Just Plain Ruff

two of the services I worked for were what you described - hospital based. Routine response times 20-30 minutes The town the ambulances are staffed in and the hospital is in constitutes 60% of the calls so the ambulances are in the place with the highest call volume. You live in a rural area you understand that services you need will not be there immediately. It's no different for the fire department. Our rural fire department was run by the city fire department with response times similar to the ambulance The sheriff's department also had tremendously long response time. It was not out of the ordinary for our ambulance to come from the county center, the first responders to come from 10 miles away from the scene, law enforcement to come from one corner of the county to the call in the opposite corner People who live in the rural areas understand response times and it was never an issue in our county.

I am going to go out on a limb and create some controversy on this formu. I do not think this person should be revealed on this forum. If this person is revealed this post will degenerate into a den of nastyness like other posts have. We all know it will. what purpose will this serve? There's nothing that we who do not know this person can do about it. AK, I urge you to take action on your own part and alert whoever in authority be it his supervisor, instructor or parents. Maybe a forced vacation from the service is just the kick in his pants but to reveal him here will only let this community vent and many will personally attack this person. I do not support outing this person.

by the way, the first Vice president was Thomas Jefferson . the way elections went back then were that the top vote getter got the presidency and the 2nd vote amount got the vice presidency. By all means this was not a happy relationship between the two. George washington always said he didn't want to be president but who could resist after he was credited with winning the revolutionary war and giving us independence. Who would not have voted for him. But it was a very close election. Thomas Jefferson was the 2nd president by a large margin after George spent two terms in office. Third president was John Adams who I believe was Jefferson's Vice president. Need I go on?

I think the above poster got it. after reading some more responses - I say Chicken pox Any childhood history of chicken pox? How sick did this guy eventually get?

1. Yourself: accomplished 2. Your boyfriend/girlfriend?: wife 3. Your hair: short 4. Your mother? awesome 5. Your Father? God 6. Your Favorite Item:laptop 7. Your dream last night: canttell 8. Your favorite drink:water 9. Your dream car: Bond's 10. The room you are in: privacyless 11. Your Ex:history 12. Your Fears: few 13. What do you want to be in 10 years:alive 14. Who you hung out with tonight?self 15. What You're Not? rich 16. Muffins: none 17: One of Your Wish List Items: fortune 18. Time: 0704est 19. Last thing you did? drink 20. What You Are Wearing? clothes 21. Your Favorite Weather: 75 22. Your Favorite Book:history 23. The last thing you ate: food 24. Your Life: ontrack 25. Your Mood: sassy 26. Your friends: few 27. What are you thinking about right now? lunch 28. Your car: boxer 29. What are you doing at the moment?: survey 30. Your summer: repeat 31. Your relationship status: married 32. What is on your tv? not 33. When is the last time you laughed? 0707 34. last time you cried? rarely 35. School? finished

multicolored rash and blisters on hands. Fever and seizures, this doesn't sound good for this guy.

one of two things I'm thinking Meningitis that hasn't gotten bad yet Strep throat which can cause the rash and the sores in his mouth. Sores on his hands I'm at a loss for.

ok, question for this wonderful group Ok, you take a clean needle and syringe, draw up the drug, mix it in a bag or larger syringe. And bam, needle stick. How many would be worried about that stick other than the fact that they were pissed they were careless or stuck themselves?

Somedic you are right, every hospital I have transported patients to and they number in the upper double digits have always taken the 12 lead I've done and looked at it and then they immediately ordered one done on their machine. As a matter of fact, I have a friend who works closely with the cardiology group at a major cardiac Hospital and she asked them the question - do pre-hospital 12leads help them? the reply was quite interesting. Yes they do help but they rely on their hospitals 12leads more than the pre-hospital. It's good to know what rhythm or reading they got prior to arriving at the hospital but it doesn't really guide their treatment since they rely on the here and now printout of their machine. Funny but interesting answer she got.

I was doing my ambulance ride-alongs/clinicals while finishing up my hospital clinicals. Once we had the ER and ICU out of the way we were free to do ride time. But that was god, 15 years ago so I'm sure the requirements have changed since this antique went to school.

