Ace844

Did they put a poster like this in their truck too!?!?!!!!! With the byline of Chechnyan's not welcome and will be left fro dead!! :wink:

"PRPG," Sadly, IMHLO, the management, administration, and owners for the most part don't want a highly trained, educated and professional EMS force, as it would force them to pay more, provide a better more professional work environment, and in general eat into their profit margin. This is part of the reason why you see some private and municipal providers fighting new equipment requirements at the state level, etc....Sadly, I think it will take nothing short of an act of god, to bring the providers, management, and docs/DPH's together to create a cohesive, functioning, progressive, educated, professional, EMS practice environment. To further answer your question, if the companies and management/marketing apparatus were to approach their contracts with a cohesive, well defined explanation of how they were planning to improve education, service, and pt care, and present it to them with a timeline, and explanation, that there may be periods of time where the service delivered will be affected but that it would be for the better. I bet, you'd find a more recptive client...and less adverse action/lost revenue, than if they were to just do it without any of the aforementioned actions... Furthermore, I think that the medical directors may be willing to put more effort into their EMS system, if they were adequately compensated for it, as well as having the support of the providers/hospital admin in the system of being willing to undergo, more training, and perhaps previously unrequired oversight for a short time until they got to know the providers...and thus their capabilities. From this they would be able to form an objective measure of system status, and the services would benefit from their insight and input into how they could best improve and grow in a positive direction. YMMV, JMHLO & .02... out here, Ace844

Hi All, I saw this article and thought it provided alittle bit of evidence at least in part to support soemthing which is punded into everyone from the lay-person, to MD...thoughts anyone?? Emergency Medicine Journal 2005;22:867-868; doi:10.1136/emj.2004.019257 © 2005 by BMJ Publishing Group Ltd, and British Association for Accident and Emergency Medicine This Article Relationship between Trendelenburg tilt and internal jugular vein diameter S Clenaghan, R E McLaughlin, C Martyn, S McGovern and J Bowra Ulster Hospital, Belfast, Northern Ireland Correspondence to: S Clenaghan Ulster Hospital, Upper Newtownards Road, Belfast, Northern Ireland; stepclen@hotmail.com Objectives: To evaluate the relationship between Trendelenburg tilt and internal jugular vein (IJV) diameter, and to examine any cumulative effects of tilt on the IJV diameter. Methods: Using a tilt table, healthy volunteers were randomised to Trendelenburg tilts of 10°, 15°, 20°, 25°, and 30°. Ultrasound was used to measure and record the lateral diameter of the right IJV at the level of the cricoid cartilage. Following each reading the table was returned to the supine position. Balanced randomisation was used to assess cumulative tilt effects. Results: A total of 20 healthy volunteers were recruited (10 men, 10 women). Mean supine IJV diameter was 13.5 mm (95% CI 12.8 to 14.1) and was significantly greater at 10° (15.5 mm, 95% CI 14.9 to 16.1). There was no significant difference between 10° and greater angles of tilt. The effect of the previous angle of tilt did not prove to be statistically significant. Conclusion: Increasing the degree of Trendelenburg tilt increases the lateral diameter of the IJV. Even a 10° tilt is effective. The cumulative effect of tilt (that is, the effect of the previous angle) is not significant. Ultrasound guided cannulation is ideal, but in its absence Trendelenburg tilt will increase IJV diameter and improve the chance of successful cannulation. While 25° achieved optimum distension, this may not be practical and may be detrimental (for example, risk of raised intracranial pressure). Out here, Ace844

Well spoken by someone with the wisdom and experience of actually having done these things to back it all up....In addaition, for all those who think it's easy try telling an 8yo who just had to call 911 because his mommy just went unresponsive and isn't breathing, because she took more than her usual 8 ball today. That she just isn't worth saving because shes a junky. Calousness isn't compassion, neither is indiscrimenate apathy warranted.. It's kind of funny sometimes how people expose their lack of experience and naivete when they post..:cheers: "asys". Having said that, I think its sad that it needs to even be explained especially to a group of people/professionals who "suppossedly" deal with these issues all the time.... out here, Ace844

Well spoken by someone with the wisdom and experience of actually having done these things to back it all up....It's kind of funny sometimes how people expose their lack of experience and naivete when they post..:cheers: "asys". Having said that, I think its sad that it needs to even be explained especially to a group of people/professionals who "suppossedly" deal with these issues all the time.... out here, Ace

I believe our esteemed colleugue from NYC's Handle is short for "ASYSTLOE IN @ LEADS">>>>..But, I'm quite sure that he will correct us both if we are wrong..!! So thus your attack and assumptions are unwarranted.. out here, Ace844

Thank you..

