These guidelines have been put together to aid neurologists in the medical care of stroke patients. Many of these guidelines apply to other general care for both neurological and neurosurgical patients. These guidelines are designed for the physicians. They were developed with input from residents, stroke fellows and staff neurologists. For straightforward care, these guidelines are designed to allow the neurologist and neurology residents to manage the care of stroke patients on the stroke unit. For complicated cases, consultation with a specialist still applies. These guidelines are also designed to rationalize drug use on the Stroke Unit and to make the maximum use of a limited pharmacy budget. Please follow these guidelines for all initial care. Table of Contents
1. Hypertension 2. Hyperglycemia 3. Temperature 4. Antiplatelet therapy 5. Statins 6. Antibiotics for pneumonia, UTI 7. Heparin use 8. DVT prevention 9. Triage of Stroke 10. Triage of TIA
Michael D. Hill, Director, Stroke Unit Guidelines for the Treatment of Hypertension in Acute Stroke
BACKGROUND The treatment of hypertension in the acute stroke setting is uncertain. Pre-clinical research suggests that acutely lowering the blood pressure may result in recruitment of penumbral tissues and infarct extension. ACUTE TREATMENT The current recommendations for ACUTE TREATMENT (first 48h) are: 1) Treat if: SBP > 200 or DBP >130 (AHA guideline) on 2 readings 15 minutes apart 2) Use an agent that works slowly and gently such as an ACE inhibitor or ACE receptor blocker
or a mixed adrenergic blocker such as labetalol. a) Begin enalapril 2.5 mg bid and rapidly titrate up at each dose time to max of 20mg bid. b) Begin atenolol 25mg daily and rapid titrate (each dosing interval) up to 100 mg daily. c) Begin hydrochlorothiazide 12.5mg taken in the morning.
3) AVOID the use of short-acting dihydropyridine calcium channel blockers (eg. nicardipine,
4) Nitrates (eg. NTG patch, nitroprusside) should be used cautiously because they increase ICP,
nitric oxide may be neurotoxic in the ischemic setting. Nitrates alter local cerebral perfusion.
GENERAL PRINCIPLES of ACUTE TREATMENT 5) Acutely, aim to bring the BP down no more than 25% from the baseline value over 24 hours. 6) Be conservative with treatment. A majority of patients will have a natural fall in their BP
7) Be CAREFUL with patients who have tight carotid or vertebrobasilar stenosis or fluctuating
lacunar disease. They may require a higher blood pressure. Ensure that you image your patients to determine the MECHANISM of stroke so that rationale management follows.
8) Treatment of ICH and elevated BP follows the same protocol. Evidence from PET and MRI
literature suggests that there is only a minimal chance to recruit penumbral tissues around the hematoma.
9) Labetalol can be used as a bolus IV medication to bring the BP down rapidly and safely.
Give labetalol in 10mg IV boluses q5-10min to treat to target. Labetalol should only be used in the ER, U112 or ICU. Optimally, labetalol may be used for initial blood pressure control and rapid transition to the oral medication should be made. **Labetalol is contraindicated among patients with bronchospasm and it may precipitate mild congestive heart failure.
CHRONIC TREATMENT (after the first week): 10) Aim for a target BP 135/85 or less on average.
a) The choice of drug(s) is less important than reaching target b) When choice of drug is possible, a thiazide diuretic and an ACE inhibitor should be the
Michael D. Hill, Director, Stroke Unit
c) A majority of patients will require dual or triple therapy. Recent evidence suggests that
dual or triple therapy at lower doses are better tolerated by most patients.
d) After beginning ACEi, please check or arrange to have checked a serum creatinine and
serum K+ to ensure that the ACEi is not precipitating prerenal azotemia.
e) Consider the cause of hypertension. A hypertension clinic is available for outpatient
Note: recall that HCTZ and chlorthalidone are sulfa drugs and may precipitate allergic skin reactions in patients allergic to sulfa based antibiotics.Michael D. Hill, Director, Stroke Unit Guidelines for the Treatment of Hyperglycemia in Acute Stroke
1. Hyperglycemia worsens experimental stroke. 2. Patients who are diabetic or who have elevated blood sugars have a poorer prognosis. 3. Patients with hyperglycemia have a significantly higher risk of ICH after thrombolytic
4. Check finger-stick glucose level at admission to stroke unit on all patients. Thereafter,
check glucose at admission only on patients who were hyperglycemic (>8mM) at baseline. Frequency of glucose assessments should be determined by attending neurologists.