I know this insults abbott and costello but this is what I thought of when I saw this. I can imagine that if anyone of them gets injured that they would call the real service covering that area to take care of them. But yes that's an imaginative way to transport multiple patients. yeeee haw!!!!!!!!!!!!!!!!!! andy and amos sled again

so true so true but the problem with that song is that it doesnt really flow well with the music. such is life in EMS where everything doesn't flow well at times. Merry Christmas everyone

I agree, every ped code unless they were obviously dead, I've worked to the hospital. L&S yes.

Whit you wrote: So Ruff you don't respond to the hospital with a: A broken arm? A headache? A CVA? A MI? My response - of course I respond to the hospital with the above. What I don't do unless I say it happens is responding code 3 back to the hospital. Why???? Maybe we just got our signals crossed. Well 1. Broken arm - stupid reason to respond code 3 back to the hospital 2. Headache - again see above 3. CVA - depends on the situation to respond code 3 back to the ER - 90% of my patients that have cva's didn't warrant a transport to the er code 3 4. MI - why stress an already stressed heart. I know time is muscle and brain but if we give them all the meds and do the checklist and 12 lead they would benefit from a rapid but not code 3 transport. Have you ever looked in your patients eyes when you are running code 3 - there is a scared look that you can bet is transferring over to stress on their cardiac system. There are only a three types of people that I will risk my life for - myself, my children and my family. To me no-one else is worth not coming home to other than the three types of people I just mentioned.

whit, a busted skull on my hard head is definately not worth it no matter who it is. If we transport, crash and kill or hurt everyone in the ambulance for basically transporting a dead body is not worth the price at any time. So now you have a dead patient(they were that way when you found them), you have at least 2 if not more caregivers not on the street because they were injured trying to save someone. We get into the hero complex, "Oh wer'e so proud of you that you got hurt while trying to save a 5 year old" or some other mushy garbage but in the end, the only one who is providing for my family is me and If I don't have to risk it I won't. We can go all around the block saying what if it was a 1 day old what if it was your son, what if it was your mom or a 5 year old or whatever but that is playing the emotional card and at the end of the day - who is gonna take care of you??:? Not your company, not your patients and not your partner - YOU are. I do not get into the arguments that what if it was a 5 year old - those are just knee jerk reactions.

40 minutes is about the right amount of time to spend on scene of a cardiac arrest unless you are 5 minutes from the hospital. I would much rather be on scene doing these things than in the back of a bouncy ambulance, trying to hold on for dear life because the EMT gets to run HOT!!!! Because you seem to have such a strong opinion of things and how things are done here is what I recommend Get a driver and go out to a large parking lot in your jurisdiction. Get all your stuff ready for a code and put a Cpr dummy in the back of your ambulance. Have that driver start to drive like he was running hot to the hospital. Now begin your code. Do cpr in the ambulance, Try to intubate and try to start an IV. If you can do that without being bounced around, thrown around and all that, come back here, post again and tell us that you would rather do it in the ambulance. After you have healed from your bruises and bumps and scrapes from your fun ride in the back of the ambulance, now go and run the same code on the floor of your station and tell me which you would rather do. Your opinion will change when you become a medic.

thanks for the clarification. It makes sense now.

This is where clarity really counts.

But to train them to read a 12 lead would be counter intuitive. What good is a tool if you cannot fix what you find wrong with the original tool.

I agree with you Somedic. I think that it is foolish to allow and EMT-B to do either of those things. It is one thing to have the tool but you also have to be able to provide care for what that tool shows you. What I wonder actually with the blind intubation the poster really meant the placement of another airway adjunct rather than blind intubation???? Original poster, please clarify

I know Missouri EMT-B's cannot. Are you saying that there are states out there that allow the EMT-B's to do Blind Intubations and 12 Lead EKG's

Two things Do these guys still have jobs? Second, at least the guy in the front could have covered his face. The patches give it away as to what service this is. AMR and then there is a 2nd patch on the right shoulder that I believe gives away the specific service name. I hope the sup's aren't looking at this.