"Asys," With all respect, this may not be true in all areas, for example. In my state the protocol is as follows:: and you can find it here;MA OEMS protocol appendix5_1 APPENDIX C: CESSATION OF RESUSCITATION (Effective 2/1/05) PURPOSE: 1) TO CLARIFY FOR EMS SERVICES AND THEIR EMTS WHEN RESUSCITATIVE MEASURES MAY BE WITHHELD FOR PATIENTS IN CARDIAC ARREST AND 2) TO DEFINE WHEN EMTS CAN CEASE RESUSCITATIVE MEASURES ALREADY INITIATED. Background and EMS Services’ Training/Support Services Obligations: Emergency Medical Technicians must begin or continue resuscitative measures for all patients in cardiac arrest except as indicated in this Protocol (also issued as Administrative Requirement (A/R) 5- 515). If in doubt, begin resuscitative efforts. All EMS services must provide appropriate training on management of death in the field, including legal, procedural, and psychological aspects; and access to support services. EMS services and EMS personnel should be aware that the nursing staff of a health care facility, such as a skilled nursing facility, may need a physician order (including a medical control physician’s order, if allowed by nursing home policy) to halt resuscitation attempts, even in the case of patients meeting EMS “obvious death†criteria, as set out below. Nursing staff and EMS personnel should come to a cooperative decision on continuation or termination of resuscitation; this process may include obtaining physician input and orders. If the medical professionals at the bedside are unable to reach agreement on attempting or terminating efforts, the presumption should be to continue resuscitative efforts and transport the patient to an emergency department. I. EXCEPTIONS TO INITIATION OF RESUSCITATION Other than in overriding circumstances such as a large mass-casualty incident or a hazardous scene, the following are the only exceptions to initiating and maintaining resuscitative measures in the field: 1. Current, valid DNR, verified per the Comfort Care Protocol. 2. Trauma inconsistent with survival a. Decapitation: severing of the vital structures of the head from the remainder of the patient’s body b. Transection of the torso: body is completely cut across below the shoulders and above the hips c. Evident complete destruction of brain or heart d. Incineration of the body e. Cardiac arrest (i.e. pulselessness) documented at first EMS evaluation when such condition is the result of significant blunt or penetrating trauma and the arrest is obviously and unequivocally due to such trauma, EXCEPT in the specific case of arrest due to penetrating chest trauma and short transport time to definitive care (in which circumstance, resuscitate and transport) 3. Body condition clearly indicating biological death. a. Complete decomposition or putrefaction: the skin surface (not only in isolated areas) is bloated or ruptured, with sloughing of soft tissue, and the odor of decaying flesh. b. Dependent lividity and/or rigor: when the patient’s body is appropriately examined, there is a clear demarcation of pooled blood within the body, and/or major joints (jaw, shoulders, elbows, hips, or knees) are immovable. Procedure for lividity and/or rigor: All of the criteria below must be established and documented in addition to lividity and/or rigor in order to withhold resuscitation: i. Respirations are absent for at least 30 seconds; and ii. Carotid pulse is absent for at least 30 seconds; and iii. Lung sounds auscultated by stethoscope bilaterally are absent for at least 30 seconds; and iv. Both pupils, if assessable, are non-reactive to light. II. Cessation of Resuscitation by EMTs Emergency Medical Technicians must continue resuscitative measures for all patients in cardiac arrest unless contraindicated by one of the exceptions below. 1. EMTs, certified at the Basic, Intermediate and Paramedic levels, may cease resuscitative efforts at any time when any “Exception to Initiation of Resuscitation†as defined in I., above, is determined to be present. 2. EMTs certified at the Paramedic level only may cease resuscitative efforts in an adult patient 18 years of age or older, regardless of who initiated the resuscitative efforts, without finding “obvious death†criteria only by the following procedure, and only if the EMS system’s Affiliate Hospital Medical Director has approved of use of this procedure, as follows: a. There is no evidence of or suspicion of hypothermia; AND b. Indicated standard Advanced Life Support measures have been successfully undertaken (including for example effective airway support, intravenous access, medications, transcutaneous pacing, and rhythm monitoring); AND c. The patient is in asystole or pulseless electrical activity (PEA), and REMAINS SO persistently, unresponsive to resuscitative efforts, for at least twenty (20) minutes while resuscitative efforts continue; AND d. No reversible cause of arrest is evident; AND e. The patient is not visibly pregnant; AND f. An on-line medical control physician gives an order to terminate resuscitative efforts. III. Special Considerations and Procedures: 1. In all cases where a decedent is left in the field, procedures must include notification of appropriate medical or medico-legal authorities. 2. EMS documentation must reflect the criteria used to determine obvious death or allow cessation of resuscitative efforts. So as mentioned earlier you should be familiar with your clinical policies, protocols/practice parameters, etc... hope this helps, Ace844

What???????......Ipratropium Bromide is related to this thread how again...? Please explain and clarify your post... out here, Ace844

"AnthonyM83 & others," I agree with "Dust, and Kev," et. al. in their posts and opinions on this. I will further say that if you don't search your patient's and or make sure they are unarmed, etc...than you are putting yourself at risk and may not go home afetr that call. Next, if you fail to search your patients as mentioned here because you are worried, about jeopardizing the "rights" of a patient or some scumbag whose intent it is to hurt you, the solution is simple. 1.) Wriet a registered letter to your areas Attorney Generals office and or presiding legal authority/court system and ask for a letter of opinion on the applicable statues, etc... 2.) Write another "registered" letter to the DPH/OEMS of the state or area in which you work and aks for a second letter of opinion/policy and for guidance on this matter. By doing the above actions you will have your answer and if you act within those guidlines, you will be protected... out here, Ace844

UPRH= Uncontrolled PortaRican Hysteria HHS= Hatian Hysterical Syndrome MARS= Met At Road with Suitcase LOLINAD= Little Old Lady In No Acute Distress Aetna Pain Radiating to the Prudential= Extensive "Pain" post a low to no speed MVC or other similar trauma...