RECOMMENDATION 1) Treat blood glucose > 8mM to maintain normoglycemia (target 4-8mM).
a) Use humulin-R initially as a single dose initially b) If BS remains elevated (>8mM), then a sliding scale is appropriate.
2) Use sliding scale insulin iv if necessary. Sliding scales are available in OSCAR. Intravenous
treatment is preferred over sc sliding scale because of better efficacy in achieving target glucose levels.
Sliding Scale SC Humulin R Target glucose 4-8mM; Glucose checks q4h. Glucose < 8mM
Sliding Scale IV Humulin R Target glucose 4-8mM; Glucose checks q2h. Glucose checks q1h if IV infusion rate has been changed. Otherwise glucose checks q2h. Begin IV infusion of D5W at 50 cc/hr [This is the only standard situation where IV fluids should include glucose] Begin infusion at 2 units/h Glucose < 3mM and patient shows signs of symptomatic hypoglycemia
Stop infusion. Give 25cc of D50. Restart infusion at rate reduced by 1 unit/h only when glucose > 5.0.
Give 8units humulin R and increase infusion rate 1 unit/h
Michael D. Hill, Director, Stroke Unit
GENERAL PRINCIPLES 3) Like hypertension, stress related hyperglycemia will resolve naturally within 24h after stroke
4) Administer fluids without glucose to patients with acute stroke. Use NS rather than D5W
CHRONIC TREATMENT 5) Chronic treatment of type II diabetes involves primarily OUTPATIENT management –
a) Diet. Have dietician assess the diet. b) Weight loss, particularly of the abdominal fat pad. The waist hip ratio is an important
predictor of type II diabetes and type II diabetic control.
1. Metformin (Glucophage™) – can be prescribed up to 2 g per day. Usually taken
500mg tid ac meals. Note: it has rarely been associated with lactic acidosis and is excreted by the kidney. When iodinated intravenous contrast dye causes mild impairment of renal function, metformin may accumulate in the body and cause lactic acidosis. Hold metformin x 48h post-procedure where X-ray contrast has been used. Avoid metformin in patients with renal failure.
2. Glyburide (Diabeta™) – is a sulfonurea. It is usually prescribed up to 5mg bid.
Glyburide and metformin form the staple of oral hypoglycaemic agents for type II diabetes.
3. Glicliazide is a sulfonurea like glyburide 4. Acarbose is an α-secretase inhibitor which reduces intestinal absorption of sugars. It
has mild hypoglycaemic effectiveness. It is the only oral hypoglycaemic which has been shown to reduce macrovascular complications of diabetes.
5. Rosiglitazone is a thiazolidinediones. The act by increasing insulin sensitivity at the
These latter drugs (acarbose, rosiglitazone) can be continued from prior outpatient management but ought to be prescribed under the direction of an internist or endocrinologist. **Recall that sulfonureas may precipitate hypoglycaemia, particularly in renal failure due to impaired excretion. Metformin may be associated with lactic acidosis, particularly in patients with renal failure.
Michael D. Hill, Director, Stroke Unit Guidelines for the Treatment of Elevated Temperature in Acute Stroke
BACKGROUND 1. Patients with elevated temperature are more likely to have a poor outcome 2. Hypothermia is a strong neuroprotectant in animal models.
POLICY 1. Treat all patients with temperature > 38.0 C with acetaminophen 650 mg q4h
regularly scheduled to reduce temperature.
2. Use cooling measures – fans, cooling blankets etc. 3. Use passive cooling – no blankets - on all patients in the first 48h 4. Avoid allowing the patient to get so cold that shivering ensues 5. MOST IMPORTANTLY – INVESTIGATE THE CAUSE OF FEVER
Michael D. Hill, Director, Stroke Unit Guidelines for the use of Aggrenox, Clopidogrel (Plavix) and Antiplatelet therapy
BACKGROUND 1. ASA 81mg is the standard of care. There is NO EVIDENCE to support using a higher dose
a. ASA 325mg should be used for the first 6 months after carotid endarterectomy b. ASA 325mg should be used for patients with lone atrial fibrillation who do not
require coumadin. [NB – this precludes any patient admitted to the stroke unit since by definition they will have suffered a TIA or stroke and therefore require coumadin]
2. Clopidogrel is a thienopyridine which has antiplatelet effect similar to ASA. It is NOT
clearly better as monotherapy for stroke patients than ASA alone. It may be most useful in patients with peripheral vascular disaease.