I did a little looking and I'm gonna go with the following APS, antiphospholipid syndrome; INR, international normalised ratio Taken from the web site http://pmj.bmj.com/cgi/content/full/79/928/81 For anyone who wants to read the abstract here it is source is above. If you don't want to read it don't but I learned some things I didn't know prior to reading it. REVIEW Migraine, memory loss, and "multiple sclerosis ". Neurological features of the antiphospholipid (Hughes’) syndrome G R V Hughes Correspondence to: Dr Graham Hughes, Lupus Unit, St Thomas’ Hospital, London SE1 7EH; graham.hughes@kcl.ac.uk Submitted 29 July 2002 Accepted 30 October 2002 ABSTRACT TOP ABSTRACT CLINICAL FEATURES RESEARCH AND SPECULATION REFERENCES The antiphospholipid syndrome (APS, Hughes’ syndrome), first described in 1983, is a prothrombotic disease in which neurological events feature prominently. Strokes, transient ischaemic attacks, and headaches (including migraine) are important complications. However, it is clear that other neurological symptoms, including diplopia, memory loss, ataxia, and "multiple sclerosis-like" features are common. A notable feature of Hughes’ syndrome is the clinical response to anticoagulants; features such as headache and memory loss often improving dramatically with appropriate warfarin dosage. APS may well become recognised as an important (and potentially treatable) cause of neurological disease. -------------------------------------------------------------------------------- Keywords: antiphospholipid syndrome; Hughes’ syndrome; migraine; memory loss; "multiple sclerosis" Abbreviations: APS, antiphospholipid syndrome; INR, international normalised ratio It is now recognised that antiphospholipid syndrome (APS) is a major neurological disease.1 The syndrome, first described in 1983, is characterised by recurrent thrombosis (both venous and arterial), recurrent miscarriage, neurological disease, including stroke, and the presence of circulating antibodies against phospholipids.2 Our early studies focused on lupus, but we recognised that the syndrome was just as prevalent outside lupus and called this syndrome the antiphospholipid syndrome. The title is not strictly correct—the antibodies are in fact directed against phospholipids and proteins. The syndrome is now recognised as a common and important prothrombotic condition with ramifications into almost all spheres of medicine, surgery, and obstetrics. While our earliest descriptions highlighted the neurological aspects of the syndrome (strokes, chorea, myelopathy, headaches, memory loss, and dementia),3,4 the full impact of the syndrome on neurology is now becoming more widely recognised. CLINICAL FEATURES TOP ABSTRACT CLINICAL FEATURES RESEARCH AND SPECULATION REFERENCES This short review addresses these nervous system features, their pathogenesis, and their management. Headache and migraine Recently, we set up a patients’ website on APS (www.hughes-syndrome.org). In the first week of operation we received over 20 000 hits. Far and away the commonest symptom reported was headache: not evidence based medicine perhaps, but a pointer to the importance of this symptom.5 The history is remarkably similar in many patients with teenage headaches that are frequently migrainous—often premenstrual—often disappearing for 10–20 years only to return in the 30s or 40s. There is, significantly, a strong family history of headaches or of migraine in many of our patients, pointing to genetic influences. In some patients the headaches are accompanied by visual or speech disturbance, or by transient ischaemic attacks. It is my view that antiphospholipid antibody testing should be among the armamentarium of those investigating migraine or recurrent headache.6 Memory loss All those dealing with large numbers of patients with the syndrome recognise memory loss as possibly the most important feature. Unfortunately, as yet, there have been few formal psychometric studies of these patients—for example, before and after anticoagulation treatment is started. In some patients, the disease, if untreated, progresses to widespread brain infarction, grossly abnormal magnetic resonance images and, ultimately, multi-infarct dementia. In the majority of patients, the memory loss is less extreme—though sufficiently frightening for the patient to worry about the possibility of Alzheimer’s disease.7 It is this aspect of the syndrome which—like headaches—often improves when anticoagulation is started. Epilepsy Seizures are