"Para," There are a few reasons a psych is transported to an ER first. A.) To rule out primary medical/tox causes which may be causing said psych issue. B.) To screen the patient to determine whether admission is waranted and to give them access to the opportunity to get EMH help. C.) To find the most appropriate facility for them and where their insurance (should they have it) pay for them to go. On your second point, about EMS vs PD, I think it is a mix of: A.) Law enforcement laziness and unwillingness to "transport" someone, potentially out of town (thus placeing the town down one less available PD unit) to an ER. B.) The fact that because some psych d/o's are caused by medical issues, if they are missed than the patient may die or suffer permenant damage, placing the PD in a potentially -/teneable litigous position as medicine is not in their "role" Thus you find yourself with the current state of affairs....In my area we take all of the psychs via EMS means period, first to an ER then potentially later to the psych facility its self. The only notable exception I have seen is when a prisoner is already in the PD system and gets brought directly to an ER by them due to EMH issues. It should be noted that even in this even sometimes we transport the patient with LE. In the end YMMV, and it depends on your area. IMHLO, its a LE function and should eb handled by them in the majority of cases. If they feel uncomfortable, then an EMS unit should meet them at their location, do a full assessment, and if they find no serious medical issues, off they go with the PD!! For those of you who work in systems where the PD does this on any kind of regular basis, consider yourself lucky. out here, Ace844

It would probably be a good idea for you to actually read the thread to which your responding. This applies to Law enforcement as noted above. Next, you are looking for weapons, and to protect yourself, not to try to "find" something to send your patient to jail. Furthermore, that doesn't mean that you may not choose to involve the police once "illegal items" are found. Also, for those who are interested. You should not be placeing your hands into pockets you can't see into. Take your trauma shears and cut the pocket down its outside seam. This will cause the objects in the pocket to fall out or be exposed. Agreed. out here, Ace844

Any one else have any input on this?????

"Buddy," I apologize, we spoke earlier about this...I was under the impression that you were conducting "Field trials-in the street" with local EMS units. I was curious about the prelim data, etc.... Also, i have the BNp stuff for you which we spoke about and i will send it vais e-mail when i get home. out here, Ace844

On the device and it's field use...and efficacy..???

"Buddy," Do you have any new info. re: your studies...on this topic...? thanks, Ace844

i guess this is as pertinent now as before....any other thoughts.....?

HMMM....Let's see, where to begin. Ok, for everyone interested, here's a "pic and article" about the machine;:: http://www.yet2.com/app/insight/techofweek/35135?sid=200 , http://www.bjhc.co.uk/news/industry/2004/ind40920.htm. As you can see it is small, portable and "space friendly". The insurance companies would most likely not re-imburse services using this technology for quite sometime, next you have to take into consideration the immense battle you would have to fight to get the FDA, State OEMS, your local service, and MD director to even allow you to use it. I mean at just a dollar per "exposure" cost it isn't prohibitively expensive in operating cost. Then as mentioned there is the huge training and saftey requirement and the actual efficacy of the machine vs its impact on patient care treatment modialities and changes it would or wouldn't take effect. I said this previously and I will say it again. I would be dumbfounded if even 2% of current cert/licenced Medics even knew the basics of interpreting an X-ray, MRI or CT !!!!!! Next, even if in this 2% there were medics who could "interpret" them, what difference would it make to your treatment. It would make little to none. Even in the ER the majority of urgent and emergent treatment is based on H/P alone. Next you have the other issues of physics...Penetration, density, etc.....add an unstable environment, a patient in extremis and "upset" and you have a recipe for many "useless" films, unned rad exposure,etc... As "rid," and others mentioned you also have the issue that the hospital may not even accept "the ambulance films" and need to "repeat them". As I mentioned before, even with "a minimal amount of training" using this machine pre-hospital would be akin to giving a FR or layperson a 12 lead monitor and training them "how to do" a 12 lead placement, etc... but leaving out all of the ancillary important stuff that goes with it. What you would have then is an item which would be "cool" but serve little clinical purpose, and not change the pt care provided...:study::dontknow::sign3:....:tongue3: CXR:: http://www.vh.org/pediatric/provider/pediatrics/ElectricAirway/RadImages/DoubleAorticArchCXR.html ://http://www.vh.org/pediatric/provide...icArchCXR.html ://http://www.vh.org/pediatric/provide...icArchCXR.html ://http://www.vh.org/pediatric/provide...icArchCXR.html ://http://www.vh.org/pediatric/provide...icArchCXR.html , neck A/p::: http://www.vh.org/pediatric/provider/pedia...alAirwayAP.html out here, Ace844 ________________________________________________________________________________ ________________________ F.REAKIN I.DIOTS R.IDE E.NGINES ONLY THE BEST DO EMS!!

Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder characterized by unexplained left ventricular hypertrophy (increased muscle thickness), myocyte disarray (disorganized cardiac cells) and fibrosis (see Figure A, below). It is the most common heritable cardiovascular disorder with an estimated prevalence of 1/1000 in the general population. Genetic studies have defined HCM as a disease of the sarcomere, with more than 250 mutations identified in 10 different components of the contractile apparatus of the heart. Although associated with an increased risk for progressive heart failure and sudden death, the complexity and diversity of HCM impose significant challenges to clinical management. Figure A: Microscopic picture of a heart with HCM showing myocyte disarray and fibrosis (blue) Figure B: Normal heart histology echocardiogram of a heart with HCM. Diagnosis, Management and Treatment of Hypertrophic Cardiomyopathy (HCM) An integrative approach is essential for optimal management of patients and families with hypertrophic cardiomyopathy, with particular attention to unique features of this disorder: · Genotypic analysis to allow for definitive diagnosis · Comprehensive evaluation of affected individuals (cardiac imaging, exercise testing, surveillance for dysrhythmias) · Family screening · Stratification regarding risk for sudden cardiac death · Implantable Cardioverter Defibrillator and pacemaker therapy · Alcohol septal ablation for treatment of refractory obstructive HCM · Surgical septal myomectomy/myotomy for treatment of refractory obstructive HCM · Management of end-stage heart failure, including cardiac transplantation Learn More About Hypertrophic Cardiomyopathy: · http://www.brighamandwomens.org/cvcenter/S...enetics/HCM.pdf · [video width=400 height=350:be943aa488]http://www.brighamandwomens.org/cvcenter/HCMHeartvideo.asp[/video:be943aa488] In case you can't get the video here is the link:: http://www.brighamandwomens.org/cvcenter/HCMHeartvideo.asp Hope this helps, ACE844

