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Monitoring of vasospasm in stroke using transcranial doppler ultrasonography
Abstracts
152 dyspnea. PE was associated with deep venous thrombosis (DVT) in 11 patients. In all patients, the DVT was located in a paralyzed leg. None of the 30 patients received DVT prophylaxis. We conclude that PE defies ante mortem diagnosis in half of the patients and may significantly contribute to early (<3 weeks) mortality. Clinical evidence of DVT was present in one third of the patients and invariably in the paralyzed leg. Physician practices of DVT prophylaxis in acute stroke were insufficient in the series. Neurologists should routinely examine the calves of patients immobilized after a stroke, especially the paralyzed leg, and strongly consider DVT prophylaxis.
Thermoregulatory Vasoconstriction and Shivering Impede Therapeutic Hypothermia Following Acute Ischemic Stroke. Richard M. Zweifler, Daniel I. Sessler (University of South Alabama Stroke Center, Mobile, AL and UCSF, San Francisco, CA) Numerous studies have indicated that only 2 to 3°C hypothermia provides substantial protection against focal and global cerebral ischemia. Induction of therapeutic hypothermia requires overcoming effective thermoregulatory protective responses including vasoconstriction and shivering. We tested the hypothesis that vasoconstriction and shivering thresholds are sufficiently reduced by acute stroke to permit induction of therapeutic hypothermia without additional pharmacological inhibition of thermoregulatory control. Methods: We studied 8 patients 2 + 1 days following ischemic stroke. Forced-air cutaneous cooling was administered until the patients shivered continuously or reached a tympanic membrane (i.e., core) temperature of 34°C. The tympanic membrane temperatures triggering vasoconstriction and shivering identified the thresholds for each response. Results: Patients had a mean age of 68+8 years and a mean National Institutes of Health Stroke Scale (NIHSS) score of 5. No patient reached the target core temperature of 34°C. Vasoconstriction and shivering thresholds were 37.1 + 0.4 and 36.6 + 0.4°C, respectively. Conclusions: Vasoconstriction and shivering were initiated at roughly normal temperatures in ischemic stroke patients and these thermoregulatory responses prevented induction of therapeutic hypothermia. Pharmacological reduction of the vasoconstriction and shivering thresholds therefore will be required if therapeutic hypothermia for stroke patients is to be easily induced by surface cooling.
Implementation of a Stroke Code System: Diagnostic and Therapeutic Yield. Richard M. Zweifler, Renay Drinkard, Sarah Cunningham, Mark BrodF and John E
Rothrock (University of South Alabama Stroke Center, Mobile,
AL) Interventional therapy for patients with acute ischemic stroke requires implementation of a system which facilitates rapid triage and diagnostic evaluation. We initiated a 24 hour/7 day per week "stroke code system" at the University of South Alabama Hospitals and prospectively collected data from the first 100 patients whose clinical presentations triggered this system. Seventy-eight (78%) were found to have acute ischemic stroke. Of the remaining 22, 9 (9%) had evidence of intracerebral hemorrhage. The most common non-stroke diagnosis was seizure (n = 5); one patient had a previously undiagnosed meningioma which was incidental to her acute stroke. Fortyeight of the 87 stroke patients (55%) presented within 6 hours of stroke onset (40/78 = 51% of the ischemic stroke patients). Thirty-one patients (31% of the group overall; 40% of the ischemic stroke patients) were eligible for acute therapy. Twenty-five of these eligible patients were entered into a treatment study, 4 declined participation, and the other 2 were treated for open-label t-PA. Conclusion: Implementation of a stroke code system may result in a high yield of patients with acute stroke and relatively few "stroke mirnickers." A significant proportion of all cases generated will be eligible for acute treatment, but the majority will not.
Monitoring of Vasospasm in Stroke Using Transcranial Doppler Ultrasonography. Nancy Newcommon (Foothills Hospital, Calgany, Alberta, Canada) Spasm of the intracranial vessels following subarachnoid hemorrhage was initially observed using the invasive angiogram technique. Vasospasm subsequently has been identified as a major cause of stroke and death during the post hemorrhage period. With the introduction of Transcranial Doppler Ultrasonography (TCD), the diagnosis of vasospasm can be confirmed noninvasively in the clinical setting. TCD offers a technique to identify patients who are in danger of developing deficits from vasospasm, as well as the potential to monitor treatment therapy. This paper/poster proposes to: 1. Review the basic principles of TCD monitoring. 2. Identify the accuracy or correlation between anglogram and TCD results in subarachnoid hemorrhage. 3. Introduce guidelines for nurses at the bedside monitoring vasospasm using the TCD technique.
