding

Consider stopping t-PA therapy if:

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

2. The patient has a known coagulopathy

3. Patient is on anticoagulants (requires INR before t-PA can be administered, ok if <1.7)

4. The patient has had a previous stroke or head injury within the last 3 months

5. The patient had a previous intracranial hemorrhage

6. The patient has had gastrointestinal bleeding for the past 3 weeks

7. The patient has had major surgery in the past 14 days

8. The patient has had an arterial puncture at a non-compressible site within the past week

9. The patient has active bleeding or signs of trauma.

10. The platelet count is < 100,000 mm³

11. Blood sugar is <50 mg/dL

12. The patient has had a seizure before

13. CT scan shows clear evidence of infarction > 1/3 hemisphere

Other considerations:

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

1. The patient is over 80 years old

2. NIH Stroke Scale Score ist >25

3. History of previous stroke and diabetes

4. Or the patient is taking anticoagulants

hemorrhagic attack

The patient is not a candidate for t-PA.

The target systolic blood pressure is < 140 mmHg.

Control your blood pressure quickly with a fast-acting calcium channel blocker:

Nicardipine: Start with 5 mg/h IV. and increase by 2.5 mg/h every 5-15 min until the systolic target is reached

Clevidipine: Start with 1 to 2 mg/h IV. and doubling the rate every 90 seconds to the target, then making small incremental changes every 5–15 min to the target

Follow the exam closely and consider re-imaging if changes are noted.

3. Diagnose

diagnostic approach

Although there are some subtle clinical features that can distinguish ischemic from hemorrhagic stroke, CT is the mainstay of diagnosis. However, there should be strong clinical suspicion of stroke before imaging studies are ordered. This must be the case because the most common CT finding in an acute ischemic stroke is a normal CT scan. Therefore, a clinical examination suggesting a common vascular region of the brain, such as e.g. hemiplegia or aphasia, arrange for a rapid CT evaluation to determine the most appropriate next step.

CT angiography may be appropriate for severe stroke symptoms. Carotid obstruction or extensive MCA are unlikely to respond to intravenous t-PA and patients should be referred to an interventionist for evaluation immediately.

Other important tests to consider are blood clotting and blood count tests. These are of relative importance since low platelets or high INR would be contraindications to t-PA administration. However, in the absence of a history of coagulation abnormalities, active anticoagulant therapy, or evidence of bleeding, administration of t-PA is not deferred for results in these laboratories.

normal laboratory values

By far the most common imaging finding in acute stroke is normal imaging. Thereafter, any subtle hypodensity should be carefully considered and evaluated for correlation with existing deficits. Some particular patterns can be observed and are important to recognize as they suggest the need for more aggressive intervention.

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

Illustration 1.

Figure 2 shows an island band signal. This finding can be very subtle and usually occurs at the beginning of large MCAs. These findings suggest a major stroke and significant deficits if left unchecked.

Figure 2.

If CT confirms a large volume stroke (Figure 3), future treatment of the increased intracranial pressure should be considered. There is good data on the role of hemicraniectomy in acute stroke, showing reduced mortality and better functional outcomes regardless of the hemisphere affected.

Figure 3.

differential diagnosis

There are few other clinical conditions that can mimic an acute stroke. These conditions include seizures, migraines, hypoglycemia, and acute infections or febrile illnesses. As expected, a careful history can help distinguish these mimics. In younger patients with lower vascular risks, it is important to consider these alternatives. Seizures can cause Todd's palsy or focal weakness, and for this reason seizures are a relative contraindication to t-PA administration. In most cases, the weakness improves quickly, although it can last 24 hours or more. Complex migraines may also present as acute vision loss or other focal deficits, and in older patients the deficits may present as part of an aura and not be associated with headache. Although these types of knockoffs are a significant source of concern among non-subspecialty providers, recent studies have shown that bleeding complications from t-PA are rare in these patients.

As with other mimics, infection and fever can cause the symptoms of an old stroke to acutely worsen or, less commonly, unmask a previously asymptomatic stroke. This acute discovery of a chronic illness can easily be mistaken for an acute event. However, a medical history can often be obtained with similar depictions, the CT scan is negative for new areas of injury or bleeding, and other evidence of developing infection can be found, such as: B. Elevated white blood cell count, blood pressure below normal or positive. . Urinalysis Like other mimics, these patients have a very low complication rate with t-PA. However, since t-PA does not need to be administered, any complications that arise are avoidable complications. This underscores the importance of careful investigation of the history of these conditions and screening of appropriate laboratories prior to administration of t-PA.

4. Specific treatment

ischemic stroke

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

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

A follow-up CT scan should be performed 24 hours after t-PA to determine stroke extent and assess bleeding conversion.