a feature of APS: indeed in a patient with lupus presenting with seizures, APS is the most likely underlying pathology—an observation with therapeutic implications. All ages are affected, and all forms of epilepsy are seen, as are subclinical (abnormal electroencephalogram) forms. The association of antiphospholipid antibody with epilepsy, first reported in 1985,8 may be of significant importance in the investigation of seizures in general.9 A typical scenario A 39 year old woman complained of headaches, fatigue, and memory loss. She was concerned about a possible diagnosis of Alzheimer’s disease. Two years earlier, she had suffered from similar headaches, associated with gait disturbance and ataxia. She had been investigated for multiple sclerosis but brain magnetic resonance imaging had been normal. Her past history included a strong teenage tendency to headaches, often migrainous. In her 20s she had been investigated for infertility, but on two occasions had conceived only to suffer a miscarriage at three months. At the age of 35 she had a successful pregnancy. In view of the possible diagnosis of APS (Hughes’ syndrome), blood tests for antiphospholipid antibodies were ordered and found to be strongly positive. She was treated initially with aspirin 75 mg daily, with moderate though incomplete resolution of the headaches. Ultimately, in view of the known prothrombotic nature of APS, and especially its neurological and obstetric sequlae, the patient was anticoagulated with warfarin. Not only did this treatment result in disappearance of the headaches, but the patient noted a marked improvement in memory. Interestingly, these two major symptoms returned whenever the international normalised ratio (INR) fell below 2.5. Stroke The commonest serious complication of APS is stroke. Indeed, the syndrome is becoming recognised as a major, and potentially preventable, cause of stroke. It has been estimated that up to one in five of all young (under 45) strokes are associated with Hughes’ syndrome, although all ages can be affected. The clinical spectrum ranges from transient ischaemic attacks and focal lesions—such as amaurosis fugax—to widespread cerebral infarction, ataxia, bladder, and gait disturbance and—in extreme cases—multi-infarct dementia. More than anything else, it is this propensity to (arterial) stroke which marks out Hughes’ syndrome from the other less serious coagulopathies such as factor V Leiden deficiency. Myelopathy Transverse myelopathy is a rare but well recognised feature of APS. It is sometimes associated with optic nerve ischaemia (Devic’s disease). The pathology of the myelopathy is poorly understood. However, some interesting observations have come from the mouse model of APS. Some of these animals which develop an APS-like disease became paraplegic. Histology of the spinal cord in these animals showed vessel thrombosis.10 These observations might be taken to support the suggestion that anticoagulation may have to be considered in addition to the more conventional steroid and immunosuppressive regimens generally given to some lupus patients with myelopathy, for example. Multiple sclerosis Not surprisingly, a number of patients with APS have carried a working diagnosis of "multiple sclerosis". In a recent study from our unit, 28 APS patients were reviewed in whom an original diagnosis of multiple sclerosis had been made.11 Some interesting lessons were learnt. Firstly, differential diagnosis was difficult—in this particular study the magnetic resonance imaging did not clearly distinguish the two conditions. Secondly, with hindsight, there had been clues to the underlying diagnosis, notably recurrent headaches, previous thrombosis, or recurrent miscarriage. Thirdly, and perhaps most significantly of all, in the majority of the patients ultimately correctly diagnosed and appropriately anticoagulated, there were no further neurological events. Clearly, there will be many similar studies to come. However, it seems probable that a small percent of patients diagnosed with multiple sclerosis do in fact have Hughes’ syndrome, a condition with totally different treatment and prognosis. Chorea Our original studies in 1983 included chorea. Although rare, this feature has been strongly associated with the presence of antiphospholipid antibodies—indeed, the combination in some APS patients of joint pains, heart murmurs and chorea has led, not unexpectedly, to a label of "rheumatic fever". Although the precise pathophysiology of the chorea