Abstract
Although, classically, stroke symptoms are maximal at onset and patients gradually recover over days, weeks, and months, patients sometimes deteriorate. People have termed the phenomenon stroke progression, stroke in evolution, stroke deterioration, and symptom fluctuation. There is no consistent terminology. The phenomenon occurs from different causes and is incompletely understood. Although the typical definition of a significant neurological deterioration in trials has been a gain of ≥ 1 point on item 1a (level of consciousness) or ≥ 4 points in the motor items of the NIHSS, any detectable deterioration should prompt careful assessment and a tailored work-up.
Although, classically, stroke symptoms are maximal at onset and patients gradually recover over days, weeks, and months, patients sometimes deteriorate. People have termed the phenomenon stroke progression, stroke in evolution, stroke deterioration, and symptom fluctuation. There is no consistent terminology. The phenomenon occurs from different causes and is incompletely understood. Although the typical definition of a significant neurological deterioration in trials has been a gain of ≥ 1 point on item 1a (level of consciousness) or ≥ 4 points in the motor items of the NIHSS, any detectable deterioration should prompt careful assessment and a tailored work-up.
This chapter discusses the evaluation of potential causes, and approaches for treatment of each cause.
Probable Causes
1. Stroke enlargement (e.g., arterial stenosis or occlusion with worsening perfusion)
2. Drop in perfusion pressure
3. Recurrent stroke (not common)
4. Cerebral edema and mass effect
5. Hemorrhagic transformation
6. Metabolic disturbance (hypoxia, hypercarbia, decreased cardiac output, increased glucose, decreased sodium, fever, sedative drugs, etc.)
7. Seizure, post-ictal state
8. Symptom fluctuation without good cause (due to inflammation?)
9. The patient is not feeling like cooperating (sleepy, drugs)
Initial Evaluation of Patients with Neurological Deterioration
1. Check airway – breathing – circulation (ABC), vital signs, laboratory tests. Is the patient hypotensive or hypoxic?
2. Talk to and examine the patient. If the patient is sleepy, is it because it’s 3 a.m. or because of mass effect? Is there a pattern of symptoms (global worsening versus focal worsening)?
3. Get an immediate non-contrast head CT (to evaluate for hemorrhage, new stroke, swelling, etc.).
4. Review medications (antihypertensives, sedatives).
5. Observe patient, and ask nurse, for subtle signs of seizure.
6. Consider MRI for brain imaging, new stroke, stroke enlargement, swelling; TCD or CT/MR angiography, CT/MR perfusion for arterial imaging; EEG to diagnose subclinical seizures. Chemistry, cultures, urinalysis, blood gases to rule out toxometabolic causes.
7. In some of these situations, the patient might benefit from closer monitoring in the neurointensive care unit.
Stroke Enlargement
This occurs when there is worsening or recurring arterial stenosis/occlusion and the hemodynamics change for some reason. There are no data to support that anticoagulation prevents hemodynamic worsening. The treatment should match what you think is the pathophysiology behind the deterioration.
Early treatment of the underlying stenosis/occlusion is undeniably the best course of action. The key is finding the high-risk patients early by performing imaging to detect large-artery stenosis/occlusion by CTA/MRA, TCD/carotid Doppler, or MRI. Patients with minor deficits but abnormal TCD, CTA, or MRA are at highest risk of progression. Perfusion imaging may indicate areas of tissue at risk. Even without an MR or CT perfusion study, the finding of a small diffusion-weighted lesion on MRI and a relatively minor neurological deficit in the presence of large-artery occlusion may indicate a high risk for progression. In such patients, you might want to consider early intervention, such as IV thrombolysis despite low NIHSS score, intra-arterial therapy, carotid endarterectomy, or carotid stenting.
Even if early treatment of the underlying stenosis/occlusion is not done, there are still treatment options for strokes that enlarge, especially in the current era of late-window reperfusion strategies (i.e., beyond 6 hours from LKW). Recent studies have shown that tPA may be effective if the FLAIR is not yet positive,1 and thrombectomy improves outcome in patients with small ischemic core lesions up to 24 hours after stroke onset.2, 3 These data should be kept in mind and guide treatment when patients deteriorate on a hemodynamic basis after admission.
Reocclusion after thrombolysis/thrombectomy may also lead to substantial stroke enlargement. These patients may benefit from repeat angiography and thrombectomy if their imaging profile on perfusion studies is still favorable to intervention (see Chapter 6). The interventionist may repeat the thrombectomy and/or deploy a stent across a tight stenosis. If an intra-arterial thrombus is identified, heparin or a direct thrombin inhibitor drip (e.g., argatroban) should be considered.
Finally, if your deteriorating patient is not already on dual antiplatelets, this should be considered (see Recurrent Stroke, below).
