Stroke presentation-Dr Mustapha.ppt

An update on the medical management of Acute Stroke Adekunle F Mustapha MB;BS(Ibadan),FMCP(Neurolo gy) MSc(Limoges France)  Stroke Objectives Review etiology of strokes Identify likely location/type of stroke based on physical exam Acute manageme...

An update on the medical management of Acute Stroke Adekunle F Mustapha MB;BS(Ibadan),FMCP(Neurolo gy) MSc(Limoges France)  Stroke Objectives Review etiology of strokes Identify likely location/type of stroke based on physical exam Acute management of ischemic stroke Acute management of hemorrhagic stroke  Stroke Fast Facts Affects ~ 800, 000 people per year Leading cause of disability, cognitive impairment, and death in the United States Accounts for 1.7% of national health expenditures. Estimated U.S. cost for 2012 = $71.5 billion – Mostly hospital (esp. LOS) & post stroke costs – Appropriate use of IV t-PA s long-term cost – Appropriate billing for AIS w/ thrombolysis ( hospital reimbursement from $5k to $11.5k) Stroke. 2013;44:2361-2375  Introductn: Brain Attack / Stroke Acute neuro-vascular syndrome 666 (revelation 13/18) (1 in 6 individual; 6 patients develop stroke q 1 min q6s 1 death recorded in its favor; 6M death worldwide) A significant economic, social, and medical problem. A Second leading cause of preventable death and disability in adults worldwide. Preventable: but preventive efforts are still far from optimal. Treatable: evidence-based Rx available, but not fully used in any region, especially low resource areas A major public health issue : international collaboration and activities are required. 4  Where We’re Headed By 2030 ~ 4% of the US population over the age of 18 is projected to have had a stroke Between 2012 and 2030, total direct stroke-related medical costs are expected to increase from $71.55 billion to $183.13 billion Total annual costs of stroke are projected to increase to $240.67 billion by 2030, an increase of 129%Stroke. 2013;44:2361-2375  What is stroke? Historical remarks: Hippocrates (460 – 370BC) “first description of phenomenon of sudden paralysis” Greek word “Apoplexy” (b/c sudden and meaning “struck by violence”), a way of dying, spiritual attacks Witch theory / Step-mum theory / Wicked Mother in law offended the gods /godesses (unable to speak, move part of the body; “Agbero”; “Ofa” “Ota”, “Ita”) 6  Definition WHO: 1970 Cerebral dysfn of vascular origin lasting >24 hrs or leading to death. S.A. H / C. I / I.C.H T.I.A./B.Tumors/Subdural hematomao T. I. A. (Transient Ischemic Attack) R. I. N. D. >24hrs < 3/52 (Rev. Isch. N. Def) CITS (Cerebral Infarction wth Transient signs ) Completed stroke  >3/52 07/12/24 7 3 types of stroke  Definition – new concept 2002 24 hrs time based: confusing; misleading; outdated Old definition does not suggest medical emergency (Brain attack). Not corroborate the mantra “time’s neurone” (cf Time’s muscle by cardiologist) Does not take into cognizance the use of thrombolytics within 270 mins (4 ½ hrs) in CI or Recombinant activated factor VII within 4 hours in ICH TIA not benign TIA and stroke = One hour Most (90%) TIA lasts 10 mins; resolve in 30 mins. If symptoms last > I hr; chances 07/12/24 of resolution:15% 9  TIA / Stroke – proposed defn 2009 Tissue – based / Time – based definition TIA: No objective evidence of acute infarction in the affected region of brain or retina; < I hour Stroke : objective evidence of infarction irrespective of duration of clinical symptoms. (cf Angina pectoris vs Myocardial infarction ) CT/MRI necessary to increase diagnostic accuracy CITS 07/12/24 = RIND. 10  Deficiencies need for Updated Defn The WHO’s definition of stroke is obsolete. Based on advanced modern brain imaging, the 24-hour inclusion criterion for CI is inaccurate and misleading, b/c permanent injury can occur much sooner. Global cerebral dysfunction is seldom caused by CVD. Common defn important in epidemiological studies and Rxic trials. Comparing and contrasting studies in which different definitions are used for inclusion of cases or ascertainment of outcomes is difficult. The advent of thrombolysis and other hyperacute Rx have added to the need to redefine stroke and TIA, because many current guidelines differentiate treatment strategies for these 2 entities.  