Stroke Management for the EMS Provider October 2014 CME Stroke Management for the EMS Provider At the completion of this module, the EMS Provider will be able to: Describe the various types of stroke and their etiology. Discuss the imperatives for best practice in regard to EMS stroke management. List 5 or more risk factors for acute stroke. Define “penumbra” and how this concept is important in stroke. Generally Discuss Identify describe the major vessels involved in acute ischemic stroke. the “therapeutic window” for thrombolytic therapy in stroke. interventions that individual EMS providers can make to improve outcomes in stroke. Is STROKE a health problem in the US today? 700,000 strokes every year • Stroke is the 3rd leading cause of death • One person dies of stroke every 3 minutes • Stroke is the leading cause of serious, long term disability • 5 million stroke survivors, but with substantial morbidity: • 18% unable to return to work • 4% require total custodial care Is STROKE a health problem in the US today? Only 50-70% of stroke survivors regain functional independence • 20% are institutionalized within 3 months • 22% of men & 25% of women die within 1 year of their first stroke • Locally, African-Americans have 50% more strokes than Caucasians, and twice as many as Asians and Hispanics (Statistics from the American Stroke Association) Women & Stroke Stroke kills more than twice as many American women every year as breast cancer More women than men die from stroke Women over age 30 who smoke and take highestrogen oral contraceptives have a stroke risk 22 times higher than average (National Stroke Association) Is STROKE a health problem in the US today? YES, stroke is a major health problem in the US today. EMS Providers are closely involved with this patient population and are a vital component of the “Stroke Chain of Survival”. Increased knowledge and personal motivation on the part of EMS providers can: Greatly reduce death and disability due to stroke. Improve stroke centers’ ability to provide thrombolytic therapy. Make a positive impact on communities’ strides to reduce costs for healthcare and improve outcomes. Goals for EMS Provider Care of Stroke Patients 1. 2. 3. 4. 5. Improve knowledge of identification of stroke signs and symptoms. Develop a rapid assessment process. Facilitate transfer of stroke victims to Primary Stroke Centers in the quickest and safest manner. Pre-notify the Stroke Center, “Possible acute stroke in route.” Encourage family members familiar with the patient care to either ride with the transfer vehicle or drive to the stroke center ASAP to provide more patient information. Goals for EMS Provider Care of Stroke Patients 6. 7. 8. 9. 10. Obtain reliable list of meds taken or bring bag of all medications taken. Obtain a set of vital signs and finger stick blood sugar at the site. Reliably identify family’s best estimation of when the patient was “last seen normal”. Administer the Cincinnati Pre-hospital Stroke Scale. Provide the receiving facility with a quick, complete verbal report that incorporates the information obtained since arrival on scene. Review: Anatomy & Physiology of Acute Ischemic Stroke What is acute ischemic stroke? What is the major vasculature involved? When circulation is suddenly reduced, how quickly is brain tissue affected? What is “penumbra”? What are the types and etiologies of stroke? What about different stroke symptoms? What Is Stroke ? A stroke occurs when blood flow to the brain is interrupted by a blocked or burst blood vessel. What is Stroke? No oxygen, nerve cells die in minutes In first three hours, some cells can be saved (up to 35% recovery) Thrombolytics (‘clot-busting’) drugs dissolve clots; prevent more strokes: Administered via IV pump Heparin (mixed results) t-PA, “Activase” Activase” (good results) Copyright 2004 MEDRAD, Inc. All rights reserved. One quarter of cardiac output goes to the 5-6 pound organ—the brain. The brain needs a constant supply of: •Oxygen •Glucose •Other nutrients Circulation is supplied via 2 pairs of arteries: •Internal carotids •Vertebrals The Major Circulation to the Brain PENUMBRA (That tissue surrounding the infarct that is salvageable, but at risk.) Rapid transfer to the stroke center will allow for protection of penumbra through emergency interventions and medical management. Cerebrovascular Disease: Pathogenesis Hemorrhagic Stroke (17%) Intracerebral Hemorrhage (59%) Ischemic Stroke (83%) Atherothrombotic Cerebrovascular Disease (20%) Cryptogenic (30%) Subarachnoid Hemorrhage (41%) Lacunar (25%) Small vessel disease Albers GW, et al. Chest. 