Rethinking Stroke Care
The treatment of suspected stroke patients has changed significantly in the past several years. Management of hypertension by EMS providers in suspected strokes has recently been challenged. The optimal strategy for brain resuscitation remains unknown; however, treating hypertension in the stroke patient is now considered dangerous. No definitive evidence exists suggesting that emergent treatment of hypertension will improve the neurological outcome.1 In fact, numerous clinical case series have reported neurological deterioration in strokes immediately following reduction of blood pressure.2 Critical care transport providers must be familiar with the physiology of strokes and the treatments for brain resuscitation in order to provide optimal care.
Management of hypertension remains permissible in limited circumstances. During hemorrhagic strokes, an elevated blood pressure may increase the bleeding. According to Norman Kaplan, MD, clinical professor of internal medicine at the University of Texas--Southwestern, "Reducing the blood pressure in patients with either subarachnoid or intracerebral bleeding may be beneficial by minimizing further bleeding and continued vascular damage. Elevated blood pressure can worsen a subarachnoid hemorrhage, since the mechanical force across the plugged bleeding site is related to the difference between the systemic blood pressure and the cerebrospinal fluid pressure."3 Although treatment in these cases may be beneficial, it is impossible in the prehospital arena to determine the nature of the cerebral insult. Eighty to 85% of strokes are ischemic, so erring on the side of a hemorrhagic stroke is not statistically viable. Much controversy exists regarding the treatment of patients with subarachnoid hemorrhage. Some neurologists recommend withholding treatment of severe hypertension because of the potential for cerebral ischemia. Currently, there is no definite evidence proving hypertension causes enlargement of an intracerebral hemorrhage or increases the risk of rebleeding.1,2 The Brain Attack Coalition also recommends the judicious treatment of hypertension only if the patient presents symptomatic for congestive heart failure or an acute myocardial infarction.4
In patients diagnosed with intracerebral hemorrhage, the drug of choice is Trandate (labetalol hydrochloride), Nitropress (nitroprusside) or Cardene (nicardipine). Some neurologists caution that Nitropress increases cerebral blood volume and therefore increases intracranial pressure.3 Also, Nitropress is known to cause a "steal phenomenon" by shunting blood and thus causing secondary focal cerebral ischemia.1
EMS agencies choosing to treat hypertension in strokes must be acutely aware of the risks. Many prehospital protocols still recommend treating systolic pressures greater than 200 and diastolic pressures greater than 110 in the presence of suspected strokes. Generally, the drug of choice for these agencies is Trandate 20 mg intravenously to control the hypertension, while some agencies still advocate the use of nitroglycerin to lower blood pressures. Nitroglycerin is still used to lower blood pressure in the hospital setting, but is not advocated prehospital because of the inability to monitor invasive pressures and the propensity to lower pressures too quickly or cause hypotension.
Although hypertension may be a contributing factor to rebleeding in the first hour of a stroke, inadvertent overcorrection of the blood pressure will most likely exacerbate ischemia. If treatment of hypertension is going to occur, it is strongly recommended that it be cautiously lowered over 12 to 48 hours, not in the prehospital arena.
Some physicians argue that the hypertension must be corrected, since it may cause the stroke to worsen; however, the hypertension most often observed is protective reflex hypertension as a result of the stroke, not as a cause.5 Cushing reflex is a protective response from the body to a rapid rise in intracranial pressure. This reflex is characterized by hypertension, bradycardia and respiratory irregularities. The brain recognizes a need for increased cerebral pressures in order to maintain adequate perfusion of the brain. This hypertension can sometimes spontaneously improve after a few hours without any intervention. According to Norman Kaplan, MD, and Burton Rose, MD, a professor of medicine at Harvard School of Medicine, "Antihypertensive therapy is more likely to lead to an exaggerated reduction in cerebral flow in this setting, since autoregulation is impaired in ischemic areas."3 The National Stroke Center does not even list antihypertensive therapy as an indicated treatment in the "Golden Hour" of strokes.6 It is interesting to note that, in the first 48 hours of a stroke, if a patient's systolic pressure drops below 100 or oxygen saturation falls below 95%, there is a 150% increase in mortality.7
Some professionals also argue that a blood pressure greater than 185/110 should be corrected, because it is an exclusion criterion for thrombolytic therapy. Research conducted by the University of Miami School of Medicine shows thrombolytic therapy is only indicated for a small number of ischemic stroke patients. Definitive verification of an ischemic stroke is accomplished with a non-contrast computed tomography (CT) with angiography scan. This must be accomplished in a hospital in the critical care setting. The deleterious effects of rapid, uncontrolled reduction of blood pressure by EMS providers in ischemic stroke patients are well documented. Physicians who advocate lowering blood pressure because of the benefit of thrombolytics are basing this theory on anecdotal evidence rather than evidence-based medical practice.8
The University of Miami School of Medicine strongly discourages prehospital providers manipulating blood pressures because of possible damage to the penumbra.8 The penumbra is an area of reversible ischemia surrounding the core of irreversible ischemia or area of insult. During the first few hours following a stroke, the penumbra is dysfunctional but still-living brain tissue. The tissue in the penumbra is unable to function due to altered and limited blood flow. The penumbra requires a minimal mean arterial pressure of 100 to perfuse, whereas the undamaged portions of the brain only require a mean arterial pressure of 70. The mean arterial pressure varies based on premorbidity. A mean arterial pressure as high as 130 may be required to ensure perfusion in patients with a history of hypertension. Determining mean arterial pressure in the field can be valuable in the hypotensive stroke patient (see Figure 1). If mean arterial pressure falls below 100, medical control should be consulted for possible blood pressure management, including a fluid challenge and/or pressor therapy.
