Use of tissue-type plasminogen activator for acute ischemic stroke: the Cleveland area experience.

CONTEXT: Little is known regarding outcomes after intravenous tissue-type plasminogen activator (IV tPA) therapy for acute ischemic stroke outside a trial setting. OBJECTIVE: To assess the rate of IV tPA use, the incidence of symptomatic intracerebral hemorrhage (ICH), and in-hospital patient outcomes throughout a large urban community. DESIGN: Historical prospective cohort study conducted from July 1997 through June 1998. SETTING: Twenty-nine hospitals in the Cleveland, Ohio, metropolitan area. PATIENTS: A total of 3948 patients admitted to a study hospital with a primary diagnosis of ischemic stroke (International Classification of Diseases, Ninth Revision, Clinical Modification code 434 or 436). MAIN OUTCOME MEASURES: Rate of IV tPA use and occurrence of symptomatic ICH among patients treated with tPA; proportion of patients receiving tPA whose treatment deviated from national guidelines; in-hospital mortality among patients receiving tPA compared with that among ischemic stroke patients not receiving tPA and with mortality predicted by a model. RESULTS: Seventy patients (1.8%) admitted with ischemic stroke received IV tPA. Of those, 11 patients (15.7%; 95% confidence interval [CI], 8.1%-26.4%) had a symptomatic ICH (of which 6 were fatal) and 50% (95% CI, 37.8%-62.2%) had deviations from national treatment guidelines. In-hospital mortality was significantly higher among patients treated with tPA (15.7%) compared with patients not receiving tPA (5.1%, P<.001) and compared with the model's prediction (7.9%; P<.006). CONCLUSIONS: A small proportion of patients admitted with acute ischemic stroke in Cleveland received tPA; they experienced a high rate of ICH. Cleveland community experience with tPA for acute ischemic stroke may differ from that reported in clinical trials.

The ciliospinal reflex in pentobarbital coma.

OBJECT: This study was conducted to delineate the ciliospinal reflex (CSR), which is defined as pupillary dilation caused by a noxious stimulus to the face or head. The authors anecdotally observed that patients in a pentobarbital coma have a CSR that can mimic pathological conditions. A pentobarbital coma obscures the results of the neurological examination in patients with potentially life-threatening cerebral edema; pupil size and reactivity are the only readily monitored signs. Any condition that incorrectly suggests evolving intracranial pathological processes can lead to unnecessary clinical actions. METHODS: The authors evaluated six consecutive patients in the neurointensive care unit in whom a pentobarbital coma had been induced, documenting the presence and duration of the CSR. The CSR was always bilateral and symmetrical, manifesting as enlarged (6-8 mm), seemingly nonreactive pupils continuing from 1 to 6 minutes and was usually seen after routine nursing maneuvers. The pupils appeared nonreactive to short flashes of direct light but did react if longer flashes were used. CONCLUSIONS: Recognition of the CSR can potentially lead to reduction of unnecessary transportation and complicating medical interventions in critically neurologically ill patients in whom a pentobarbital coma has been induced.

Is in-hospital stroke mortality an accurate measure of quality of care?

We examined the validity of using in-hospital stroke mortality as predicted by the Cleveland Hospital Outcomes Indicators of Care Evaluations (CHOICE) model as a measure of quality of care. A total of 223 patients admitted to the hospital for stroke were evaluated by the CHOICE model, which predicted that 19 stroke deaths would occur. We reviewed the 19 patients with the highest predicted mortality, according to CHOICE, and three additional patients who died following stroke. We found that The CHOICE model accurately predicts in-hospital stroke mortality for large populations but not for individual patients. CHOICE and other stroke outcome models rely heavily on early Do Not Resuscitate orders and coma but exclude important variables found in the literature on stroke. No correlation between in-hospital stroke mortality and quality of care was demonstrated. Mortality prediction models used to guide consumers on where to receive stroke care are potentially misleading, as they do not assess functional neurologic recovery or the process of care that are essential elements of quality.

Thrombolytic therapy in neurointensive care.

Thrombolytic therapy has been studied in acute ischemic stroke, intracranial hemorrhage, intraventricular hemorrhage, subarachnoid hemorrhage, and sagittal sinus thrombosis. This form of therapy has an evolving role in contemporary neurologic practice, and increased investigational fervor will ensure more exacting therapeutic alternatives for stroke victims in the future.

Prediction of worsening consciousness from edema after hemispheric infarction.

We sought to develop a risk profile that would predict worsening consciousness from edema after hemispheric infarction. Charts were reviewed correlating initial computed tomography scan, neurologic examination, demographic features, and ischemic mechanism with worsening consciousness from massive edema after hemispheric infarction. An edema risk profile composed of two of three clinical factors (gaze preference, hemiplegia, or hemineglect) and evidence of acute cortical infarction on initial computed tomography scan highly correlated with the later development of worsening consciousness from edema. The edema risk profile correlated with worsening consciousness from edema after hemispheric infarction. The profile requires prospective verification before use for family counseling, for anticipatory care, and for randomizing patients in acute stroke trials aimed at controlling the formation and sequelae of edema after ischemic stroke.

Malignant cerebral edema and intracranial hypertension.

Cerebral edema and intracranial hypertension occur frequently in neurologic patients. Proper understanding of the pathophysiology of each entity allows prompt recognition and rational therapeutic goals, allowing for better neurologic outcome in many disease states. The recognition of cerebral edema as a distinct entity allows the clinician to treat focal pressure gradients in the brain separately from more diffuse intracranial pressure elevations, appreciating the benefits and pitfalls of directed therapies for each process. The treatment of many of the disorders that cause cerebral edema and intracranial hypertension is heuristic, challenging the managing physician's thorough understanding of cerebral hemodynamics and his or her ability to encounter the human aspects of determining appropriate levels of care for individual patients.