is unclear, an interesting clinical observation has been made that in a small number of patients, the chorea has ceased with the institution of anticoagulants. Neuropathy Possibly one of the more surprising findings has been the association in some patients between antiphospholipid antibodies and neuropathy, both peripheral and cranial. In classical lupus, peripheral neuropathy is relatively uncommon, and larger numbers will be required before this possible association can be confirmed. Behavioural disorders A number of cases of frontal lobe ischaemia, with its attendant behavioural disorder, have been seen (this author was referred one 3 year old boy with an aggressive behavioural disorder found to be associated with multiple cerebral infarcts). To date there have been surprisingly few studies detailing the neuropsychiatric manifestations of APS. Treatment Anticoagulation is required. Current experience shows that antiphospholipid antibodies constitute a significant risk for thrombosis, including stroke. For example, in our clinic, in a 10 year retrospective analysis, no fewer than 50% of those individuals (mainly lupus patients or women with recurrent miscarriage) with positive antibodies in 1985 had developed thrombosis by 1995.12 A more difficult decision is whether to use aspirin alone or to anticoagulate with warfarin. Most data currently available point to the superiority of warfarin if there has been clear cut cerebral ischaemia. Khamashta et al analysed APS patients over a 10 year period.13 Of those treated with aspirin alone, over half developed further thrombosis. Likewise, in those treated with warfarin to an INR of less than 3, one half developed further thrombosis. Only in those maintained at an INR of 3 or over was there a significant 10 year benefit. Our study had two possible weaknesses. Firstly, it was retrospective. Secondly, it was directed mainly to patients with arterial rather than venous thrombosis—it could be argued that subsets of patients with venous thrombosis alone might require less aggressive anticoagulation. One point, however, is clear. The danger of thrombosis and stroke in these patients far outweighs the risks of anticoagulant induced bleeding. The traditional fear of cerebral haemorrhage has, almost certainly, resulted in the under-treatment of many patients with APS. Finally, what of the "non-thrombotic" neurological features? What of the patient with severe, recurrent headaches who has antiphospholipid antibodies but who has not had a previous thrombosis. It is a common observation that warfarin treatment when finally given (for example, for a deep vein thrombosis) results in dramatic improvement in headache. Recently, we have introduced a "clinical trial" of heparin in this situation. A two week trial of self administered heparin (for example, Fragmin 5000 units daily) is both safe, and, in our preliminary studies, has provided a clear indication (for example, immediate disappearance of the headaches) as to whether anticoagulation might be suitable.5,14 We are involved in a prospective controlled trial of this treatment in APS associated headache and migraine. RESEARCH AND SPECULATION TOP ABSTRACT CLINICAL FEATURES RESEARCH AND SPECULATION REFERENCES Epidemiology APS (Hughes’ syndrome) may well prove to be a much more common neurological diagnosis than hitherto realised. Multicentre studies are now in progress in migraine, multiple sclerosis, memory loss, epilepsy, and stroke clinics. The observation that some patients have strong family histories of APS features (especially migraine) suggests that genetic studies should broaden the clinical spectrum beyond "classical" cases. Why the brain? The 20 year experience of the syndrome has shown that the central nervous system appears to be particularly at risk. The reasons (if this observation proves correct) are uncertain. However, interactions between brain and clotting processes have a long history. The coagulation mechanism within the central nervous system has clear differences from that found in other organs. For example, the brain endothelium expresses little thrombomodulin, unlike other endothelial surfaces. While some experimental work has suggested that antiphospholipid antibodies may have direct antineuronal ties, at the present time, the available evidence suggests that the major underlying mechanism in the cerebral features of Hughes’ syndrome is either vascular thrombosis or sludging. Future trends As imaging techniques improve, so presumably will