Updating Definition of  Stroke Advances in basic science, neuropathology, neuroimaging and technology improved the understanding of ischemia, infarction, hemorrhage in CNS. “stroke” is not consistently defined in clinical practice, in clinical research, or in assessments of the public health and public policy including surveillance and reporting, national and international statistics, disease classification coding systems, and existing health surveys. Another concern for stroke surveillance is the inclusion of spinal and retinal arterial infarctions within the definition of stroke. For global reporting of the public health impact of stroke, symptomatic CNS infarction and symptomatic hemorrhage should be recorded and, where available, silent subgroups recorded. Having separate recording of these subgroups would allow for more valid analysis of temporal and geographic trends in the surveillance of stroke. Universal definition and reclassification of stroke cases are mandatory for incidence, prevalence, mortality, prognosis.  JULY 2013:universal defn of stroke Stroke Council: AHA/ASA Expert Consensus Document An Updated Definition of Stroke for the 21st Century A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Ralph L. Sacco, MD, MS, FAHA, FAAN, Co-Chair*; Scott E. Kasner, MD, MSCE, FAHA, FAAN, Co-Chair*; Joseph P. Broderick, MD, FAHA; Louis R. Caplan, MD; J.J. (Buddy) Connors, MD; Antonio Culebras, MD, FAHA, FAAN; Mitchell S.V. Elkind, MD, MS, FAHA, FAAN; Mary G. George, MD, MSPH, FAHA†; Allen D. Hamdan, MD; Randall T. Higashida, MD; Brian L. Hoh, MD, FAHA; L. Scott Janis, PhD‡; Carlos S. Kase, MD; Dawn O. Kleindorfer, MD, FAHA; Jin-Moo Lee, MD, PhD; Michael E. Moseley, PhD; Eric D. Peterson, MD, MPH, FAHA; Tanya N. Turan, MD, MS, FAHA; Amy L. Valderrama, PhD, RN†; Harry V. Vinters, MD on behalf of the American Heart Association Stroke Council, Council on Cardiovascular Surgery and Anesthesia, Council on Cardiovascular Radiology and Intervention, Council on Cardiovascular and Stroke Nursing, Council on Epidemiology and Prevention, Council on Peripheral Vascular Disease, and Council on Nutrition, Physical Activity and Metabolism New definition incorporates clinical and tissue criteria CNS infarction: clinical spectrum: SUBTYPES of CI Ischemic stroke: CNS infarction + overt sym Silent infarction: no known symptoms.  CNS infarction Brain, spinal cord, or retinal cell death attributable to ischemia, based on pathological, imaging, or other objective evidence of cerebral, spinal cord, or retinal focal ischemic injury in a defined vascular distribution; OR Clinical evidence of cerebral, spinal cord, or retinal focal ischemic injury based on symptoms persisting ≥24 h or until death, and other etiologies excluded. Silent CNS infarction: Imaging or neuropathological evidence of CNS infarction, without a history of acute neurological dysfunction attributable to the lesion. Captures infarcts discovered incidentally, when autopsy/imagn study is performed outside of a setting consistent with CI. TIA: focal arterial ischemia with transient symptoms (lasting 95% in the first 5 days after SAH and 99.7% overall.  SAH Although SAH may be caused by trauma, only spontaneous nontraumatic SAH is considered under the defn of stroke. Nontraumatic SAH: cerebral aneurysm rupture, AV malformation, intracranial artery dissections, mycotic aneurysms, bleeding disorders, substance abuse, reversible cerebral vasoconstriction syndrome, vasculitis, moyamoya, and cerebral amyloid angiopathy. Nontraumatic SAH rarely occurs without any of the previously mentioned causes. Subtype: Perimesencephalic SAH is a type of SAH with a characteristic pattern of blood collected only in the pretruncal cisterns, the absence of an identifiable aneurysm, and associated with a benign prognosis and natural history}.  