Large hemispheric infarction, deterioration, and intracranial pressure.

Neurologic deterioration from large hemispheric infarction with edema (LHIE) often leads to the use of therapies directed at decreasing intracranial pressure (ICP). Many of these ICP therapies can potentially accentuate tissue shifts from unilateral mass lesions and lead to rebound ICP elevations. We sought to determine whether ICP elevation is a common cause of deterioration from LHIE by measuring the initial ICP and cerebral perfusion pressure (CPP) in 19 patients deteriorating to stupor from LHIE within 3 hours of deterioration, after ruling out metabolic aberrations, medication side effects, infection, and seizures and prior to commencement of any ICP-lowering therapies. We evaluated 19 patients aged 23 to 77 years--14 with complete middle cerebral artery and five with complete internal carotid artery territory infarctions. Stupor began 59 +/- 37 hours after the stroke onset. ICP monitoring (12 ipsilateral Camino, five contralateral ventriculostomy, and two ipsilateral epidural) demonstrated elevation of ICP (> 15 mm Hg) in only five patients (26.3%), with group mean initial ICP = 13.4 +/- 10 mm Hg. Similarly, the initial CPP was diminished (< 55 mm Hg) in only two patients (10.5%), with group mean initial CPP = 74.9 +/- 14 mm Hg. Globally elevated ICP is not a common cause of initial neurologic deterioration from LHIE mass effect.

Automatic stepping in the pontomedullary stage of central herniation.

Both spontaneous and reflexive movements may occur during the final stages of herniation and following brain death. We describe spontaneous, rhythmic (0.2 to 0.5 Hz), alternating flexion of the hip, knee, and ankle in two patients during the pontomedullary phase of central herniation following a massive hemispheric infarct. Automatic stepping is likely a spinal automatism generated within the spinal locomotion center and regulated by both ascending and descending brainstem tracts. Clinicians and family members of neurologically devastated patients should be aware that this and other movements can occur during the late stages of central herniation preceding and following brain death.

Respiratory failure with cervicomedullary infarctions.

Respiratory failure from brainstem and spinal cord infarction has been described without attention to ventilatory characteristics and prognosis. We describe two patients who suffered from complete aventilation with cervicomedullary infarctions. One achieved full recovery of spontaneous breathing, and the other had persistent aventilation until her death 4 months after her stroke from sepsis. The anatomical extent of the infarction as identified by magnetic resonance imaging was predictive of the recoverability of spontaneous breathing, and important clinical considerations are emphasized when considering weaning a patient from mechanical ventilation after respiratory failure from cervicomedullary infarction.

An unusual case of postpartum stroke.

Intracranial hemorrhage is a rare peripartum complication. We report a 28-year-old woman, 24 h postpartum, with acute onset of aphasia, right lower facial paresis, and spastic right hemiplegia secondary to hemorrhage into a previously undiagnosed large left parasagittal meningioma. Prompt diagnosis and surgical intervention led to an excellent outcome. Intrameningiomal hemorrhage as a treatable cause of peripartum stroke is discussed.

Management of intracranial hypertension.

Intracranial hypertension is the final common denominator of morbidity and mortality for diverse neurologic problems, and its proper treatment requires the heuristic application of the available therapeutic alternatives when the clinical situation and patient's prognosis warrants treatment. The initial therapeutic focus for ICP reduction should be control of factors that may aggravate intracranial hypertension such as inappropriate head and body position, elevated body temperature, pain, noxious stimuli, elevated airway pressure, elevated blood pressure, seizures, and hypotonic intravenous fluids. The appropriate conventional therapies (e.g., hyperventilation, osmotic agents, sedatives, barbiturates, and cerebrospinal fluid removal) should be selected based on the details of each individual case. Surgical removal of intracranial mass lesions may be indicated in some circumstances, particularly for intractable intracranial hypertension and progressive, severe brain tissue shifts.

Acute intracranial lesions and respiratory sinus arrhythmia.

We studied the effects of acute intracranial lesions on the respiratory sinus arrhythmia (RSA) with the use of computerized measurements of the ratio of expiratory to inspiratory R-R intervals. The RSA was reduced below the 95th percentile for age in 20 of 27 patients, an average of 2 days after an acute event. Only four patients, without neurological deficits, had a normal RSA. Two patients, with signs of secondary brain-stem compression from a mass, had an increased RSA, without the bradycardia that is usually associated with Cushing's response. Twenty-three patients had their respiratory rate controlled by positive pressure ventilation during testing, and our preliminary findings suggested that this was not responsible for reducing the RSA. Acute intracranial lesions caused a diminished RSA, perhaps by reducing supratentorial influences on vagal cardioinhibitory activity. In contrast, once signs of secondary brain-stem compression occur, the RSA is greatly increased while the heart rate remains unchanged, offering a possible method of noninvasive monitoring for this complication.

Vasodepressor carotid sinus syncope associated with a neck mass.

We present the hemodynamic and autonomic features of recurrent purely vasodepressor syncope episodes in a patient with left-sided malignant cervical adenopathy involving the carotid sinus. Extreme hypotension lasting 10 to 30 minutes, without change in heart rate, occurred spontaneously and 20 seconds after head-turning. The baseline respiratory sinus arrhythmia, heart rate response to standing and Valsalva's maneuver, and cold-induced blood pressure elevation were normal, indicating normal baroreceptor function between episodes. The episodes abated after 1 week of bedrest but reappeared within 1 day of discharge from the hospital. Syncope no longer occurred after intracranial section of the left glossopharyngeal nerve and upper rootlets of the left vagus. Autonomic testing remained normal postoperatively. A review of the literature indicates that purely vasodepressor syncope has been more common with left carotid sinus lesions.