Unplanned Transfers from Hospital Wards to the Neurological Intensive Care Unit.

BACKGROUND: The aim of this study is to evaluate the characteristics of unplanned transfers of adult patients from hospital wards to a neurological intensive care unit (NICU). METHODS: We retrospectively reviewed consecutive unplanned transfers from hospital wards to the NICU at our institution over a 3-year period. In-hospital mortality rates were compared between patients readmitted to the NICU ("bounce-back transfers") and patients admitted to hospital wards from sources other than the NICU who were then transferred to the NICU ("incident transfers"). We also measured clinical characteristics of transfers, including source of admission and indication for transfer. RESULTS: A total of 446 unplanned transfers from hospital wards to the NICU occurred, of which 39% were bounce-back transfers. The in-hospital mortality rate associated with all unplanned transfers to the NICU was 17% and did not differ significantly between bounce-back transfers and incident transfers. Transfers to the NICU within 24 h of admission to a floor service accounted for 32% of all transfers and were significantly more common for incident transfers than bounce-back transfers (39 vs. 21%, p = .0002). Of patients admitted via the emergency department who had subsequent incident transfers to the NICU, 50% were transferred within 24 h of admission. CONCLUSIONS: Unplanned transfers to an NICU were common and were associated with a high in-hospital mortality rate. Quality improvement projects should target the triage process and transitions of care to the hospital wards in order to decrease unplanned transfers of high-risk patients to the NICU.

Predictors of resource use after acute hospitalization: the Northern Manhattan Stroke Study.

OBJECTIVE: To determine demographic and clinical predictors of discharge destinations following acute care hospitalization for stroke in the community of northern Manhattan. METHODS: A group of 893 patients (mean age, 70 +/- 12 years; 56% women; 51% Hispanic, 30% African-American, 19% white) who survived acute care hospitalization for a first ischemic stroke were followed prospectively. Stroke severity was assessed by the NIH Stroke Scale and categorized as mild (< or = 5), moderate (6 to 13), and severe (> or = 14). Polytomous logistic regression was used to determine predictors for rehabilitation and nursing home placement versus returning home. RESULTS: Among the survivors of acute stroke care hospitalization, 611 (68%) patients were discharged to their homes, 168 (19%) to rehabilitation, and 114 (13%) to nursing homes. Patients with moderate and severe neurologic deficits had more than a threefold increased risk of being sent to a nursing home and more than an eightfold increased risk of being sent to rehabilitation. Age over 65 and cognitive impairment were associated with placement to a nursing home (age over 65: OR, 2.4; 95% CI, 1.0 to 5.6; cognitive impairment: OR, 2.9; 95%, CI 1.4 to 5.7), and rehabilitation (age over 65: OR, 1.8; 95% CI, 1.1 to 2.9; cognitive impairment: OR, 2.9; 95% CI, 1.4 to 5.7). CONCLUSION: Our results demonstrated that one-third of patients with acute stroke from the community of northern Manhattan required placement in a temporary or a long-term disability care institution following acute care hospitalization. Severity of stroke is an important factor that influences discharge planning following acute care hospitalization and its reduction can improve health care resource usage.

Cost and outcome of mechanical ventilation for life-threatening stroke.

BACKGROUND AND PURPOSE: Hospital mortality rates of 50% to 90% have been reported for stroke patients treated with mechanical ventilation. These data have raised serious questions about the cost-effectiveness of this intervention. We sought to determine how often stroke patients are mechanically ventilated, identify predictors of 30-day survival among ventilated patients, and evaluate the cost-effectiveness of this intervention. METHODS: We identified mechanically ventilated patients in a population-based multiethnic cohort of 510 incidence stroke patients who were hospitalized between July 1993 and June 1996. Factors affecting 30-day survival were identified in a multiple logistic regression analysis. We calculated the cost per patient discharged alive, life-year saved, and quality-adjusted life-year saved using a zero-cost, zero-life assumption. RESULTS: Ten percent of patients (n=52) were mechanically ventilated. Thirty-day mortality was 65% overall and did not differ significantly by stroke subtype. Glasgow Coma Scale score on the day of intubation (P:<0.01) and subsequent neurological deterioration (P:=0.02) were identified as predictors of 30-day mortality. The cost (1996 US dollars) of hospitalization per patient discharged alive was $89 400; the cost per year of life saved was $37 600; and the cost per quality-adjusted life-year saved was $174 200. Functional status of most survivors was poor; at 6 months, half were severely disabled and completely dependent. In a worst-case scenario of quality of life preferences, mechanical ventilation resulted in a net deficit of meaningful survival. CONCLUSIONS: Two thirds of mechanically ventilated stroke patients die during their hospitalization, and most survivors are severely disabled. Survival is particularly unlikely if patients are deeply comatose or clinically deteriorate after intubation. In our multiethnic urban population, mechanical ventilation for stroke was relatively cost-effective for extending life but not for preserving quality of life.