Measurement of the Free Radical-Derived Isoprostane, 8-EPI Prostaglandin F2x, in Acute Stroke. Norman Delanty, Daniel MacGowan, Muredach Reilly, John Lawson, and Garret FitzGerald (Department of Neurology,
152 dyspnea. PE was associated with deep venous thrombosis (DVT) in 11 patients. In all patients, the DVT was located in a paralyzed leg. None of the 30 patients received DVT prophylaxis. We conclude that PE defies ante mortem diagnosis in half of the patients and may significantly contribute to early (<3 weeks) mortality. Clinical evidence of DVT was present in one third of the patients and invariably in the paralyzed leg. Physician practices of DVT prophylaxis in acute stroke were insufficient in the series. Neurologists should routinely examine the calves of patients immobilized after a stroke, especially the paralyzed leg, and strongly consider DVT prophylaxis.
Thermoregulatory Vasoconstriction and Shivering Impede Therapeutic Hypothermia Following Acute Ischemic Stroke. Richard M. Zweifler, Daniel I. Sessler (University of South Alabama Stroke Center, Mobile, AL and UCSF, San Francisco, CA) Numerous studies have indicated that only 2 to 3°C hypothermia provides substantial protection against focal and global cerebral ischemia. Induction of therapeutic hypothermia requires overcoming effective thermoregulatory protective responses including vasoconstriction and shivering. We tested the hypothesis that vasoconstriction and shivering thresholds are sufficiently reduced by acute stroke to permit induction of therapeutic hypothermia without additional pharmacological inhibition of thermoregulatory control. Methods: We studied 8 patients 2 + 1 days following ischemic stroke. Forced-air cutaneous cooling was administered until the patients shivered continuously or reached a tympanic membrane (i.e., core) temperature of 34°C. The tympanic membrane temperatures triggering vasoconstriction and shivering identified the thresholds for each response. Results: Patients had a mean age of 68+8 years and a mean National Institutes of Health Stroke Scale (NIHSS) score of 5. No patient reached the target core temperature of 34°C. Vasoconstriction and shivering thresholds were 37.1 + 0.4 and 36.6 + 0.4°C, respectively. Conclusions: Vasoconstriction and shivering were initiated at roughly normal temperatures in ischemic stroke patients and these thermoregulatory responses prevented induction of therapeutic hypothermia. Pharmacological reduction of the vasoconstriction and shivering thresholds therefore will be required if therapeutic hypothermia for stroke patients is to be easily induced by surface cooling.
Implementation of a Stroke Code System: Diagnostic and Therapeutic Yield. Richard M. Zweifler, Renay Drinkard, Sarah Cunningham, Mark BrodF and John E
Rothrock (University of South Alabama Stroke Center, Mobile,
AL) Interventional therapy for patients with acute ischemic stroke requires implementation of a system which facilitates rapid triage and diagnostic evaluation. We initiated a 24 hour/7 day per week "stroke code system" at the University of South Alabama Hospitals and prospectively collected data from the first 100 patients whose clinical presentations triggered this system. Seventy-eight (78%) were found to have acute ischemic stroke. Of the remaining 22, 9 (9%) had evidence of intracerebral hemorrhage. The most common non-stroke diagnosis was seizure (n = 5); one patient had a previously undiagnosed meningioma which was incidental to her acute stroke. Fortyeight of the 87 stroke patients (55%) presented within 6 hours of stroke onset (40/78 = 51% of the ischemic stroke patients). Thirty-one patients (31% of the group overall; 40% of the ischemic stroke patients) were eligible for acute therapy. Twenty-five of these eligible patients were entered into a treatment study, 4 declined participation, and the other 2 were treated for open-label t-PA. Conclusion: Implementation of a stroke code system may result in a high yield of patients with acute stroke and relatively few "stroke mirnickers." A significant proportion of all cases generated will be eligible for acute treatment, but the majority will not.
Monitoring of Vasospasm in Stroke Using Transcranial Doppler Ultrasonography. Nancy Newcommon (Foothills Hospital, Calgany, Alberta, Canada) Spasm of the intracranial vessels following subarachnoid hemorrhage was initially observed using the invasive angiogram technique. Vasospasm subsequently has been identified as a major cause of stroke and death during the post hemorrhage period. With the introduction of Transcranial Doppler Ultrasonography (TCD), the diagnosis of vasospasm can be confirmed noninvasively in the clinical setting. TCD offers a technique to identify patients who are in danger of developing deficits from vasospasm, as well as the potential to monitor treatment therapy. This paper/poster proposes to: 1. Review the basic principles of TCD monitoring. 2. Identify the accuracy or correlation between anglogram and TCD results in subarachnoid hemorrhage. 3. Introduce guidelines for nurses at the bedside monitoring vasospasm using the TCD technique.
Measurement of the Free Radical-Derived Isoprostane, 8-EPI Prostaglandin F2x, in Acute Stroke. Norman Delanty, Daniel MacGowan, Muredach Reilly, John Lawson, and Garret FitzGerald (Department of Neurology,