Drop in Perfusion Pressure
Since autoregulation is compromised in ischemic brain, any reduction in blood pressure will reduce flow to penumbral regions, thereby potentially worsening the clinical deficit. This is true in both cortical and subcortical strokes. Lacunar strokes are notorious for fluctuating pressure-dependent symptoms due to the paucity of collateral flow in subcortical areas. As a rule of thumb, mean arterial pressure (MAP) should be kept at pre-stroke levels (as a general guideline, at least 130 mmHg in hypertensive patients, and 110 mmHg in normotensive patients) in the first 24 hours, and, if MAP drops below this level and the patient deteriorates, the MAP should be increased by fluid boluses and possibly initiation of a pressor. Some data suggest that blood-pressure fluctuations are particularly deleterious, so wide fluctuations in MAP should be avoided.
Laying patients flat may temporarily optimize cerebral perfusion and result in improvement in symptoms. The recent HeadPoST trial, which randomized patients to either lying flat or sitting up at 30 degrees for 24 hours post-stroke, showed no differences in stroke recovery at 90 days or rate of pneumonias.4 However, this study mainly included patients with mild strokes, which may not have been the group most likely to benefit, and the intervention was not carried out in the first hours after stroke.
Recurrent Stroke
Unfortunately some patients go on to have recurrent strokes. Recent data suggest that most patients with acute non-cardioembolic strokes, and certainly those at highest risk of recurrent stroke such as those with intracranial atherosclerosis, multiple infarcts, or large-artery occlusion, should be treated with dual antiplatelets (aspirin + clopidogrel) starting within the first 24 hours (see Chapter 8).5–7 Ticagrelor may be an alternative and is under study either alone or in combination with aspirin.
Among atrial fibrillation patients, the stroke recurrence risk is 5–8% in the first 2 weeks.8–10 There are no data to show that immediate or “early” anticoagulation helps, even in the setting of atrial fibrillation, because anticoagulation can lead to hemorrhagic complications (see Hemorrhagic Transformation, below). Yet we might be underestimating the magnitude of frequency of stroke recurrence if we rely on clinical deterioration alone. One study reported that stroke recurrence was detected by MRI in 34% of patients in the first week, whereas clinically only 2% stroke recurrence was noted.11 Furthermore, some patients may be at higher risk of re-embolization, especially those with associated mitral stenosis or left atrial thrombus. Therefore, our recommendation in atrial fibrillation patients is to anticoagulate once we determine by repeat brain imaging that the infarct is small or, if it is large, that any acute hemorrhagic transformation or vasogenic edema is resolving. This usually means waiting 48–96 hours after the acute stroke.
In a large population-based study, large-artery atherosclerosis was associated with the highest risk of stroke recurrence (Figure 7.1, Table 7.1).12 This supports the recommendation to perform carotid revascularization (endarterectomy or stenting) earlier rather than later (see Carotid Stenosis in Chapter 8).
Figure 7.1 Stroke recurrence risk by stroke mechanism.
Table 7.1 Stroke mechanisms and risk of early recurrence
Cerebral Edema and Mass Effect
This is a worry with large strokes, such as large MCA strokes involving the basal ganglia, often with some involvement of the ACA or PCA territories as well, and large cerebellar strokes. It is particularly concerning in young patients who do not have much atrophy and thus not much room for the brain to swell inside the skull. Monitor for any neurological change, decline in level of consciousness, rising blood pressure, periodic breathing, hiccups, headache, new cranial nerve abnormalities, and pupils (late phenomenon).
Medical Management
1. Reduction of intracranial pressure (ICP) starts with head-of-bed positioning at > 30 degrees, head in neutral position to optimize venous outflow, immediate correction of fever, electrolyte imbalance, and hyperglycemia, and careful optimization of MAP and cardiac output to ensure adequate cerebral perfusion (cerebral perfusion pressure = MAP – ICP; should be kept ≥ 60 mmHg).
2. Osmotherapy (i.e., mannitol or hypertonics) is a temporizing measure that may help in some cases. Give mannitol (1–1.5 g/kg bolus over 30–60 minutes) upon signs of deterioration. The aim is to increase baseline serum osmolality by 10%, but no higher than 320 mOsm. Check serum osmolality every 12 hours and hold mannitol if > 320 mOsm. Hypertonics (e.g., 3% or 23.4% NaCl) can also be bolused to achieve the same effect. Intubation and mechanical ventilation (maintain SpO2 > 95% and PaCO2 30–35 mmHg), judicious sedation, and at times paralysis may be necessary to control ICP.
3. Importantly, do not give steroids after a stroke (grade A recommendation). Randomized studies have shown that steroids may be more harmful than beneficial after an acute stroke.
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