Hi All, Here's part 4 in my CHF series.... Hope this helps, ACE844 Cardiomyopathy Definition Cardiomyopathy refers to heart muscle disease. The damaged heart does not effectively pump blood. The disease usually progresses to the point where patients develop life-threatening heart failure. In addition, people with cardiomyopathy are more likely to have irregular heartbeats or arrhythmias. There are two major categories of cardiomyopathy. When the heart muscle is damaged from heart attacks due to coronary artery disease that is called ischemic cardiomyopathy. The less common category of cardiomyopathy is nonischemic. That category includes types of cardiomyopathy that are not related to coronary artery disease. There are three main types of nonischemic cardiomyopathy: Dilated Damaged heart muscles lead to an enlarged, floppy heart. The heart stretches as it tries to compensate for weakened pumping ability. Hypertrophic Heart muscle fibers enlarge abnormally. The heart wall thickens, leaving less space for blood in the chambers. Since the heart does not relax correctly between beats, less blood fills the chamber and is pumped from the heart. Restrictive ? Portions of the heart wall become rigid and lose their flexibility. Thickening often occurs due to abnormal tissue invading the heart muscle. Hypertrophic Heart :: , http://catalog.nucleusinc.com/generateexhi...TL=9985&A=2 Causes In many cases, the exact cause is not known. Possible causes include: Dilated The cause of the initial damage is often not found but may include: · Ischemic heart disease, with decreased blood flow to the heart · Infections, usually viral · Chronic exposure to toxins, including alcohol and some chemotherapy drugs · A rare complication of pregnancy or childbirth (probably immune related) · Rarely, other illnesses, including rheumatoid arthritis, diabetes, or thyroid disease Hypertrophic · Inherited: sometimes present at birth but often developing in teens · With aging: associated with hypertension Restrictive usually related to another condition, such as: · Amyloidosis ? protein fibers collect in the heart muscle · Sarcoidosis ? small inflammatory masses (granulomas) form in many organs · Hemochromatosis ? too much iron in the body Risk Factors A risk factor is something that increases your chance of getting a disease or condition. · Family members with cardiomyopathy · Alcoholism · Obesity · Diabetes · Hypertension · Coronary artery disease · Certain drugs Symptoms Symptoms vary, depending on the type of cardiomyopathy and its severity. Patients with hypertrophic cardiomyopathy often do not notice any symptoms. Sudden cardiac death may be the first indication of the condition. In dilated cardiomyopathy, it may take years for symptoms to develop. Blood clots may form due to the abnormal pooling of blood in the heart. If a clot moves to another part of the body (embolism), symptoms associated with that organ (the brain, for example) may be the first sign of the heart disease. Cardiomyopathy ultimately leads to heart failure and the following symptoms: · Fatigue · Weakness · Shortness of breath, often worse when lying down and with exertion · Cough · Swelling in feet or legs · Chest pain · Irregular heart rhythm Diagnosis The doctor will: · Ask about your symptoms and medical history · Perform a physical exam · Listen to your heart with a stethoscope (cardiomyopathies often produce heart murmurs and other abnormal heart sounds) Tests may include: Chest X-ray ? to look for heart enlargement Electrocardiogram ? a test that records the heart's activity by measuring electrical currents through the heart muscle Echocardiogram? a test that uses high-frequency sound waves (ultrasound) to examine the size, shape, and motion of the heart Blood Tests ? to check for damage to the heart and other organs, and possibly the underlying cause(s) of the cardiomyopathy Cardiac Catheterization ? a tube-like instrument inserted into the heart through a vein or artery (usually in the arm or leg) to detect problems with the heart and its blood supply Heart Biopsy ? removal of a sample of heart tissue for testing Treatment No treatment, short of a heart transplant, can reverse the damage already done to the heart muscle. Treatment aims to relieve symptoms and prevent further damage. If a treatable underlying cause is found, treatment will be started to address the problem. Lifestyle Modification Changes aim to eliminate anything that contributes to the disease or worsens symptoms: · Avoid alcohol. · Lose weight, if you are overweight. · Eat a low-fat diet to minimize the risk and extent of coronary artery disease. · Limit salt intake to decrease fluid retention. · Follow your doctor's advice for exercise. You may need to limit physical activity. Medications Medications may include: · Diuretics ? to eliminate extra fluid · ACE inhibitors ? to help relax blood vessels, lower blood pressure and decrease the heart's workload · Digitalis ? to slow and regulate the heart rate, and modestly increase its force of contractions · Calcium channel blockers ? to lower blood pressure and relax the heart · Beta blockers ? to slow the heart and limit disease progression · Anti-arrythmia agents ? to prevent irregular heart rhythms · Immune system suppressants ? including steroids (depending on underlying cause) Surgery Surgical options include: · A pacemaker may be implanted to improve the heart rate and pattern. · For patients with hypertrophic disease, doctors may remove part of the thickened wall separating the heart's chambers. Surgery may be needed to replace a heart valve. · A heart transplant may be possible for otherwise healthy patients who do not respond to medical treatment. Candidates often wait a long time for a new heart. Those waiting may temporarily receive a ventricular assist device, which is a mechanical pump that assumes some or most of the heart's pumping function. Prevention Aggressively treating hypertension, coronary artery diseases, and their risk factors is the best way to prevent most cases of cardiomyopathy. Other less common causes, however, are not preventable. People with a family history of the disease should ask the doctor about screening tests, especially before starting an intense exercise program. RESOURCES: American Heart Association http://www.americanheart.org The Cardiomyopathy Association http://www.cardiomyopathy.org/homepage.htm References: Braunwald E, Zipes DP, Libby P, et al. Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, PA: W. B. Saunders Company; 2001. Cecil RL, Goldman L, Bennett JC. Cecil Textbook of Medicine, 21st ed. Philadelphia, PA: W. B. Saunders Company; 2000. Dambro MR. Griffith's 5-Minute Clinical Consult, 2001 ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001. National Heart, Lung, and Blood Institute website. Available at: http://www.nhlbi.nih.gov/. Accessed October 13, 2005. Primary Care Medicine, 4th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2000