3. Clopidogrel is appropriate in the ASA intolerant patient. 4. Clopidogrel 75mg daily + ASA 81mg daily is increasingly used based upon the positive
results of the CURE trial for unstable coronary syndromes. Therefore use clopidogrel in addition to ASA when:
a. Use clopidogrel + ASA ONLY when proximal large vessel disease has been proven
(eg. Carotid stenosis or vertebral artery stenosis). If proximal large vessel disease has been excluded as a cause of stroke, discontinue the clopidogrel.
b. If a decision is made to use clopidogrel in a clopidogrel naïve patient, load the patient
with 300mg one-time dose then 75mg daily
c. If ASA is being given to an ASA naïve patient, give 160mg one-time loading dose d. Because of the results of an increased risk of intracranial hemorrhage with ASA and
clopidogrel in the MATCH trial, we do not use double anti-platelet therapy for lacunar stroke.
5. Ticlopidine (ticlid) is no longer prescribed because of hematologic toxicity. 6. Aggrenox (ASA + dipyridamole slow release) may or may not be better than ASA alone.
One trial suggests that it is superior, a meta-analysis suggests that there is no additional benefit to dipyridamole over ASA. Aggrenox is an acceptable alternative to ASA or clopidogrel.
ASA FAILURES – Recurrent event while on ASA 7. Do not increase the ASA dose 8. You may choose to add clopidogrel or change to Aggrenox 9. The most important thing to do is to reassess the mechanism of stroke (rule out atrial
fibrillation, carotid stenosis) and to aggressively treat hypertension. Treatment of hypertension has a far larger magnitude of effect than switching antiplatelet therapy.
Michael D. Hill, Director, Stroke Unit Guidelines for the use of statins
BACKGROUND Simvastatin was shown in the Heart Protection Study to reduce the five-year risk of stroke among patients with previous stroke or TIA at any time in the past. It was given as 40mg qhs without regard for the lipid profile. The effect of simvastatin on stroke reduction was independent of the baseline LDL-C level. Based upon meta-analysis of cardiac trials, pravastatin has also been shown to prevent stroke. Atorvastatin is currently in a long term secondary prevention trial and data should be known in the next two years.
1. Simvastatin 20mg shall be starting dose of the statin of choice in the stroke unit. If
tolerated, the dose will be increased to 40mg daily in the stroke follow-up clinic. For simplicity for the patient, patients who were already on a statin at the time of admission should stay on their previous statin.
2. Measure ALT, ALP and CK at baseline on all patients starting a statin. Counsel about
the small risk of liver and muscle toxicity including myalgias without CK rise. Explain the symptoms. Remeasure enzymes only if symptoms arise.
Michael D. Hill, Director, Stroke Unit Guidelines for Antibiotic Use on the Stroke Unit
Principle: Use simple protocols because most stroke-related pneumonias are caused by common, antibiotic-sensitive drugs. Exceptions will arise, particularly among patients who have been intubated. Begin with these empiric regimens and change according to culture results and clinical progress.