Three Stroke Types Ischemic Intracerebral Subarachnoid Stroke Hemorrhage Hemorrhage Clot occluding Bleeding Bleeding around artery into brain brain 85% 10% 5% www.acponline.org/about_acp/ chapters/ok/gordon.ppt http://www.phillystroke.org/ content/learn_about_stroke/ act_fast.asp  NIHSS NIHSS (National Institute of Health Stroke Scale) – Standardized method used by health care professionals to measure the level of impairment caused by a stroke – Purpose Main use is as a clinical assessment tool to determine whether the degree of disability is severe enough to warrant the use of tPA Another important use of the NIHSS is in research, where it allows for the objective comparison of efficacy across different stroke treatments and rehabilitation interventions – Scores are totaled to determine level of severity – Can also serve as a tool to determine if a change in exam has occurred  Breaking Down the Scale 13 item scoring system, 7 minute exam Integrates neurologic exam components CN (visual), motor, sensory, cerebellar, inattention, language, LOC Maximum score is 42, signifying severe stroke Minimum score is 0, a normal exam Scores greater than 15-20 are more severe  NIHSS and Outcome Prediction NIHSS below 12-14 will have an 80% good or excellent outcome NIHSS above 20-26 will have less than a 20% good or excellent outcome Lacunar infarct patients had the best outcomes Adams HP Neurology 1999;53:126-131 Baseline NIH Stroke Scale score strongly predicts outcome after stroke (TOAST)  Brain Infarction The four most frequent subtypes of cerebral infarction are: large-vessel atherosclerotic, cardioembolic, small vessel (lacunar), and cryptogenic  Etiology of Ischemic Strokes LARGE VESSEL THROMBOTIC: Virchow’s Triad…. Blood vessel injury - HTN, Atherosclerosis, Vasculitis Stasis/turbulent blood flow - Atherosclerosis, A. fib., Valve disorders Hypercoagulable state - Increased number of platelets - Deficiency of anti-coagulation factors - Presence of pro-coagulation factors - Cancer  Etiology Of Ischemic Stroke: LARGE VESSEL EMBOLIC: The Heart – Valve diseases, A. Fib, Dilated cardiomyopathy, Myxoma Arterial Circulation (artery to artery emboli) – Atherosclerosis of carotid, Arterial dissection, Vasculitis The Venous Circulation – PFO w/R to L shunt, Emboli  Cortical Signs RIGHT BRAIN: LEFT BRAIN: - Right gaze - Left gaze preference preference - Neglect - Aphasia If present, think LARGE VESSEL stroke  Large Vessel Stroke Syndromes MCA: – Arm>leg weakness – LMCA cognitive: Aphasia – RMCA cognitive: Neglect,, topographical difficulty, apraxia, constructional impairment ACA: – Leg>arm weakness, grasp – Cognitive: muteness, perseveration, abulia, disinhibition PCA: – Hemianopia – Cognitive: memory loss/confusion, alexia Cerebellum: – Ipsilateral ataxia  Aphasia Broca’s – Expressive aphasia – Left posterior inferior frontal gyrus Wernicke’s – Receptive aphasia – Posterior part of the superior temporal gyrus – Located on the dominant side (left) of the brain  Determining the Location Large Vessel: – Look for cortical signs Small Vessel: – No cortical signs on exam Posterior Circulation: – Crossed signs – Cranial nerve findings Watershed: – Look for watershed pattern – S/S of Hypo-perfusion  Etiology of Stroke SMALL VESSEL (Lacunes = 24 hrs Assessment and diagnosis (exclude mimics) early assessment of nursing and therapy needs Early mobilisation, prevention of complications, Rx of hypoxia, >glycaemia, pyrexia and dehydration. 4H:Hydration, Hypoxia, Hyperglycaemia, Hyperpyrexia Ongoing rehabilitation; Coordinated multidisciplinary team care; early assessments of needs > discharge 07/12/24 48  Outline of activities for early supportive care 1. Ensure clear airway and good ventilation: Given oxygen if necessary but not routinely. 