1998;114:683S-698S. Rosamond WD, et al. Stroke. 1999;30:736-743. Embolism (20%) Acute Ischemic Stroke Deficits: (What do you see?) Unilateral (though not always) weakness Unilateral sensory deficit Visual deficits (blindness, gaze palsy, double) Speech (slurred – a motor dysfunction) Language (aphasia – damage to the brain’s speech center) Ataxia (lack of coordinated movement) Cognitive impairment Like real estate—Location, Location, Location What Parts of the Brain Are Affected by Stroke? What Are the Effects of Stroke? Left Brain What Are the Effects of Stroke? Right Brain Stroke Assessment Scale (Cincinnati Pre-hospital Stroke Scale) “The sky is blue in Cincinnati.” Any abnormality means an abnormal Cincinnati scale for stroke. Probably accurately detects stroke 80% of the time. Act F.A.S.T for stroke The National Stroke Association recommends using the FAST method for recognizing and responding to stroke symptoms. F (face) A (arms) S (speech) T (time) Stroke Assessment in the Field Administer Cincinnati Scale. If abnormal, facilitate a rapid transfer to an approved stroke center. Pre-notify the receiving stroke center— ”possible acute stroke in route”. Identify Time “Last Seen Normal” A 75 year old man with HTN and diabetes finishes dinner with a friend at 8pm. He drives himself the short distance home that night, and a daughter stops by the next morning to find him still in bed and with right side weakness and severe aphasia. When do we assume the stoke occurred? (Answer: “last seen normal at 8pm) A 35 year old hypertensive man who is known to be non-compliant with meds is found slumped over in his car in a job site parking area at 3pm. In the ED he was found to have a massive left hemispheric ischemic stroke. His wife said he left for work at 7am that morning as normal, and she had a clear and normal cell phone conversation with him at 12:30pm. At 1pm a co-worker stated the man said he wasn’t feeling well and was going to his car to rest. At the time the co-worker noticed his speech was slurred. What time can we use as the time “last seen normal”? (Answer: 12:30pm) Types of Acute Ischemic Strokes Middle Cerebral Artery Stroke Vertebral—Basilar Artery Strokes Lacunar Strokes Types of Strokes (Middle Cerebral Artery – MCA) CT Scan of Acute Ischemic Stroke (Left MCA territory stroke) Types of Strokes (Middle Cerebral Artery – MCA) The most common artery occluded in AIS— can be proximal or from carotid circulation. Features: Motor/Sensory Deficit: face, arm, leg Speech deficit – dysarthria (slurred speech) Language deficit – if in dominant hemisphere Gaze palsy – eyes directed towards side of AIS Blindness – visual field cut (homonymous hemianopsia) Types of Strokes (Vertebral—Basilar Artery) Features: Cranial nerve involvement – hearing, visual, facial, swallowing Can have bilateral weakness Cerebellar signs – ataxia Sensory deficits Vertigo – often nystagmus Nausea and vomiting Common to have waxing and waning symptoms Lacunar Strokes These strokes are ischemic in nature. Mainly caused by HTN. Occurs in the small penetrating arteries of the brain. Presentation – affects the arm, leg, and face, sometimes silent. Deficits are equal to all areas. Conditions That Mimic AIS Bell’s Palsy Todd’s Paralysis Hemorrhagic Stroke Subdural Hematoma Other conditions Conditions That Mimic AIS Bell’s Palsy Bell’s Palsy is a viral infection of the facial nerve which causes stroke-like symptoms: unilateral facial droop, sensory