1) Aspiration pneumonia / nosocomial pneumonia • Cefazolin 1g IV q8h and metronidazole 500mg IV q8h intravenously
• Switch to oral medication after 48h afebrile for 7-10d complete course • AVOID use of cefuroxime as it is a potent inducer of VRE
• Culture the sputum, blood so that treatment may be adjusted appropriately when the culture
2) UTI / nosocomial UTI • Amoxicillin 500mg po tid for 5-7 days • AVOID unnecessary use of quinolones (ciprofloxacin, norfloxacin)
• Most UTIs are caused by gram negative bacteria (e.coli, klebsiella pneumoniae, citrobacter
freundii etc.) sensitive to amoxicillin or enterococcus faecalis which is also sensitive to amoxicillin
• Prevent UTI by removing the foley catheter as soon as possible. • Do not treat asymptomatic bacteruria which is common in older women
• Culture the urine so that treatment may be adjusted appropriately when the culture results are
Note: Among patients allergic to penicillins, cross-reactivity to cephalosporins can occur but is uncommon. An alternative choice for amoxicillin for UTI is sulfamethoxazole-trimethoprim (septra) 1 DS tab bid. Michael D. Hill, Director, Stroke Unit Guidelines for the Prophylaxis of DVT/PE in Acute Stroke
BACKGROUND Deep venous thrombosis (DVT) and pulmonary embolus (PE) are manifestations of the same disease, and are important causes of morbidity and mortality among stroke patients. Prevention of DVT/PE is an important way to improve outcome after stroke. The rate of clinically evident DVT/PE on the stroke unit over 2 years in less than 2%.
Prophylactic Treatment 1. Consider all patients who are confined to bed or chair, or have a hemiparetic leg as candidates for DVT/PE prophylaxis. 2. Heparin 5000U sc bid is an effective measure to reduce DVT. However, it does increase the risk of hemorrhage very slightly. 3. ASA also has a small effect in preventing DVT. 4. Intermittent pneumatic compression stockings are an effective measure for DVT prophylaxis - but they must be on the patient to be effective. IPC stockings probably have an additive effect with low-dose sc heparin. 5. Among patient with ICH, it is safe to commence sc heparin after 48-72h where the patient is
6. Low-molecular weight heparins are also available for use and among hip-fracture patients
result in lower bleeding rates. It remains unclear if LMWH is superior to regular heparin or IPC stockings in stroke patients.
POLICY Standard protocol will be to use: early mobilization, unfractionated heparin 5000U sc BID AND/OR IPC stockings. The emphasis should be on all patients being mobilized as early as possible.
Page 10 Version: 8 September 2005 Michael D. Hill, Director, Stroke Unit Guidelines for the Use of Intravenous Heparin in Acute Stroke
BACKGROUND Despite much past use, there is considerable randomized trial evidence, supported by meta- analysis from the Cochrane collaboration that heparin use results in more ischemic stroke patients dead or dependent than no use at all. In short, heparin is dangerous and should be discouraged from general use. In selected circumstances, intravenous heparin according to the stroke heparin protocol may be useful as an off-label treatment. As a principle of use, heparin should only be used when the mechanism of stroke is known. Therefore, heparin should be used with knowledge of the vascular anatomy and location of thrombus. This information can now be very rapidly acquired non-invasively and acutely with CT or MR angiography. Demonstrated (imaging-proven) intraluminal thrombus is a common reason for using heparin. In one post-hoc analysis, heparin was found to useful for large artery (ie. Carotid stenosis) stroke. POLICY 1. Do not use heparin for stroke as a general rule. 2. There is no evidence that heparin is useful for lacunar stroke or “fluctuating stroke” due to
3. There is no evidence that heparin is useful for arterial dissection. 4. There is no evidence that patients with atrial fibrillation should be immediately treated with
heparin prior to coumadin. In one randomized trial of LMWH vs. placebo for patients with storke due to proven atrial fibriilation, there was no difference in recurrent stroke in the first 2 weeks between those treated with heparin and those who were not treated. Such patients may be started on coumadin directly.
5. Use of heparin should be highly selective and based upon image-proven pathophysiology.
• Fluctuating or unstable symptoms due to proven carotid artery
• Fluctuating or unstable symptoms due to basilar artery atherosclerotic disease
6. All use of full anticoagulation should be undertaken cautiously among patients with large
volume ischemic stroke. Large volume stroke is associated with a greater risk of hemorrhage when patients are anticoagulated.