Decreased cerebral perfusion and vasospasm frequently occur in the penumbra. Although chronic hypertension may be a predisposing factor for stroke events, the elevation in pressure may be beneficial to maintain blood flow in the potentially viable ischemic areas. A reduction in pressure may result in cerebral vasospasms,3 which is the leading cause of death and disability following a subarachnoid hemorrhage.9 Vasospasms commonly occur adjacent to intracerebrellar bleeding. The resultant decrease in the mean arterial pressure will aggravate cerebral ischemia.1 Although the University of Miami School of Medicine strongly encourages prehospital providers not to manipulate blood pressures, patients being treated inside hospitals are often treated with the same judiciously delivered treatment. As in the field, a rapid decrease in blood pressure will result in possible extension of the infarct into the area that was once penumbra.2
The treatment of prehospital hypertension is limited by an array of factors. Patient and caregiver interaction time is often limited. Scene transport times frequently do not allow in-depth interventions and associated monitoring necessary in antihypertensive therapy. Although times have changed from "load and go" on most emergency calls, it seems that the trend in stroke management is to rapidly transport the patient to a critical care setting for definitive intervention. As seen in Figure 2, the goal is to rapidly transport the patient to a qualified stroke care facility, because stroke treatment is extremely time-dependent.
During interfacility transports, providers may transport patients who already have arterial pressure lines and other devices in place that help monitor their progress toward a normotensive state. With these devices, providers are able to monitor subtle changes in intravascular pressures and prevent rapid decreases in pressure leading to frank hypotension. If treatment modalities include pharmacological management of hypertension, the reduction should be achieved in a controlled environment, not in an aircraft or ambulance.
What is the appropriate prehospital treatment for suspected strokes? Transport personnel must perform accurate patient evaluations that include either the Cincinnati or Los Angeles PreHospital Stroke Scale. The patient must also be transported to a hospital that has a stroke management team, preferably a Level One, or primary stroke center, facility. Figure 3 lists the elements required by the Joint Commission on Accreditation of Healthcare Organizations (JCAHO).
Treatment is centered on management of life-threatening symptoms that are resultant of the stroke. This includes aggressive airway management with rapid sequence induction, if indicated. Patients with a Glascow Coma Score of less than eight or those who cannot maintain their own airway should have definitive airway control. Suspicion of a stroke should not be a contraindication for rapid sequence induction. The patient should be intubated if any of the following are present:12
- Inability to maintain airway
- Failure to maintain adequate oxygenation or ventilation
- Intubation is indicated as part of the patient's anticipated clinical course of treatment.
Providers should be familiar with the concept of neuroprotective rapid sequence induction, which utilizes premedication agents in addition to the sedative and paralytic. The two most common premedication agents are lidocaine and a defasciculating agent. However, the use of pretreatment agents in neuroprotective rapid sequence induction is theory-based, not evidence-proven. Providers should know the indications for pretreatment agents and be aware of the controversy surrounding their use.
Lidocaine is administered at 1 mg/kg intravenous push. The theory is that lidocaine will blunt an increase in intracranial pressure. The mechanism behind this action is unknown, and the benefits of lidocaine have not been definitively proven. The decrease in intracranial pressure is most likely related to its sympatholytic activity.13 Lidocaine also decreases cerebral metabolism and stabilizes cell membranes by means of its ability to block membrane sodium channels. Prophylactic lidocaine has also been shown to obtund the rise in intraorbital pressure that accompanies tracheal manipulation. Several new research articles contest the efficacy of lidocaine, and clinical trials have shown that there is no decrease of intracranial pressure.14 Currently, the use of lidocaine as a pretreatment agent is based on physician preference.