deficit, dysarthria, etc. Conditions That Mimic AIS Differential dx: Hx: women, pregnancy, viral illness Can’t close eye completely or raise forehead May have facial pain No other stroke symptoms May have no risk factors for stroke Conditions That Mimic AIS Todd’s Paralysis: unilateral weakness that occurs after a seizure. Can involve speech, language, visual and sensory May be due to hyperpolarization in the area of the seizure Resolves within 48 hours Key concern in regard to thrombolytic therapy Conditions That Mimic AIS Hypoglycemia Metabolic conditions – fever, hyponatremia, drugs, etc. Psychogenic Complex migraines Hypertensive crisis What are the risks factors for Ischemic Stroke? Modifiable Risks HTN CAD/Carotid Disease/PVD Atrial Fibrillation Diabetes Weight High Cholesterol/Diet Lack of exercise ETOH/Drug abuse Coagulopathy- Cancer, Sickle Cell Anemia Non-Modifiable Risks Age->55 Race- African Americans have 2x the risk of death and disability. Asians have 1.4x the risk of death and disability. Sex- 9% greater chance in men. (61% of stroke deaths occur in women) Previous Stroke or TIA Family History of Stroke Goals for Treatment in the ED EMS rapid identification & pre-notification of the Emergency Dept. Quick evaluation in ED. Last seen normal < 3 hr. Door-to-CT scan < 25 minutes CT-to-Radiologist Reading < 20 minutes IV TPA administration < 15 minutes (Door-to-needle within 60 minutes.) What can be done for an acute ischemic stroke? These patients may be appropriate for “clot busting” drugs. Tissue Plasminogen Activator (TPA). Requires a rapid, coordinated response. IV TPA can only be given within the first 3 hours of symptom onset. Expected response: “60 minutes from door to needle.” Tissue Plasminogen Activator Natural body substance. Recombinant TPA converts Plasminogen to plasmin, which in turn breaks down fibrin and fibrinogen, thereby dissolving the clot. IV window of opportunity is < 3 hours of known symptom onset. Transition Hemorrhagic Stroke Hemorrhagic Stroke (Intracranial Hemorrhage—ICH & Subarachnoid Hemorrhage—SAH) Intracranial Hemorrhage (Hypertensive): > twice as common as SAH more likely to result in death or severe disability 37,000 Americans/year 35-52% dead within 1 month (half of deaths in the first 2 days) Only 10% living independently in 1 month; improves to only 20% within 6 months Hemorrhagic Stroke (Intracranial Hemorrhage—ICH & Subarachnoid Hemorrhage—SAH) Risk factors: Hypertension Advancing age Coagulation disorders & therapy ETOH abuse Drug use (meth, cocaine, crack, etc.) Ischemic stroke—hemorrhagic transformation Hemorrhagic Stroke (Intracranial Hemorrhage—ICH & Subarachnoid Hemorrhage—SAH) Presenting signs: Sudden—signs over minutes to hours Headache Nausea and vomiting Decreasing LOC Extremely elevated blood pressure (All of these are signs of increased ICP) Hemorrhagic Stroke (Intracranial Hemorrhage—ICH & Subarachnoid Hemorrhage—SAH) Differential Diagnosis: AIS—often high BP AIS—rare decreased LOC AIS—rare or vague H.A. AIS—rare nausea & vomiting AIS—often wake up with the symptoms • Final ICH—usually very high BP ICH—50% of the time ↓ LOC ICH—40% of the time H.A. ICH—50% of time vomiting ICH—rarely wake up with symptoms (15%) diagnosis is by CT scan. Weakened blood vessels in a Hypertensive Bleed Autopsy of Intracerebral Hemorrhage Small hemorrhagic stroke Large hemorrhagic stroke ICH: Goals for Early Management Airway management Assure adequate oxygenation & reduce hypercapnea (Remember: ↑CO2 = ↑ ICP) Prevent aspiration (Remember: 50% of ICH patients vomit and have ALOC) Seizures Versed – If seizure activity > 2-3 minutes administer 2.5mg IV. May repeat 2.5mg once in 5 minutes Versed may be given IM if no IV established Oxygenation Oxygen is a free radical, meaning that it is a highly reactive species owing to its two unpaired electrons. From a physics perspective, free radicals have potential to do harm in the body Normally, the body fends off free radical attacks using antioxidants. With aging and in cases of trauma, stroke, heart attack or