2. Nurse in slight head-up tilt (0 – 45 - 900) to improve venous drainage from the head region. 07/12/24 49  Outline of activities 3. continuous monitoring of neurological deficit for deterioration, including the level of consciousness, which may herald impending herniation. 4. Continuous cardiac monitoring, if indicated, particularly if risk factors for coronary heart disease are present. 07/12/24 50  Outline of activities 5. Do not feed orally if patient is unconscious or drowsy. Swallowing test should be done in conscious patients before oral feeding and feed in the semi-recumbent position (450) – ensure correct consistency of food. 07/12/24 51  Outline of activities 6. If hemiplegia is dense, commence DVT prophhylaxis 7. Do not give hypotonic solution, eg 5% Dextrose in water, as it may worsen cerebral oedema. Monitor serum sodium. 8. Do not treat hypertension except mean blood pressure is above 145mmHg, systolic BP is > 220mmHg or diastolic BP is > 120mmHG. Even then, use oral agents (captopril, calcium channel blockers). 07/12/24 52  Outline of activities 9. Treat hyperglycaemia as usual 10.Treat fever symptomatically, Search for source and treat appropriately. 11.Avoid urinary catheterisation, as much as possible. 12.Treat neurological complications. 07/12/24 53  Assessment All pts: Brain Imaging: CT or MRI Chest X-ray; ECG; Echocardiography; Cbc; platelet count, PT or INR, PTT; CRP/ESR electrolytes, glucose; LFT / Renal fn correlation between lacunar stroke and HB, None between Hb and non-lacunar; leucocytosis is associated with poor prognosis Urinalysis - Microalbuminuria predicts haemor transformation in CI– endothelial dysfunctn In selected patients: Duplex / Doppler ultrasound MRA or CTA Diffusion and perfusion MR or perfusion CT Pulse oximetry and arterial blood gas analysis Lumbar 07/12/24 puncture; EEG ;Toxicology screen 54  Imaging CT scan MRI Non- contrast CTH Superior for showing remains the gold underlying structural standard as it is superior lesions for showing IVH and ICH Contraindications CT with contrast may help identify aneurysms, AVMs, or tumors but is not required to determine whether or not the patient is a tPa candidate  Acute (4 hours) Subacute (4 days) Infarction Infarction R L R L Subtle blurring of gray-white Obvious dark changes & junction & sulcal effacement “mass effect” (e.g., ventricle compression) www.acponline.org/about_acp/ chapters/ok/gordon.ppt  Multimodal Imaging Multimodal CT Multimodal MRI Typically includes non- Standard MRI sequences contrast CT, perfusion ( T1 weighted, T2 CT, and CTA weighted, and proton Two types of perfusion density) are relatively insensitive to changes in CT cerebral ischemia – Whole brain perfusion Multimodal adds diffuse- CT weighted imaging (DWI) – Dynamic perfusion CT and PWI (perfusion- weighted imaging)  Differential Diagnosis Deciphered by history, PE, diagnostics DDx: TIA vascular disorders seizure infections (endocarditis) trauma complex migraine mass lesions metabolic abnormalities  tPa Fast Facts Contraindications Tissue plasminogen Hemorrhage activator SBP > 185 or DBP > 110 “clot buster” Recent surgery, trauma IV tpa window 3 hours or stroke Coagulopathy IA tpa window 4.5 Seizure at onset of hours symptoms Disability risk  30% NIHSS >21 despite ~5% Age? symptomatic ICH risk Glucose < 50  Mechanical Thrombolysis Often used in adjunct with tPa MERCI (Mechanical Embolus Removal in Cerebral Ischemia) Retrieval System is a corkscrew-like apparatus designed to remove clots from vessels PENUMBRA system aspirates the clot  Blood Pressure Management BP Management – The goal is to maintain cerebral perfusion!! – CPP = MAP – ICP (needs to be at least 70) – Higher BP goals with Ischemic stroke – Lower BP goals with Hemorrhagic