Hi everyone, After talking with both an ER doc and a Neurologist in my area I came to realize that even after almost 5 years of evidence based research showing that intraarterial TPA is useful and helps decrese mortality, it is still quite scarsely used around here. So it got me to wondering if it is available in your area...Included in the post are some images of normal anatomy, and some info on CVA Rx as well. It seems that here it is available at our level 1 Center during bankers houyrs or when they "call in the team", yet in Boston, and Providence they have it 24/7 at 2 level 1 Centers... January 2005 Stroke: While Current Treatment Is Limited, New Options Are on the Horizon MARC FISHER, MD, and JURGEN BARDUTZKY, MD Current therapy for acute ischemic stroke remains limited to intravenous recombinant tissue plasminogen activator (tPA) administered within 3 hours of symptom onset, but despite strong evidence supporting its effectiveness,1-5 only 2% to 4% of all stroke patients currently receive tPA.4 The major impediment to use of tPA is the late arrival of many stroke patients at the emergency department for evaluation and treatment. Fortunately, other treatment options are on the horizon. THE 3- TO 6-HOUR WINDOW The value of intravenous tPA given outside the 3-hour window is being studied. Although the efficacy of thrombolysis initiated later than 3 hours after the onset of acute ischemic stroke has not been proved in a clinical trial, 2 metaanalyses suggest that intravenous tPA significantly reduces the risk of disability and death when started between 3 and 6 hours later. The number needed to treat (NNT) was 11 (0 to 6 hours) or 25 (3 to 6 hours); for intravenous tPA initiated within 3 hours, the NNT was 8.6,7 Additional trials in the 3- to 6-hour window are needed to establish efficacy and to determine tablish efficacy and to determine which patient subgroups are most responsive. For now, however, thrombolytic therapy with tPA in the 3- to 6-hour window should not be initiated outside of research protocols. Although administration of tPA more than 3 hours after symptom onset may benefit some patients, the interval between onset of symptoms and initiation of thrombolysis remains an essential factor in treatment, because therapeutic efficacy decreases even within the 3-hour window.2 To achieve optimal results, thrombolysis should be initiated as soon as possible after the onset of stroke.8 Thus, the ability to achieve rapid stroke onset" to-hospital and door-to-needle times will continue to be an important factor in the management of acute stroke. Appropriate patient selection is crucial—especially to prevent bleeding. How to determine which patients are the best candidates for tPA treatment is a matter of ongoing investigation. In a recent report from a single center, among 216 patients treated with tPA, predictors of lack of response to treatment were glucose levels greater than 144 mg/dL, cortical involvement determined by clinical features, and time to treatment.9 In addition, other factors that appear to affect the risk/benefit ratio of thrombolysis for a particular patient include: · Extent of signs of early infarct on CT scan. · Initial severity of stroke, based on National Institutes of Health Stroke Scale (NIHSS) score. · The patient's age. Whether patients with extensive early ischemic changes on the initial CT scan are eligible for tPA during the first 3 hours after symptom onset remains an unanswered question. The only CT cri- terion currently required for intravenous tPAtreatment (based on results of the National Institute of Neurological Disorders and Stroke [NINDS] trial) is the exclusion of intracerebral hemorrhage (ICH). A reevaluation of NINDS CT data showed no correlation between early infarct signs and either outcome or ICH rate.10 However, other studies have reported that an early CT hypodensity covering more than half of the middle cerebral artery (MCA) territory is associated with an 85% risk of fatal outcome and that patients with a hypodense area of more than one third of the MCA territory receive no benefit from tPA treatment and are at increased risk for symptomatic ICH.11,12 These large hypodensities represent irreversibly damaged tissue. Among stroke experts, there is a growing consensus that patients with signs of profound ischemia and a large hypodensity on a CT scan should not be treated with tPA—even within the 3-hour window— because of the excessive risk of ICH and the likelihood that they will not respond to therapy. Some experts advise against the use of intravenous tPA in patients with very mild (NIHSS score less than 4) or severe (NIHSS score greater than 25) stroke. In the former setting, the natural history is favorable, and in the latter, the risk of ICH and poor outcome is high.13,14 However, precise clinical criteria for these exclusions have not been established. The prognosis for patients with basilar artery occlusion is poor, with a high degree of associated mortality. In some centers, intra-arterial thrombolytic therapy is used and improved outcome has been observed. In a recent study, the efficacy of intravenous tPA for basilar occlusion was reported. Patients were treated up to 12 hours after onset when onset of symptoms was sudden and up to 48 hours after onset when symptoms were determined to be gradually progressing.15 Partial or complete reperfusion was observed in 26 (60%) of 43 patients with followup vascular imaging. At 3 months, 20 of 50 had died, and 12 patients (24%) were performing activities of daily living independently. As for elevated blood glucose levels, the effects of admission hyperglycemia on stroke outcome are still not fully understood, and there