other tissue injury, the balance of free radicals to antioxidants shifts Cell damage occurs when free radicals outnumber antioxidants, a condition called oxidative stress Oxygenation Tissue damage is directly proportionate to the quantity of free radicals present at the site of injury. Supplemental oxygen administration during the initial moments of a stroke may well increase tissue injury by flooding the injury site with free radicals. Oxygen saturations should be measured on every patient. Administer oxygen to keep saturations between 94 and 96 percent. Rarely does a patient need oxygen saturations above 97 percent. ICH: Goals for Early Management Blood Pressure Management: Very poor outcomes if BP is allowed to stay very high—more bleeding Very poor outcomes if BP is allowed to drop precipitously—removes the brain’s attempt to perfuse a “tight” brain Guidelines: In general, keep BP about 160/90 or MAP <130 In the first 48 hours: no BP drop > 15-25% of presenting value Hemorrhagic Stroke (Subarachnoid Hemorrhage) Acute bleeding around the outside of the brain and into the subarachnoid space. Usually from an aneurysm or arteriovenous malformation. Statistics: 50% are fatal 1--15% die before reaching the hospital Those who survive are often impaired 1-7% of all strokes Hemorrhagic Stroke (Subarachnoid Hemorrhage) Diagnosis: “Thunderclap” headache. “It is the worst headache of my life!” Xanthochromic lumbar puncture (blood in the CSF not due to traumatic tap) “Star pattern” on CT scan Aneurysmal bleed Classic “Star Pattern” of Subarachnoid Hemorrhage Subdural Hematoma (Not a true stroke but symptoms can mimic stroke.) Subdural Hematoma Symptoms: Unilateral weakness, sensory deficit Facial weakness Dysarthria Altered level of consciousness Onset: Can be rapid Can take months to show symptoms Subdural Hematoma Causes Anticoagulation (Heparin, Coumadin) Antithrombotics (Aspirin, Plavix) ETOH abuse Trauma (could be recent or months ago) Advanced age (most common cause) Subdural Hematoma Small bridging veins from the dura mater to the brain are stretched and can rupture releasing blood into the subdural space and causing pressure on that part of the brain. This leads to the deficits seen. Subdural Hematoma on CT Scan Subdural Hematoma Treatment Options Medical Management: Correct Coags Monitor neuro signs Surgical Management: Correct Coags Burr hole drainage Craniotomy for removal of solid clot Summing Up The best stroke care is a coordinated approach and developed in a stroke center system of care. Requires everyone to be on board: Patients/Families EMS ED Stroke Unit Stroke Rehabilitation Summing Up How well a patient does; whether a patient has a life-long serious disability; whether he/she lives or dies; may depend on you and how you respond. A few minutes delay may make a very big difference. What you do really matters! Emergent Stroke Care and the Chain of Survival Patient Calling Knowledge 911 EMS System ED Staff Stroke Team Stroke Unit EMS Treatment SMO Code 38 “Suspected Stroke” “Initiate rapid transport.” ESRH – Emergent Stroke Ready Hospital PSC – Primary Stroke Center Stroke Centers On Oct 22, 2013, the Illinois Legislature’s Joint Committee on Administrative Rules formally approved the Administrative Rule for the 2009 Illinois Primary Stroke Center Law. The 2009 Primary Stroke Center Law was designed to improve stroke care in two complementary ways: Help hospitals to improve the quality of their inpatient stroke care systems It would ensure that regional emergency medical services (EMS) medical directors draft and implement stroke care protocols to better identify stroke patients in the field and take them directly to the nearest designated stroke center for treatment, bypassing a less-specialized hospital if necessary. Silver Cross Hospital EMS System Within SCEMSS, there are 3 IDPH approved PSC or ESRH facilities: Silver Cross Hospital – PSC Presence St Joseph Medical Center – PSC South Suburban Hospital – PSC Other associate/participating facilities within SCEMSS have IDPH