Depolarizing paralytics like Anectine (succinylcholine) can cause fasciculations, which are asynchronous contractions of muscles as they are stimulated by depolarizing paralytics. These fasciculations can cause several untoward effects, including aspiration (due to increased gastric pressure), hyperkalemia, complication of major fractures, increased intraocular pressure and increased intracranial pressure. The defasciculating agent is the nondepolarizing paralytic given at 10% of the paralyzing dose. For example, Norcuron (vecuronium) is administered at 0.1 mg/kg for long-term paralysis, but is given at 0.01 mg/kg as a defasciculating dose. This subtherapeutic dose does not paralyze the patient, but instead prevents the fasciculations from occurring with the depolarizing agent.
The use of defasciculating agents is also not without controversy. Ronald D. Miller, MD, professor and chairman of the Department of Anesthesia and Perioperative Care at the University of California, San Francisco, School of Medicine, notes in his text, Miller's Anesthesia, that a defasciculating dose of a nondepolarizing relaxant may actually slow the onset of succinylcholine and produce poorer conditions for tracheal intubation.15 However, despite the questionable pharmacologic reasoning and controversy, concomitant administration of an AChR-antagonist (the nondepolarizing relaxant) and an AChR-agonist (succinylcholine) is an accepted practice.
Some neurologists prefer that long-term paralytics like Norcuron not be used in suspected stroke patients so that a comprehensive neurological exam can be performed at the hospital. These physicians prefer benzodiazepines like Valium (diazepam) or Versed (midazolam) for sedation. The use of a long-term paralytic should be encouraged if there is potential for losing a secured airway to a combative patient. All patients should have a well-documented neurological exam prior to administration of any paralytics or sedatives.
All patients with suspected stroke who are displaying signs of hypoxia should be treated with supplemental oxygen. Treatment should be aimed at maintaining oxygen saturation levels at or above 95% and CO2 levels between 28 and 35.16 As previously stated, if the oxygen saturation falls below 95%, there is a 150% increase in mortality.7 However, there is conflicting evidence that supernormal oxygenation improves outcome. Some neurologists are advocating withholding supplemental oxygen unless the patient presents with signs or symptoms of hypoxia. Prophylactic hyperventilation of the head-injured patient is no longer recommended, and providers are encouraged to determine ventilatory support on CO2 levels and results of arterial blood gas analysis, if they are available.
Ideally, suspected stroke patients should have two intravenous lines established and blood drawn for laboratory analysis. Manage blood glucose levels below 50 (or patients with relative hypoglycemia) with dextrose, and obtain a complete set of vital signs, including a 12-lead electrocardiogram if available. Critical care transport providers should remember that all blood drawn must be appropriately labeled in order to be processed in the hospital.
Other treatment consists of elevating the head of the bed 30 to 35 degrees to aid in subtle reduction of intracranial pressure. Patients can also be placed in cervical collars to maintain the head in an upright position and aid in blood flow from the brain. Some critical care transport systems also advocate the use of ear and eye protection to prevent spikes in intracranial pressure due to outside stimulus from aircraft or sirens. Patients should also be properly assessed to determine if they will be potential candidates for thrombolytic therapy (see Figure 4).
We are fierce advocates for aggressive treatment by critical care transport providers; however, in the case of strokes, aggressive treatment by out-of-hospital personnel may be detrimental to overall patient morbidity and mortality. Treatment modalities and methodology vary by region, service and facility. As with any treatment, providers must abide by their local protocols. The risks of acutely lowering blood pressure in the field outweigh the benefits of simple transport and symptomatic care. "Primum non nocere"--first, do no harm.18
Take-Home Points joins two top-notch EMS resources: the print edition of the magazine you're presently perusing and its associated website, www.EMSResponder.com. Each month, we have more interesting and important information to share than our number of print pages allows. Some of that extra content ends up on EMSResponder. In Take-Home Points, we will offer brief summaries of some of those stories, with key information distilled for your quick consumption and immediate use. We encourage readers to digest these appetizers, then log on to EMSResponder.com/onlineexclusives and read the full articles in their entirety. Because EMS just doesn't stop after that last page.
Stroke: When Time Is REALLY of the Essence
Stroke is the No. 3 killer of middle-aged and older patients worldwide and costs around $43 billion each year in the U.S. alone. But what do you know about treating it and, potentially more important, preventing it?
Above all else, know this: Time matters in stroke as much as it does in anything. From the time a victim first experiences the signs/symptoms of stroke, there's a window of about three hours to administer tPA (tissue plasminogen activator), the fibrinolytic "gold standard" for managing the most common kind of stroke. That window must include recognition of symptoms; a call to 9-1-1 and activation of EMS; EMS response, assessment, management and transport; ED admission and assessment; and a CT scan to rule out hemorrhagic stroke.