are still no data that show the impact that maintenance of euglycemia during an acute stroke has on outcomes. However, several clinical studies have shown an association between admission hyperglycemia and poor outcome.16,17 In a retrospective analysis of 1205 patients with acute ischemic stroke who received intravenous tPA, a normal pretreatment blood glucose level was an independent predictor of a good outcome.18 An analysis of the NINDS trial data showed that higher glucose levels on admission were associated with a significantly reduced likelihood of a desirable outcome and a significantly increased risk of symptomatic ICH—regardless of tPA treatment.19 It remains to be determined whether these findings represent a cause-and-effect relationship or a stress response reflective of more severe stroke. Lowering an elevated blood glucose level during acute stroke to as close to a normal value as possible may be an optimal strategy. However, at this time, no clear evidence exists to justify withholding tPA treatment because of hyperglycemia in patients who have acute ischemic stroke. Imaging of cerebral ischemia has progressed in recent years and holds promise as a tool that can improve patient selection. In patients with acute stroke, diagnostic imaging must be able to: · Accurately assess vascular status (the presence and location of vessel occlusion). · Accurately assess tissue injury (demonstrate both irreversibly damaged brain tissue and potentially salvageable ischemic tissue). · Reliably exclude ICH. New MRI sequences and modern CT techniques, such as CT angiography and perfusion CT, may have the potential to fulfill these criteria. Diffusion-weighted MRI (DWI) can delineate ischemic brain tissue within minutes of stroke onset, while perfusionweighted MRI (PWI) defines the area of cerebral hypoperfusion. The absolute volume difference— or ratio of PWI to DWI ("mismatch")— reveals ischemic tissue that may be at risk for irreversible damage but is still potentially salvageable (the "ischemic penumbra"). MR angiography can reliably assess vessel status, and T2 sequences can establish a diagnosis of ICH within the first hours after stroke onset.20 Together, these MRI findings make it unnecessary to rely on a therapeutic window that is defined strictly by time and permit individualization of the time window for each patient, although controversy over specific MRI criteria for thrombolysis remains. A recent nonrandomized trial that involved 139 patients showed that "stroke MRI""guided tPA therapy appears to be safe and effective beyond a 3-hour window.21 This observation will have to be proved in a randomized placebo-controlled clinical trial. There have been concerns that MRI might be insensitive for the detection of ICH and could not be used alone for early stroke diagnostic imaging. A recent study comparing MRI with CT for detection of acute ICH demonstrated that gradient-recalled echo MRI was more sensitive than CT for hemorrhage detection.22 INTRA-ARTERIAL THROMBOLYSIS Intra-arterial thrombolysis may offer the advantages of higher recanalization rates and shorter times to eventual recanalization. 23,24 In patients who have vertebrobasilar thrombosis, intra-arterial thrombolysis is the only therapy to date that has reduced mortality and improved outcomes. Moreover, the window for thrombolysis in the posterior circulation— while not currently established— may be 12 hours or more after stroke onset. However, these findings are not from a randomized trial. There are only 2 published randomized studies of intra-arterial thrombolysis, and the procedure is not FDA-approved. The Prolyse in Acute Cerebral Thromboembolism (PROACT) trials I and II showed that intra-arterial thrombolysis administered within 6 hours of stroke onset was more beneficial than an intravenous approach in patients with severe stroke (NIHSS score between 11 and 20) secondary to proximal occlusion of the MCA.23 However, the investigators employed an agent (recombinant prourokinase) that is not available for clinical use. Most centers that perform intra-arterial thrombolysis use tPA, and data on the efficacy and safety of intra-arterial administration of tPA are limited. Two additional problems restrict the use of this therapy: · Limited availability of centers with experienced personnel and immediate access to angiography and interventional neuroradiology. · The delay required to mobilize the resources to perform the intraarterial procedure. A pilot study that investigated the combination of low-dose intravenous tPAgiven within 3 hours of symptom onset and intra-arterial tPA given later demonstrated the feasibility and safety of this approach. Additional study is required to prove its effectiveness.25 OTHER EXPERIMENTAL RECANALIZATION STRATEGIES Thrombolytic agents. Reteplase, a third-generation tPA, has been used in small series of patients with acute stroke but has yet to be evaluated in a controlled trial.26 The lytic agent desmoteplase (which has a longer half-life than tPA) was tested in the Desmoteplase in Acute Stroke (DIAS) study in a 3- to 9-hour window in patients with proven MCA occlusion and a significant PWI/DWI mismatch. The study demonstrated substantially better early reperfusion with desmoteplase and also clinical efficacy with the highest dose used in this dose-escalation study.27 An additional study to confirm this preliminary finding has been completed, and more extensive studies are being planned. Evidence from a series of clinical trials suggests that another agent, ancrod, an enzyme that degrades fibrinogen, may improve outcomes in patients treated within 3 hours of the onset of stroke.28 Further, 2 studies have shown that