Page 11 Version: 8 September 2005 Michael D. Hill, Director, Stroke Unit Guidelines for the Triage of STROKE Acute Stroke – Stroke Team to See Urgently – Pager 0379
• Ischemic stroke < 12h from symptom onset
• Ischemic stroke – wake up with deficits, any disabling deficit
o Disabling deficit = (a) loss of antigravity strength; (b) cannot walk; (c) cannot see;
(d) cannot speak or understand speech; (d) decreased LOC
• Intracerebral hemorrhage (spontaneous/non-traumatic) • Venous sinus thrombosis
• Applies to all of Calgary Health Region. Acute stroke team to work in co-ordination with
• For Southern Alberta, pass call on to the Acute Stroke Team (page 0379)
Stroke Service and Stroke Unit
• Stroke (ischemic and ICH and venous sinus thrombosis) from unit 112 and from ER or
o PROCESS ISSUES ARE IMPORTANT o Please transfer patients rapidly from U112 or U111 to stroke unit 100 o When there is no room on U100, patients can be admitted to U111 or U112 as
o Please see Guidelines for Admission to U100 o Please do not admit non-stroke patients to the Stroke Service; admit to General
Page 12 Version: 8 September 2005 Michael D. Hill, Director, Stroke Unit Admission Criteria - Stroke Unit 100 (updated Jan 15, 2002) Criteria for Admission Patients will be admitted from the ER, from Unit 112 and uncommonly from other wards. Inclusion Criteria A. Patients with a diagnosis of acute ischemic stroke (AIS), intracerebral hemorrhage (ICH), or
transient ischemic attack (TIA) or venous sinus thrombosis.
B. Patients with stable clinical status who do not require telemetry, blood pressure monitoring,
C. AIS patients who are >24h post-thrombolysis and have a stable clinical status. D. Patients with a reasonable potential to benefit from stroke unit care; patients who have
E. Patients must be admitted under the care of the Stroke Service Neurologist to occupy a bed in
F. All patients will have a Stroke Team consult at the discretion of the attending Stroke Service
Exclusion Criteria A. Patients with subarachnoid hemorrhage, epidural hemorrahge or subdural hemorrhage as the
B. Patients who are palliative due to the severity of stroke. C. Patients who are likely not to benefit from stroke unit care and are poor candidates for
rehabilitation; patients who will require long-term care from the outset.
D. Patients who require an isolation room. (eg. MRSA positive). E. Patients who require a WanderGuard™ device. Patients who do NOT have a stroke.
Page 13 Version: 8 September 2005 Michael D. Hill, Director, Stroke Unit Guidelines for the Triage of TIA
Background The risk of stroke after incident TIA is approximately 10% within the first 90d. Half of this risk is realized in the first 48h after TIA. Risk factors for early recurrence include age, motor or speech symptoms, diabetes and duration of symptom. Triage Rules ADMIT PATIENT. Patients with symptoms in the past 24h of a - -hemispheric TIA (speech or clear motor deficit) -transient monocular blindness/amaurosis fugax (lower risk but high probability of ICA stenosis). Refer directly to the TIA Reference unit by calling the Stroke Team Pager (0379). CLINIC PATIENT. Patients with isolated sensory deficits, vertigo or dizziness only and you believe the symptoms to be ischemic in nature, may be safely referred to the Stroke Clinic by fax - 944-1154. See attached form below. Page 14 Version: 8 September 2005 Michael D. Hill, Director, Stroke Unit TIA Referral Form Source of Referral: Patient Name: __________ Phone #: ( ) -
Referring Physician: __________ Circle All that Apply:
• Call stroke pager #0379 if: one red AND both blue criteria are met.
• Otherwise: Fax form and Emergency Record to SPC @ 944-1154
• If there are no contraindications, give all patients ASA 160mg to chew.
Referrals will not be accepted without completed form.
DAVID L. PEARLE, M.D. DAVID L. PEARLE, M.D. PERSONAL INFORMATION HOME ADDRESS: (202) 444-8833 / (877) 303-1461 Facsimile EDUCATION 1964 M.D., Harvard Medical School, Boston, Massachusetts TRAINING/ PROFESSIONAL POSITIONS 1968-1969 Internship in Medicine, New York Hospital Residency in Medicine, New York Hospital Commissioned Officer, Public Health Servic
ABSTRACT. Margaret Gilbert explores the phenomenon referred to in everyday ascrip-tions of beliefs to groups. She refers to this type of phenomenon as “collective belief” andcalls the types of groups that are the bearers of such beliefs “plural subjects”. I argue thatthe attitudes that groups adopt that Gilbert refers to as “collective beliefs” are not a speciesof belief in an import