Effect of hypervolemic therapy on cerebral blood flow after subarachnoid hemorrhage : a randomized controlled trial.

BACKGROUND AND PURPOSE: Cerebral blood flow (CBF) is reduced after subarachnoid hemorrhage (SAH), and symptomatic vasospasm is a major cause of morbidity and mortality. Volume expansion has been reported to increase CBF after SAH, but CBF values in hypervolemic (HV) and normovolemic (NV) subjects have never been directly compared. METHODS: On the day after aneurysm clipping, we randomly assigned 82 patients to receive HV or NV fluid management until SAH day 14. In addition to 80 mL/h of isotonic crystalloid, 250 mL of 5% albumin solution was given every 2 hours to maintain normal (NV group, n=41) or elevated (HV group, n=41) cardiac filling pressures. CBF ((133)xenon clearance) was measured before randomization and approximately every 3 days thereafter (mean, 4.5 studies per patient). RESULTS: HV patients received significantly more fluid and had higher pulmonary artery diastolic and central venous pressures than NV patients, but there was no effect on net fluid balance or on blood volume measured on the third postoperative day. There was no difference in mean global CBF during the treatment period between HV and NV patients (P=0.55, random-effects model). Symptomatic vasospasm occurred in 20% of patients in each group and was associated with reduced minimum regional CBF values (P=0.04). However, there was also no difference in minimum regional CBF between the 2 treatment groups. CONCLUSIONS: HV therapy resulted in increased cardiac filling pressures and fluid intake but did not increase CBF or blood volume compared with NV therapy. Although careful fluid management to avoid hypovolemia may reduce the risk of delayed cerebral ischemia after SAH, prophylactic HV therapy is unlikely to confer an additional benefit.

Myocardial injury and left ventricular performance after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Electrocardiographic abnormalities and elevations of the creatine kinase myocardial isoenzyme (CK-MB) occur frequently after subarachnoid hemorrhage. In some patients, a reversible and presumably neurogenic form of left ventricular dysfunction is demonstrated by echocardiography. It is not known whether cardiac injury of this type adversely affects cardiovascular hemodynamic performance. METHODS: We retrospectively studied 72 patients admitted to our neuro-ICU for aneurysmal subarachnoid hemorrhage over a 2.5-year period. We selected patients who met the following criteria: (1) CK-MB levels measured within 3 days of onset, (2) pulmonary artery catheter placed, (3) echocardiogram performed, and (4) no history of preexisting cardiac disease. Hemodynamic profiles were recorded on the day after surgery (n=67) or on the day of echocardiography (n=5) if surgery was not performed (mean, 3. 3+/-1.7 days after onset). The severity of cardiac injury was classified as none (peak CK-MB <1%, n=36), mild (peak CK-MB 1% to 2%, n=21), moderate (peak CK-MB >2%, n=6), or severe (abnormal left ventricular wall motion, n=9). RESULTS: Abnormal left ventricular wall motion occurred exclusively in patients with peak CK-MB levels >2% (P<0.0001), poor neurological grade (P=0.002), and female sex (P=0.02). Left ventricular stroke volume index and stroke work index were elevated above the normal range in patients with peak CK-MB levels <1% and fell progressively as the severity of cardiac injury increased, with mean values for patients with abnormal wall motion below normal (both P<0.0001 by ANOVA). Cardiac index followed a similar trend, but the effect was less pronounced (P<0.0001). Using forward stepwise multiple logistic regression, we found that thick subarachnoid clot on the admission CT scan (odds ratio, 1.9; 95% confidence interval [95% CI], 1.0 to 3.4; P=0.04) and depressed cardiac index (odds ratio, 2.1; 95% CI, 1.0 to 4.1; P=0.04) were independent predictors of symptomatic vasospasm. CONCLUSIONS: Myocardial enzyme release and echocardiographic wall motion abnormalities are associated with impaired left ventricular performance after subarachnoid hemorrhage. In severely affected patients, reduction of cardiac output from normally elevated levels may increase the risk of cerebral ischemia related to vasospasm.