abciximab, a glycoprotein (GP) IIb/IIIa receptor antagonist, has a reasonable safety profile and shows a trend toward benefit in treated patients.29 Combinations of tPA or reteplase and a GP IIb/IIIa receptor antagonist (abciximab30 or integrilin31) used in intra-arterial therapy in small series of patients with acute ischemic stroke appeared to be safe. In 37 patients who had severe stroke (average NIHSS score, 19), use of intravenous integrilin and intra-arterial tPA showed a trend toward better revascularization and clinical outcome compared with intra-arterial tPA alone.31 Endovascular interventional techniques include balloon angioplasty, mechanical removal of clots,32 laser-assisted thrombolysis of emboli, and use of ultrasoundassisted devices.33 All of these techniques are still in the experimental stage. Recently, however, the FDA approved a clot retriever that takes its name from the Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial. The Merci Retriever removes clots within the intracranial vessels. It has been approved only for clot removal, not stroke treatment. It remains unclear how safe or effective the Merci Retriever is in the setting of acute ischemic stroke. Multimodal approaches. Intravenous or intra-arterial administration of thrombolytic agents or GP IIb/IIIa inhibitors has been used to enhance the effect of mechanical clot lysis.29,30 Ongoing and future trials of various thrombolytic agents combined with different mechanical devices (and based on advanced imaging techniques) may provide important information about the feasibility and efficacy of multimodal therapy for acute stroke. An interesting recent report describes the use of continuous 2- MHz transcranial Doppler ultrasound in conjunction with intravenous tPAinitiated within 3 hours of stroke onset in 126 patients.34 The primary end points of the study were complete recanalization demonstrated within 2 hours or dramatic clinical improvement. Complete recanalization occurred in 46% of patients treated with ultrasound and tPA and in only 18% of the patients treated with tPA alone. Clinical recovery within 2 hours occurred in 29% of patients in the group that received ultrasound and tPA and in 21% of patients in the tPA-alone group. This preliminary study suggests that continuous ultrasound can enhance early clot lysis and may improve clinical outcome. NEUROPROTECTIVE THERAPY The time required for brain tissue ischemia to progress to irreversible injury varies depending primarily on the severity of the reduction in cerebral blood flow.35 The cellular events associated with the progression of injury—collectively referred to as the ischemic cascade— are complex and multifactorial. The existence of an ischemic penumbra, which is suggested by the DWI/PWI mismatch, implies that neuroprotective therapies that target aspects of the ischemic cascade might potentially salvage some portion of the penumbra, if therapy is initiated in a timely fashion and the drug can reach the affected tissue. The Table lists the types of agents that have been evaluated in clinical trials as neuroprotective drugs. Unfortunately, so far none has demonstrated unequivocal efficacy, and none is currently approved for use in patients with stroke. However, many new trials of neuroprotective drugs are under way. The complexity of the ischemic cascade suggests that a drug that targets only 1 aspect of brain injury caused by ischemia will likely have only modest benefits at best.36 Targeting multiple aspects of the ischemic cascade simultaneously is another approach to neuroprotection. 37 This can be done by using combinations of drugs that each attack a different aspect of the cascade. However, a "cocktail" approach to neuroprotective therapy will be difficult because of regulatory concerns about the testing of 2 unapproved drugs simultaneously and the potential for drug-drug interactions that could affect the safety of the trial. An alternative neuroprotective strategy that targets multiple aspects of the ischemic cascade is the use of a single drug with multiple effects. Currently available drugs such as desferrioxamine, nicotinamide, and tacrolimus have multiple mechanisms of action. An approach that used one of these drugs would avoid many of the pitfalls associated with trials of unapproved drug combinations. However, none of these drugs has been studied in patients with acute ischemic stroke; they have only been suggested for study. Neuroprotective drugs also might be used in combination with thrombolysis. This strategy has the potential to provide maximum Categories of neuroprotective drugs evaluated in clinical trials Voltage-regulated calcium channel antagonists NMDA and AMPA antagonists Sodium channel antagonists GABA antagonists Free radical scavengers and antagonists Serotonin agonists Maxi-K channel agonists Growth factors Antiadhesion molecules Nootropic agents NMDA, N-methyl-D-aspartate; AMPA, 2-(aminomethyl)phenylacetic acid; GABA, -aminobutyric acid. benefit. One way to do this would be to give a safe and effective neuroprotective drug before a patient's arrival at the hospital.38 The neuroprotective drug would enhance the survival of the ischemic penumbra, which would both increase the amount of ischemic tissue that is potentially salvageable and extend the time window for successful thrombolysis. Another way to combine neuroprotection and thrombolysis might be to give a neuroprotective drug after successful thrombolysis to impede the development of reperfusion injury. 