applications pending approval Patient advocacy… Per CODE 38 If the Cincinnati Stroke Scale is positive; And “last known normal” is less than 3 hours; Transport to the closest Primary Stroke Center or Emergent Stroke Ready Hospital Code 38 – Suspected Stroke Initial Medical Care Cincinnati Stroke Scale If Positive, begin transport to nearest MOST APPROPRIATE facility Initiate rapid transport 12-Lead EKG Obtain blood glucose reading and treat appropriately “If available” refers to the ability of your cardiac monitor to perform a 12-lead EKG. If you have 12-lead capabilities, you must perform one. Other SMO CODE’s as indicated Coma of Unknown Origin Seizures Run of the month… Atrial Fibrillation 1) P waves are absent. 2) There are fibrillation (f) waves instead of P waves. The f waves result in an oscillating irregular baseline. 3) The R-R intervals are not equal resulting in an irregular rhythm (irregularly irregular) Atrial rate 400-600bpm Ventricular rate 75-175bpm Clinical significance Atrial fibrillation patients usually have a ventricular rate of 75-175 beats/minute A lower ventricular rate should suggest AV block or the use of medications decreasing the ventricular rate (digoxin, beta blocker, verapamil, diltiazem, amiodarone) High ventricular response may cause syncope or even death in these patients Since the R-R intervals continuously change in atrial fibrillation patients, the heart rate on the monitor also changes continuously. In such patients, the instantaneous heart rates depicted on the monitor usually does not give the average ventricular rate of that patient Since there is no atrial contraction, the presence of atrial fibrillation decreases cardiac output by 20-25% Atrial fibrillation results in “atrial statis” which predisposes to the thrombus formation in the atria. This results in increased risk of systemic embolism Unless contraindicated, patients with atrial fibrillation are generally advised to be on blood thinners In patients with a very high ventricular rate, it may be difficult to recognize the irregularity of the R-R intervals at first glance Coumadin (warfarin sodium) is the most common medication prescribed for A-Fib Adenosine is often used in the clinical setting to slow the rate to differentiate between SVT/V-Tach. A-fib will not respond to the effects of adenosine. THIS IS NOT PART OF REGION VII SMO’s In some patients, atrial fibrillation is not persistent. (Transient A-Fib) Assessment/Treatment Symptomatic A-Fib patients – Signs of hypoperfusion with elevated heart rate, altered mental status Consider Synchronized Cardioversion Region VII – Code 83, “Synchronized Cardioversion” Code 83 - “Synchronized Cardioversion” Consider use of Versed for pain management and/or sedation 2.5mg to 5mg, slow IVP Constantly assess pulse oximetry and be prepared to place advanced airway if necessary! Place patient in safe environment, away from pooled water and metal surfaces Apply monitor-defibrillator electrode pads to patient chest or appropriate conductive medium paddles Turn on defibrillator Set energy level Activate “synchronous” mode Charge capacitor Ensure proper placement of electrodes on chest: Apical and high parasternal If using hand-held paddles, apply firm pressure and maintain until machine discharges Assure that no personnel are in direct contact with the patient (Call “clear”) Deliver shock by depressing discharge button. Hold button down until machine discharges Reassess patient Drug of the Month Dextrose 50% Dextrose 50% Adult Dose/Route 25 gm/50ml of 50% solution IVP Peds Dose/Route > 8 years 2 mL/kg of 50% solution 1 – 8 years 2 mL/kg of 25% solution Infants under 2months 4 mL/kg of 12.5% solution Action Increase blood glucose concentration Indications Hypoglycemia ContraIndications Adverse Reactions Intracranial and intraspinal hemorrhage, hypovolemia, hypotension 2° tachydysrhythm ias, delerium tremens. Hyperglycemia, warmth / burning from IV injection, diuresis, thrombophlebit is, tissue necrosis if IV infiltration. The End… Thanks for all you do !!!