Effect of 5% albumin solution on sodium balance and blood volume after subarachnoid hemorrhage.

OBJECTIVE: Subarachnoid hemorrhage (SAH) predisposes patients to excessive natriuresis and volume contraction. We studied the effects of postoperative administration of 5% albumin solution on sodium balance and blood volume after SAH. We also sought to identify physiological variables that influence renal sodium excretion after SAH. METHODS: Forty-three patients with acute SAH were randomly assigned to receive hypervolemia or normovolemia treatment for a period of 7 days after aneurysm clipping. In addition to a base line infusion of normal saline solution (80 ml/hr), 250 ml of 5% albumin solution was administered every 2 hours for central venous pressure (CVP) values of < or =8 mm Hg (hypervolemia group, n = 19) or < or =5 mm Hg (normovolemia group, n = 24). RESULTS: Both groups demonstrated relative volume expansion in base line measurements. The hypervolemia group received significantly more total fluid, sodium, and 5% albumin solution than did the normovolemia group and had higher CVP values and serum albumin levels (all P < 0.02). Cumulative sodium balance was even in the hypervolemia group and persistently negative in the normovolemia group, because of sodium losses that occurred on Postoperative Days 2 and 3 (P = 0.03). In a multiple-regression analysis of all patients, 24-hour sodium balance correlated negatively with glomerular filtration rate (GFR) and positively with serum albumin levels, after correction for sodium intake (P < 0.0001). Hypervolemia therapy seemed to paradoxically lower GFR (P = 0.10) and had no effect on blood volume, which declined by 10% in both groups. Pulmonary edema requiring diuresis occurred in only one patient in the hypervolemia group. CONCLUSION: Supplemental 5% albumin solution given to maintain CVP values of >8 mm Hg prevented sodium and fluid losses but did not have an impact on blood volume in our patients, who were hypervolemic in base line measurements. The natriuresis that occurs after SAH may be mediated in part by elevations of GFR. In addition to acting as a colloid volume expander, 5% albumin solution lowers the GFR and promotes renal sodium retention after SAH. These properties may limit the amount of total fluid required to maintain a given CVP value and hence may minimize the frequency of pulmonary edema.

Amphetamine in recovery from brain injury.

A chart review of dextroamphetamine treatment in 27 traumatic brain injury patients during rehabilitation therapy suggests that amphetamine treatment enhanced the recovery and functional status of 15 patients.

Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage.

A reversible and presumably neurogenic form of myocardial dysfunction may occur following subarachnoid hemorrhage (SAH), but the relationship of this finding to electrocardiographic abnormalities remains unclear. To clarify this issue, serial electrocardiograms (ECGs, mean 6.2 per patient) and echocardiograms (mean 3.4 days after SAH) were obtained in 57 SAH patients without preexisting cardiac disease. The goal was to determine which specific electrocardiographic changes, if any, reflect abnormal left ventricular wall motion in acute SAH. Wall motion abnormalities were identified in five (8%) of 57 patients. Four of these affected patients experienced hypotension (systolic blood pressure < 100 mm Hg) and three exhibited pulmonary edema within 6 hours of SAH, compared to none of the 52 patients with normal wall motion (p < 0.0001). Patients with abnormal wall motion were more likely than patients with normal echocardiograms to have symmetrical T wave inversion (five of five vs. seven of 52, p < 0.001) and severe (> or = 500 msec) QTc segment prolongation (five of five vs. three of 52, p < 0.001) on serial ECGs. These associations maintained their significance with analysis limited to single ECGs performed on or near the day of echocardiography. Abnormal wall motion was also associated with borderline (2% to 5%) creatine kinase MB elevation (five of five vs. three of 52, p < 0.001) and poor neurological grade (p < 0.0001). Although no combination of findings on a single ECG resulted in 100% sensitivity for abnormal wall motion, the presence of either inverted T waves or severe QTc segment prolongation on serial ECGs was associated with 100% sensitivity and 81% specificity. These results demonstrate an association between reduced left ventricular systolic function, mild creatine kinase MB elevation, and electrocardiographic repolarization abnormalities in acute SAH. Symmetrical T wave inversion and severe QTc segment prolongation best identified patients at risk for myocardial dysfunction and may serve as useful criteria for echocardiographic screening following SAH.