stroke (avoid hemorrhagic expansion, especially in AVMs and aneurysms)  BP-AIS Relationship Penumbra BP increase is due to arterial occlusion (i.e., an effort to Core perfuse penumbra) Failure to recanalize (w/ or w/o thrombolytic therapy) results in high BP and poor neuro outcomes Lowering BP starves penumbra, worsens Clot in outcomes Artery www.acponline.org/about_acp/ chapters/ok/gordon.ppt Save the Penumbra!! Normal 20 function 15 Neuronal CBF PENUMBRA dysfunctio 8-18 10 n 5 Neuronal CBF CORE death 130 or Sys BP > 220 MAP= [(2x DP)+SP]3 – NSA: 220/115  Hypertension - Ischemic Stroke Drugs - short acting, titrate Labetalol IV: 10-20 mg increments, double dose Q 20 min, max cumulative dose 300mg Enalapril Oral: 2.5 - 5.0 mg/day, max 40mg/day IV : 0.625-1.25 mg IV Q 6hrs, max 5.0 Q 6 hrs  Hypertension -Ischemic Stroke Nitroglycerine Paste: 1-2 inches to skin IV Drip: 5mcg/min, increase in increments of 5-10mcg every 3-5 min Nitroprusside IV Drip: 0.3 - 10 mcg/min/kg Continuos BP monitoring check thiocyanate levels AVOID NIFEDIPINE  Supportive Therapy Glucose Management – Infarction size and edema increase with acute and chronic hyperglycemia – Hyperglycemia is an independent risk factor for hemorrhage when stroke is treated with t-PA Antiepileptic Drugs – Seizures are common after hemorrhagic CVAs – ICH related seizures are generally non-convulsive and are associated to with higher NIHSS scores, a midline shift, and tend to predict poorer outcomes  Hyperthermia Treat fevers! – Evidence shows that fevers > 37.5 C that persists for > 24 hrs correlates with ventricular extension and is found in 83% of patients with poor outcomes Future directions/experimental therapies II Therapeutic Hypothermia It is now well accepted that hypothermia reduces ischemia in animal models of stroke. Current efforts are directed towards translating this to patients with ischemic stroke. There remain unresolved technical issues surrounding the timing and method for inducing hypothermia, and the deleterious effect of re-warming. Hypothermia can be combined with thrombolysis. Future directions/experimental therapies III Trophic factors and Cell based therapies These are approaches that seek to promote repair and recovery. They can be divided into two categories- trophic factor treatments (e.g. growth factors like NDF) that seek to amplify and augument endogeneous processes of neurovascular plasticity and recovery, and cell-based therapies (e.g. neural stem cells) that seek to replace damaged or lost brain cells. These approaches have met with variable degrees of success in animal models. A lot more work is needed to translate these promising results into effective stroke therapies.  Summary Supportive Care Secure airway; basic and advanced methods Protect C-spine Assure oxygenation and ventilation Maximize perfusion, IV fluids Blood pressures (both arms), treat carefully Normalize the temperature and glucose Treat seizure if occurs Reevaluate  References Adams, H., del Zappo, G., Alberts, M., Bhatt, D., Brass, L., Furlan, A., Grubb, R., & Higashida, R. (2007). Guidelines for the early management of adults with ischemic stroke. Stroke, 38, 1655-1711. Bradley G Walter, Daroff B Robert, Fenichel M Gerald, Jancovic, Joseph; Neurology in clinical practice, principles of diagnosis and management. Philadelphia Elsevier, 2004. Castillo, J., Leira, R., Garcia, M., Serena, J., Blanco, M. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 2004: 35: 520- 526. Goals for Management of Patients With Suspected Stroke Algorithm. http://circ.ahajournals.org/content/112/24_suppl/IV-111/F1.expansion.ht ml. Accessed May 8, 2012 Gordon, D. L. (n.d.). Update in stroke management. Retrieved from www.acponline.org/about_acp/chapters/ok/gordon.ppt Hesselink, J. Imaging of cerebral hemorrhages and AV malformations. http://spinwarp.ucsd.edu/neuroweb/Text/br-740.htm. accessed May 10, 2012. Questions?