39 Reperfusion injury is now well documented in experimental studies, and preliminary MRI data in humans also suggest that secondary injury does occur in some patients with stroke after blood flow to ischemic brain tissue has been reestablished. -- American Journal of Neuroradiology 26:2595-2601, November-December 2005 © 2005 American Society of Neuroradiology INTERVENTIONAL Intravenous Glycoprotein IIb/IIIa Inhibitor (Tirofiban) followed by Intra-Arterial Urokinase and Mechanical Thrombolysis in Stroke Salvatore Mangiaficoa, Martino Cellerinia, Patrizia Nencinib, Gianfranco Gensinic and Domenico Inzitarib a Department of Neuroradiology, Careggi Hospital, Florence, Italy b Department of Neurological and Psychiatric Sciences, Careggi Hospital, Florence, Italy c Department of Critical Care Medicine and Surgery, Careggi Hospital, Florence, Italy Address correspondence to Martino Cellerini, U.O. Neuroradiologia-CTO-Azienda Ospedaliera Universitaria Careggi, Largo Palagi, 1, 50100 Firenze, Italy BACKGROUND AND PURPOSE: The purpose of this study was to evaluate preliminarily the efficacy and safety of intravenous tirofiban combined with intra-arterial pharmacologic and mechanical thrombolysis in patients with stroke. METHODS: Twenty-one consecutive patients with an acute ischemic stroke due to major cerebral arteries occlusion and a National Institutes of Health Stroke Scale [NIHSS] score 18 were treated with an intravenous bolus of tirofiban and heparin followed by intra-arterial administration of urokinase coupled with mechanical thrombolysis. RESULTS: Thirteen patients had an anterior circulation stroke (T-siphon internal carotid artery [iCA]=7; middle cerebral artery [MCA]=6), 6 patients a posterior circulation stroke, and 2 patients an anterior plus posterior circulation stroke (left ICA or M1 tract of MCA plus basilar artery occlusions). Mean NIHSS score on admission was 21 (range, 18–27). Immediate recanalization was successful (thrombolysis in myocardial infarction [TIMI] 2–3) in 17 of 21 patients. The following day, 14 of 19 patients improved substantially and complete vessel patency (TIMI 3–4) was confirmed by digital subtraction angiography. Intracranial bleeding occurred in 5 of 21 patients (3 symptomatic cerebral hemorrhages and 2 subarachnoid hemorrhages) and was fatal in the case of 3 patients. At discharge, the mean NIHSS was 5.4 (range, 0–25). Overall, at 3-month follow-up the functional outcome was favorable (modified Rankin Scale score = 0–2) in 13 of 21 (62%) patients. Death (including all causes) at 90 days occurred in 6 of 21 (28%) cases. CONCLUSIONS: The combination of intravenous tirofiban with intra-arterial urokinase and mechanical thrombolysis may be successful in reestablishing vessel patency and result in a good functional outcome in patients with major cerebral arteries occlusions. (Stroke. 2005;36:865.) © 2005 American Heart Association, Inc. Derivation of Transcranial Doppler Criteria for Rescue Intra-arterial Thrombolysis Multicenter Experience From the Interventional Management of Stroke Study Maher Saqqur, MD; Ashfaq Shuaib, MD, FRCPC; Andrie V. Alexandrov, MD; Michael D. Hill, MD; Sergio Calleja, MD; Thomas Tomsick, MD; Joseph Broderick, MD Andrew M. Demchuk, MD From the Department of Medicine (Neurology) (M.S., A.S.,), University of Alberta, Alberta, Canada; University of Texas–Houston Medical School (A.V.A., S.C.), Houston, Tex; the Department of Clinical Neurosciences (M.D.H., A.M.D.), University of Calgary, Alberta, Canada; the Department of Medicine and Department of Community Health Sciences (M.D.H.), University of Calgary; and the University of Cincinnati (T.T., J.B.), Ohio. Correspondence to Dr Andrew M. Demchuk, Department of Clinical Neurosciences, Seaman Family MR Research Centre, 1403 29 St, NW Calgary, AB Canada. E-mail ademchuk@ucalgary.ca Background and Purpose— Transcranial Doppler (TCD) has the potential to identify acute stroke patients with arterial occlusion when treatment with intravenous recombinant tissue plasminogen activator (rtPA) may fail to open the vessel. We examined clinical utility and prognostic value of TCD flow findings in patients enrolled in an intravenous/intra-arterial rtPA pilot trial (Interventional Management of Stroke [iMS] study). Methods— Patients enrolled in the IMS trial who underwent urgent TCD performed before intra-arterial rtPA treatment were included. TCD findings were analyzed by a mean flow velocity (MFV) ratio using reciprocal middle carotid artery (MCA) depths bilaterally (affected MCA-to-contralateral MCA MFV ratio [aMCA/cMCA MFV ratio]). The clinical utility of TCD was determined by its ability to predict outcome and identify a proximal arterial occlusion that requires intra-arterial lysis per protocol. Results— Twenty-nine of 80 patients enrolled in IMS trial had pre–intra-arterial lysis TCD (mean age, 61±11; men-to-women ratio: 17:12; median baseline National Institutes of Health Stroke Score, 17). No temporal window was found in 3 patients (10%). Cerebral angiography was performed at mean 174±36 minutes from stroke onset. TCD was performed at median 93.5 minutes from onset. The aMCA/cMCA MFV ratio <0.6 had a sensitivity of 94% (95% confidence interval [CI], 63% to 99%), specificity of 100% (97.5%; lower CI of 54%), positive predictive value of 100% (lower CI, 80%); and negative predictive value of 86% (CI, 42% to 99%) for identifying proximal occlusion in the anterior circulation that require intra-arterial lysis. All patients with absent MCA flow (n=6) had poor outcomes (modified Rankin Scale 3) (P=0.014). Conclusion— TCD is a useful modality for evaluating the arterial circulation in acute ischemic stroke patients; it may have significant potential as a screening tool for intravenous/intra-arterial lysis protocols. Images:: Anatomy Anatomy 2 Pathophys CVAPatho phys 2Acute Stroke therepy Beyond TPA Hope this helps, Ace844