Noninvasive monitoring of cardiac output by Doppler echocardiography in patients treated with volume expansion after subarachnoid hemorrhage.

OBJECTIVE: To assess the validity and potential clinical utility of cardiac output monitoring using Doppler echocardiography in patients treated with volume expansion after subarachnoid hemorrhage. DESIGN: Observational study of patients in a randomized, clinical trial. SETTING: Neurologic intensive care unit. PATIENTS: Simultaneous, blinded measurements of cardiac output by thermodilution and Doppler echocardiography were performed in 48 patients 1 or 2 days after aneurysmal clipping. Follow-up Doppler echocardiography was performed an average of 3.9 days later (range 3 to 6) in 15 patients assigned to normovolemia and 24 patients assigned to hypervolemia. INTERVENTION: Patients received supplemental 5% albumin in order to maintain increased (hypervolemia) or normal (normovolemia) cardiac filling pressures. MEASUREMENTS AND MAIN RESULTS: The overall degree of correlation between the two measures was moderate (r = .67, r2 = .45, p < .0001). Bias and precision calculations (-0.75 +/- 1.34 L/min) showed a tendency for Doppler echocardiography to underestimate thermodilution, particularly when cardiac output was very high. Although hypervolemia patients received more 5% albumin than normovolemia patients, mean percent change in Doppler echocardiography cardiac output did not differ between the two groups. Multiple regression analysis showed that the percent change in Doppler echocardiography cardiac output correlated strongly with changes in heart rate (p < .0001), but not with daily net fluid balance or 5% albumin administration. CONCLUSIONS: Agreement was poor between Doppler echocardiography and thermodilution measurements of cardiac output, and trends reflected variations in heart rate rather than fluid status. Monitoring of cardiac output by this technique cannot be recommended in patients treated with volume expansion after subarachnoid hemorrhage.

Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorrhage.

OBJECTIVE: To describe the clinical features of cardiac injury associated with neurogenic pulmonary edema (NPE) in patients with acute subarachnoid hemorrhage (SAH). BACKGROUND: NPE is generally viewed as a form of noncardiogenic pulmonary edema related to massive sympathetic discharge. METHODS: Case series. RESULTS: We found echocardiographic evidence of reduced global and segmental left ventricular (LV) systolic function in five women (mean age, 44; range, 36 to 57) with SAH and NPE. None had a history of heart disease. Four patients were Hunt/Hess grade III and one was grade IV. All five patients experienced (1) sudden hypotension (systolic blood pressure < 110 mm Hg) following initially elevated blood pressures, (2) transient lactic acidosis, (3) borderline (2 to 4%) creatine kinase MB elevations, and (4) varied acute (< 24 hours) electrocardiographic changes followed by widespread and persistent T wave inversions. Pulmonary artery wedge pressures were normal in 3/3 patients at the onset of pulmonary edema but reached high levels (> 16 mm Hg) in all four patients studied beyond this period. Reduced cardiac output and LV stroke volume were identified in three patients; the fourth patient demonstrated normal values on high doses of intravenous pressors. Cerebral infarction due to vasospasm occurred in four patients and resulted in two deaths. Follow-up echocardiography performed 2 to 6 weeks after SAH revealed normal LV function in all three survivors. CONCLUSIONS: A reversible form of cardiac injury may occur in patients with NPE following SAH and is associated with characteristic clinical findings. Impaired LV hemodynamic performance in this setting may contribute to cardiovascular instability, pulmonary edema formation, and complications from cerebral ischemia.

Transcranial Doppler detection of anterior cerebral artery vasospasm.