Note: Some centers have considered a lack of improvement at the end of the infusion as a treatment failure and, in severely disabled patients, attempt to remove the intra-arterial clot in patients even less than 6 hours after the onset of symptoms. This is currently being investigated as part of a large multi-centre study and is currently not recommended due to the high risk of bleeding.

hemorrhagic attack

The target systolic blood pressure is below 140

Control your blood pressure quickly with a fast-acting calcium channel blocker:

Nicardipine: Start with 5 mg/h IV. and increase by 2.5 mg/h every 5-15 min until the systolic target is reached

Clevidipine: Start with 1 to 2 mg/h IV. and doubling the rate every 90 seconds to the target, then making small incremental changes every 5–15 min to the target

Follow the exam closely and consider re-imaging if changes are noted.

Candidates for ischemic stroke without t-PA

In patients who are not candidates for t-PA or are outside the t-PA window but have less than 6 hours from symptom onset for anterior circulation infarctions or less than 12 hours for posterior circulation strokes, intra-arterial intervention should be considered are taken into account.

5. Monitoring, follow-up and treatment of the disease

Expected response to treatment

All stroke patients should be admitted to an intensive care unit or lower level of care to ensure close neurological monitoring. It is important to document early speech and swallowing assessments so that adequate nutrition can be provided and complications from aspiration can be minimized. For the first 24 hours, serial scans every 2-4 hours are recommended. This is especially true for patients with significant deficits that quickly disappear. Documentation of examination standardization is critical because recurrences are common in this cohort and they may be candidates for t-PA or other interventions if symptom onset can be clearly defined. In many cases, a CT or MRI follow-up within 24-36 hours is sufficient to determine the extent of the stroke and the risk of complications from increased intracranial pressure.

In the case of an ischemic stroke, a cause of the stroke should be sought. Therefore, an ECHO with microcavitation examination, lipid profile, hemoglobin A1c and thyroid function tests should also be performed. If FOP is found on the ECHO, a bilateral lower extremity ultrasound should be considered to examine a clot source for emboli. Platelet aggregation inhibition should be considered early as a secondary prevention of stroke. In the case of major strokes, this can be delayed by a few days. DVT prophylaxis should also be started early, within 48 hours, unless the stroke is very large or hemorrhagic.

Pictures

Vascular imaging should always be performed in patients with acute stroke. If an MRI is used, an MRI of the head and neck should also be done. Although MRA can be overly sensitive, in cases where high-grade lesions or occlusion are suspected, formal ultrasonography or angiography can be performed in this small subpopulation. The ultrasound examination alone is only of limited value in the case of an acute stroke, as it does not allow any statement to be made about the condition of the intracranial vessels and therefore additional imaging is required in the case of lesions anyway.

consequences

Patients with negative sequelae should raise concerns about a simulated stroke or an alternative underlying process. This is especially true for patients with declining mental status. Although stroke can often impair speech function and make patients drowsy and lethargic, nonresponsiveness in acute stroke is uncommon and should indicate posterior circulatory catastrophe or a non-alternative diagnosis. In these cases, an EEG, follow-up laboratory tests (with toxicological screening if not already done), and a lumbar puncture should be considered.

pathophysiology

Ischemic strokes are caused by an acute blockage of blood flow through a vessel that supplies a specific region of the brain. Decreased blood flow quickly leads to neuronal dysfunction within the vascular territory supplied by the vessel. The extent of neuronal death depends on the size of the blocked vessel, the duration of the blockage, and the extent of collateral flow to the region. The cause of the blockage can be different. Local atherosclerotic disease, similar to heart disease, can occur intracranially and lead to acute local thrombosis.

In other cases, acute vascular injury, such as B. cause a dissection, a vascular obstruction or an embolic disease. A venous clot can also cause an arterial blockage if there is a bypass path between the two circuits. Classically, the patent foramen ovale (PFO) is considered the main pathway; However, recent studies have found that transcranial Doppler has a higher sensitivity for shunt detection than traditional cardiac ultrasonography of microcavities, suggesting that there are other occlusions that may allow clot migration into the arterial circulation. Finally, clots can also be seen in the heart due to valvular disease, wall motion abnormalities, or abnormal rhythms.

Bleeding is less complicated since high blood pressure is often the main cause. Cerebral hemorrhages result from a tear in the vessel wall. In some regions, such as Asia, ICH is more common and accounts for a higher percentage of strokes. There is some data to suggest that very low lipid levels may contribute to ICB; however, this relationship does not impact acute care. The relationship to blood pressure explains the places where ICH is commonly seen. The most common are the basal ganglia with rupture of the lenticulostriatic vessels.

Lobe hemorrhages in the frontal and temporal lobes are the second most common, followed by hemorrhages in the cerebellum and posterior fossa. This lower tendency to bleed in the posterior fossa explains the longer time between onset of symptoms and intra-arterial intervention. In the elderly, amyloidosis causes recurrent lobe hemorrhage. These patients often have less symptomatic bleeding initially because the bleeding tends to be more superficial and smaller. Over time, cognitive decline is common, and a progressive decline in function is seen with recurrent bleeding.