(Hemorrhagic strokes result from bleeding within the brain or between the brain and skull. These represent a minority of strokes; around 80%-85% of cerebrovascular events are occlusive strokes, which result from a blockage of a cerebral artery. These blockages can be embolic [caused by a clot that breaks free elsewhere in the body and migrates] or thrombotic [formed at the site of occurrence in the brain]. Embolic events happen suddenly, while thrombotic events develop over time.)
It is imperative, then, for EMS providers to recognize the signs and symptoms of stroke and act decisively to aid its victims. Look for things like severe headache; weakness or paralysis on one side of the body; slurred, inappropriate or unintelligible speech; drooping of one side of the face; and altered mental status. Sufferers may also display memory/judgment problems, impaired vision or problems reading and writing.
As you arrive at the scene of a potential stroke, form a general impression as you approach. Work to rule out possibilities that manifest similarly (drug/alcohol use, diabetes, head trauma, seizure). Use the Cincinnati Prehospital Stroke Scale--if any of your findings are abnormal, load and get moving to a destination hospital equipped to manage stroke. Call ahead and get the stroke team activated, and provide supportive care in transit.
The risk of stroke can be cut by reducing tobacco/alcohol/drug consumption, and treating hypertension and underlying cardiac disease. Encourage this, and fast action when signs and symptoms occur.
For more on the recognition and prehospital treatment of strokes, see Christopher Potter's associated article Brain Attack! What to Look For and How to Deal With Stroke on www.EMSResponder.com. Potter, NREMT-P, CCEMT-P, is a paramedic supervisor with Huntsville (AL) Emergency Medical Services and affiliate faculty with the Alabama ITLS program, as well as an instructor in ACLS, CPR, PALS, PHTLS and EVOC. Contact him at firstname.lastname@example.org.
- Mann JA. Guide Map to Hypertensive Emergencies. www.emguidemaps.homestead.com/files/hypertension.html.
- Tintinalli JE, et al. Emergency Medicine: A Comprehensive Study Guide, 5th Edition. American College of Emergency Physicians. McGraw-Hill Companies, 2000.
- Kaplan NM, Rose BD, Treatment of Hypertension Following CVA. MCOMS Doctor's Network. http://mcomsdoctors.8m.com/htncva.html.
- The Brain Attack Coalition. www.stroke-site.org/orders/ischemic_stroke_tia_orders.doc.
- Alberts MJ. Diagnosis and treatment of ischemic strokes. Am J Med 106(2):211-221, 1999.
- Jauch EC. The Golden Hour of the Acute Ischemic Stroke, 2001. www.strokecenter.org/education/jauch/02.htm#NIH.
- Critical Care Paramedic (CCEMT-P) curriculum. University of Maryland, Baltimore County.
- Gordon DL, et al. The Emergency Management of Acute Stroke. University of Miami School of Medicine, Center for Research in Medical Education.
- McGrath BJ, Guy J, Borel CO, et al. Perioperative management of aneurysmal subarachnoid hemorrhage. Part 2: Postoperative management. Anesth Analg 81:1295-1302, 1995.
- National Institute of Neurological Disorders and Stroke (NINDS) 2005. www.ninds.nih.gov/.
- Joint Commission on Accreditation of Healthcare Organizations. www.jcaho.org.
- Walls et al. Manual of Emergency Airway Management, Second Edition. Lippincott, 2004.
- Lafferty K, et al. Rapid Sequence Induction. www.emedicine.com/emerg/topic939.htm.
- Robinson N, Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lidocaine lead to an improved neurological outcome? A review of the literature. Emerg Med J 18(6):453-457, Nov 2001.
- Miller R. Miller's Anesthesia, 6th Edition. Volume 1, Chapter 12, p. 424.
- Jauch E, Kissela B. Acute Stroke Management. www.emedicine.com/neuro/topic9.htm.
- Harold PA et al. Guidelines for thrombolytic therapy for acute stroke: A supplement to the guidelines for the management of patients with acute ischemic stroke. Circulation 94:1167-1174, 1996.
- Rodenburg H. Less is more in the prehospital management of hypertension. J Emerg Med Serv, November 2004.
Mike Clumpner, AA, AAS, BS, MBA, NREMT-P, CCEMT-P, EMT-T, FP-C, is a firefighter/paramedic for the Charlotte Fire Department where he is assigned to the Special Operations Division. He is also a paramedic/rescue technician assigned to North Carolina Urban Search and Rescue Task Force 3 (NCTF-3) and he works as a flight paramedic with Regional One Air Medical Service in Spartanburg, SC. He can be reached at Clumpner@aol.com.
Jim Mobley, BSN, RN, CEN, CFRN, NREMT-P, FP-C, is the program director/chief flight nurse for Regional One Air Medical Service in Spartanburg, SC. A former Army combat medic, Mobley served several tours in Desert Storm. He can be reached at FlightNurseJim@aol.com.