The performance of transcranial Doppler in the detection of anterior cerebral artery vasospasm and vasospasm in patients after subarachnoid haemorrhage was analysed. Transcranial Doppler and cerebral angiography were performed within the same 24 hours on each of 41 patients with acute subarachnoid haemorrhage. Sensitivity and specificity of transcranial Doppler to classify middle cerebral arteries, anterior cerebral arteries, and patients with angiographic vasospasm were determined at mean velocities of 120 and 140 cm/s. Accuracy of transcranial Doppler was better at 140 than at 120 cm/s. For the middle cerebral artery, sensitivity was 86%, specificity 98%. For the anterior cerebral artery, sensitivity was 13%, specificity 100%. Among all patients, sensitivity was 45%, specificity 96%. Among patients with anterior communicating artery aneurysms, sensitivity was 14%, specificity 90%. Therefore, transcranial Doppler accurately differentiates between middle cerebral arteries with and without vasospasm on angiography, but has a very low sensitivity for detecting anterior cerebral artery vasospasm and vasospasm in patients with anterior communicating artery aneurysms. Since vasospasm may involve anterior cerebral arteries while sparing middle cerebral arteries, especially after rupture of an anterior communicating artery aneurysm, caution should be exercised in using negative transcranial Doppler results to make treatment decisions based on the assumed absence of vasospasm.

The clinical spectrum of unruptured intracranial aneurysms.

OBJECTIVE: A retrospective study was performed to delineate the clinical characteristics of symptomatic unruptured aneurysms. DESIGN: Patient histories, operative reports, and angiograms in 111 patients with 132 unruptured aneurysms were reviewed. SETTING: Tertiary care university hospital. PATIENTS: One hundred eleven patients with 132 unruptured intracranial aneurysms were studied. There were 85 women and 26 men, with a mean age of 51.2 years (age range, 11 to 77 years). Many patients were referred by community neurologists and neurosurgeons for further evaluation and neurosurgical management. RESULTS: Fifty-four symptomatic patients were identified. Group 1 (n = 19; mean aneurysm diameter, 2.1 cm) had acute symptoms: ischemia (n = 7), headache (n = 7), seizure (n = 3), and cranial neuropathy (n = 2). Group 2 (n = 35; mean aneurysm diameter, 2.2 cm) had chronic symptoms attributed to mass effect: headache (n = 18), visual loss (n = 10), pyramidal tract dysfunction (n = 4), and facial pain (n = 3). Group 3 (n = 57; mean aneurysm diameter, 1.1 cm) had asymptomatic aneurysms. CONCLUSIONS: Acute severe headache, comparable to subarachnoid hemorrhage headache, but without nuchal rigidity, was associated with the following mechanisms: aneurysm thrombosis, localized meningeal inflammation, and unexplained. Unruptured aneurysms may be misdiagnosed as optic neuritis or migraine, or serve as a nidus for cerebral thromboembolic events. Internal carotid artery and posterior circulation aneurysms were more likely to cause focal symptoms from mass effect than were anterior cerebral artery and middle cerebral artery aneurysms. Weeks to years may elapse before their diagnosis. The absence of subarachnoid blood does not exclude an aneurysm as a cause for acute or chronic neurologic symptoms.

Acute quadriplegic myopathy: a complication of treatment with steroids, nondepolarizing blocking agents, or both.

We studied two patients who were given high-dose intravenous steroid therapy and were intubated for status asthmaticus. Both became quadriplegic and wasted within 2 weeks. EMG had myopathic abnormalities. Muscle biopsy revealed severe atrophy of most muscle fibers, with disorganization of myofibrils and selective loss of thick (myosin) filaments. Immunohistologic stains for myosin isoforms confirmed the decrease or absence of this protein. Both patients clinically improved over several months.

The role of transcranial Doppler in confirming brain death: sensitivity, specificity, and suggestions for performance and interpretation.

We performed transcranial Doppler (TCD) examinations on 54 comatose patients over a 1-year period. Of 49 patients with technically adequate TCD examinations, 23 met criteria for determination of brain death by clinical and EEG criteria (21) or clinical criteria alone (2; EEG not performed). A TCD waveform abnormality, consisting of absent or reversed diastolic flow, or small early systolic spikes, in at least 2 intracranial arteries, occurred in 21 brain-dead patients, but in none of the other patients in coma. With appropriate guidelines for performance and interpretation, TCD could be incorporated into institutional protocols as a rapid and convenient alternative to EEG for confirmation of brain death.

Early aneurysm surgery and prophylactic hypervolemic hypertensive therapy for the treatment of aneurysmal subarachnoid hemorrhage.