Epidemiology

Stroke is currently the third leading cause of death and the leading cause of acquired disability. There are approximately 795,000 strokes per year and half that number are transient ischemic attacks (TIAs). Interestingly, there is an uneven distribution of stroke across the country, with a significantly higher rate of stroke in the Southeast. This region is known as the "conspicuous belt" because of this disparity, and the reasons for this difference in conspicuous distribution remain an area of ​​study.

The proportion of hemorrhagic and ischemic strokes also varies worldwide, with the highest proportion of bleeding in Asian countries. The lower serum lipid profiles in these regions of increased bleeding, combined with the observation that induced ultralow lipid levels appear to be associated with higher rates of bleeding, suggest a potential role for diet and lipid profiles in this distributional variation.

Primary and secondary prevention of stroke has been a major focus of cardiovascular research over the years. Much of what we know about risk factors associated with stroke comes from cardiovascular studies looking at the treatment of various heart conditions where stroke is one of the endpoints of clinical trials. Atrial fibrillation is a good example. The appropriate treatment of atrial fibrillation has been investigated in large international studies comparing rhythm control with rate control and anticoagulation.

These studies were designed and conducted by cardiologists; However, stroke is one of the main complications of atrial fibrillation and was an important finding of the study. From this large study we learn that rate control and anticoagulation lead to reduced stroke rates. This approach led to our current prevention strategies to reduce the overall rate of cardiovascular events, which include daily aspirin, low-density lipoprotein and cholesterol goals, strict glycemic control in diabetics, and normalization of blood pressure.

forecast

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

Even in these cases, increasing lower extremity tone often allows these patients to carry weight and assist in transfers. Most can also recover to oral feeding. These findings have prompted neurologists to find ways to prevent subsequent strokes and physical therapists to find new ways to maintain and improve function in stroke victims. Therefore, while some patients may find a loss of independence unacceptable, it is important not to be nihilistic when presenting with these patients.

Early prediction of outcome is easier in hemorrhagic stroke, where a scoring system has shown good correlation with outcome. In general, hemorrhagic stroke patients do not fare as well as ischemic stroke patients. Volume for volume, hemorrhagic stroke patients have greater disability at presentation and less recovery over time. The reasons for this are not entirely clear, but are likely related to mass effects and tissue destruction occurring as a result of hematoma formation. However, there is some bimodal distribution in hemorrhagic stroke patients, with some devastating and others showing relatively minimal symptoms.

what is the proof

Characteristics and diagnosis of a stroke

Fonarov. "Characteristics, performance measurements, and hospital outcomes of the first million stroke and transient ischemic attack admissions in Get with the Guidelines-stroke."Qualitative Results Circ Cardiovasc.vol. 3. May 2010. pg. 100-1 291-3

Albert, MJ. "Diagnosis and therapy of ischemic stroke".I'm JMedvolume 106 February 1999. Pages. 211-221.

Garbage. “Hospital costs, length of stay and mortality from cerebrovascular events in community hospitals.”Neurology.vol. 57. 2001. S. 305-314.

Treatment of ischemic strokes

Albert, MJ. "Diagnosis and therapy of ischemic stroke".I'm JMedvolume 106 February 1999. Pages. 211-221.

Wardrecht. "Thrombolysis for Acute Ischemic Stroke".Cochrane database system rev.7. Oktober 2009. S. CD000213

ossi. "Hospital management of acute ischemic stroke after intravenous thrombolysis".Experto Rev Cardiovasc Ther.vol. 9. April 2011, p. 463-72.

Treatment of hemorrhagic strokes

parkers "Management of non-traumatic spontaneous intracranial hemorrhage".Pharmacy Practice J.vol. 23. October 2010 P. 100-1 398-4

morning star. "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: An American Heart Association/American Stroke Association Guide for Healthcare Professionals."Attack.volume September 41, 2010 pages. 100-1 2108-2

Treatment of subarachnoid hemorrhage

forecast

ischemic stroke

Tissue. "Rate, Grade, and Predictors of Recovery from Disability After Ischemic Stroke."Neurology.vol. 68. 2007. S. 1583-1587.

hemorrhagic attack

Hemp. "The ICH score: a simple and reliable rating scale for intracerebral hemorrhage".Attack.vol. 32. 2001. S. 891-897.

Brother. "New clinical and surgical management strategies in the evaluation and treatment of intracerebral hemorrhage".Mayo Clinic Procedure.vol. 80. 2005. S. 420-433.

Mayer, S.A., Rincon, F. "Treatment of Intracerebral Hemorrhage."Lanzette Neurol..vol. 4. 2005. S. 662-672.

Qureshi. "Spontaneous intracerebral hemorrhage".N Engl. J Med.vol. 344. 2001. S. 1450-1460.

Garbage. “Hospital costs, length of stay and mortality from cerebrovascular events in community hospitals.”Neurology.vol. 57. 2001. S. 305-314.

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