The prevailing sentiment of North American neurosurgeons is that there is no significant difference in overall morbidity between patients who are treated with early aneurysm surgery and those who are treated with delayed aneurysm surgery. This concept is based primarily on the high incidence of ischemic events after early intervention. Recent experience, however, indicates that prophylactic hypervolemic hypertensive therapy may be beneficial in reducing delayed ischemia after early aneurysm surgery. During the preceding 21 months, we have performed 125 operations for intracranial aneurysms. Fifty-six patients in this group presented less than 7 days after subarachnoid hemorrhage (SAH) (47 within 3 days) and were treated by a prospective protocol of urgent aneurysm surgery performed within 24 hours after presentation. In all cases, the aneurysm was clipped with the use of mannitol and spinal drainage for brain relaxation. All patients were then treated with prophylactic volume expansion therapy and induced hypertension with a central venous pressure or a Swan-Ganz catheter until the 14th day after SAH. Preoperatively, 17 patients were Hunt and Hess Grade I, 9 were Grade II, 28 were Grade III, and 2 were Grade IV. In this group of 56 patients at risk for delayed ischemia from vasospasm, 5 patients had significant intraoperative complications. Ten patients (18%) had delayed cerebral ischemia, totally reversible in 6 cases, with small infarcts in 3 cases, and with 1 death (2% mortality from delayed ischemia), there were 5 cases of shunted hydrocephalus, and 3 deaths from other complications. Overall, 41 patients (73%) returned to their premorbid occupations without neurological deficit.(ABSTRACT TRUNCATED AT 250 WORDS)

Complications of long-term anticoagulation.

We used life-table techniques to determine risks of morbidity and mortality associated with long-term warfarin treatment in an anticoagulation clinic. Cumulative risks for life-threatening complications and warfarin-related death among all patients were 1% at 6 months, 5% at 1 year, and 7% at 2 and 3 years. Cox regression analysis using age as a continuous variable failed to show an effect of age on cumulative risks of complication. The occurrence of a minor complication during the course of therapy did not place patients at higher risk for developing a major complication that would prompt discontinuation of therapy or cause death. There was no statistically significant difference between the cumulative risks of patients anticoagulated for cerebrovascular disease and the cumulative risks of patients anticoagulated for other indications.

Prophylactic volume expansion therapy for the prevention of delayed cerebral ischemia after early aneurysm surgery. Results of a preliminary trial.

From June 1986 to June 1987, 47 consecutive patients with ruptured intracranial aneurysms were treated with immediate aneurysm surgery and prophylactic volume expansion therapy for ten to 14 days after subarachnoid hemorrhage (SAH). Twenty-four patients were admitted within three days of SAH. Twenty-three of these patients had an excellent result, and one patient died. There were no cases of delayed cerebral infarction. In 18 of 23 patients admitted more than three days after SAH, there was an excellent result. The other five patients had permanent morbidity related to the original SAH. These preliminary data suggest that immediate aneurysm surgery and aggressive postoperative prophylactic volume expansion in all patients can substantially reduce rebleeding and delayed cerebral ischemia, potential causes of morbidity, after aneurysmal subarachnoid hemorrhage. A more extensive prospective trial of this approach will be required to test this hypothesis.

Lack of association between carotid plaque hematoma and ischemic cerebral symptoms.

To investigate the association between carotid plaque hematoma and symptoms of cerebral ischemia a retrospective review of 200 consecutive carotid endarterectomies at the Neurological Institute of New York was carried out. Data analyzed included cerebral ischemic symptoms, angiographic findings, preoperative use of antithrombotic agents, and microscopic pathology of endarterectomy specimens. No association was found between ischemic symptoms ipsilateral to the endarterectomy and presence, size, or age of plaque hematomas. Plaque hematomas were less common among patients who took antithrombotic agents preoperatively than among those who did not. The presence of plaque hematoma was associated with angiographic carotid cross-sectional area stenosis of greater than 75%. Patients with stenosis of less than 75% were more likely than those with stenosis of greater than 75% to have ischemic symptoms ipsilateral to the endarterectomy, suggesting that criteria for surgical treatment of carotid atherosclerosis differ for those who are symptomatic vs. those who are asymptomatic. These results demonstrate the limitation of using a surgical series to extend causal inferences about the relation between plaque hematoma and cerebral ischemic symptoms to the general population of people with carotid atherosclerosis.