the diagnostic yield. Conventional magnetic resonance imaging may be normal in some cases of classical APS (as in the case presented at the beginning of this review). The standard blood tests—anticardiolipin and lupus anticoagulant—are reasonably standardised internationally, but do have limitations. To date, the addition of other tests such as IgA anticardiolipin, anti-ß2 GP1, antiprothrombin, and antiphosphatidyl serine, for example, have not added much in the way of further clinical definition.15 Health economics The links between APS and stroke, migraine, and epilepsy are well established. The links between APS and memory loss and between APS and multiple sclerosis are recognised but require further validation. In any event the diagnosis of this prothrombotic condition, and its response to anticoagulation, has major therapeutic and economic implications. Up to one in five of all strokes in the under 45 year olds are associated with APS and are potentially preventable. The economic cost of strokes per annum in the UK has been estimated at £2.3 billion and in the USA at £23 billion. More frequent and earlier diagnosis of APS and precise anticoagulant therapy could have an impact on these costs, both economic and human. ACKNOWLEDGEMENTS This review is based on a lecture given at the 6th European Lupus Congress, May 2002. REFERENCES TOP ABSTRACT CLINICAL FEATURES RESEARCH AND SPECULATION REFERENCES Narvarreta MG, Boey RL, Levine SR. Cerebral disease in the antiphospholipid syndrome. In: Khamashta MA, ed. Hughes syndrome: antiphospholipid syndrome. London: Springer-Verlag, 2000: 43–58. Hughes GRV. Thrombosis, abortion, cerebral disease and the lupus anticoagulant. BMJ 1983;287:1088–9.[Medline] Khamasha MA. Hughes syndrome: history. In: Khamashta MA, ed. Hughes syndrome: antiphospholipid syndrome. London: Springer-Verlag, 2000: 3–7. Harris EN, Gharavi AE, Asherson RA, et al. Cerebral infarction in systeic lupus. Association with anticardiolipin antibodies. Clin Exp Rheumatol 1984;2:47–51.[Medline] Cuadrado MJ, Khamashta MA, Hughes GRV. Sticky blood and headache. Lupus 2001;10:392–3.[Medline] Cuadrado MJ, Khamashta MA, Hughes GRV. Migraine and stroke in young women. Q J Med 2002;93:317–19. Hughes GRV. Off the beaten track: a clinician’s view. In: Khamashta MA, ed. Hughes syndrome: the antiphospholipid syndrome. London: Springer-Verlag, 2000:105–10. Mackworth-Young CG, Hughes GRV. Epilepsy: an early symptom of SLE. J Neurol Neurosurg Psychiatry 1985;48:185.[Medline] Peltola JT, Haapala A, Isojarvi JI, et al. Antiphospholipid and antinuclear antibodies in patients with epilepsy or new-onset seizure disorders. Am J Med 2000;109:712–17.[CrossRef][Medline] Blank M, Krause I, Shoenfeld Y. The contribution of experimental models to our understanding of etiology, pathogenesis and novel therapies in the antiphospholipid syndrome. In: Khamashta MA, ed. Hughes syndrome: antiphospholipid syndrome. London: Springer-Verlag, 2000:379–90. Cuadrado MJ, Khamashta MA, Ballesteros A, et al. Can Hughes (antiphospholipid) syndrome be distinguished from multiple sclerosis? Analysis of 27 patients and review of the literature. Medicine (Baltimore) 2002;79:57–68.[CrossRef] Shah MN, Khamashta MA, Atsumi T, et al. Outcome of patients with anticardiolipin antibodies: a ten year follow-up of 52 patients. Lupus 1998;7:3–6.[Medline] Khamashta MA, Cuadrado MJ, Mujic F, et al. The management of thrombosis in the antiphospholipid antibody syndrome. N Engl J Med 1995;332:993–7.[Abstract/Free Full Text] Cuadrado MJ, Khamashta MA, D’Cruz D, et al. Migraine in Hughes syndrome—heparin as a therapeutic trial. Q J Med 2001;94:114–15. Bertolaccini ML, Atsumi T, Escudero A, et al. The value of IgA antiphospholipid testing for the diagnosis of antiphospholipid (Hughes) syndrome in SLE. J Rheumatol 2001;28:2637–43.[Medline]

do not call in service without knowing where your partner is or you could get in trouble. What I would do is this, you call dispatch on your cell phone and say, the unit is back in service but my partner is not around. Tell them you do not know where she/he is but the ambulance is ready. That way your job has been completed by getting the unit in service. By no means go in service if your partner is not available to respond to a call. By the jist of your original post I sense that management is already aware of this person and is taking steps to kick her ass to the curb and they are using you to help them. I would also keep a personal log of incidents where it could be her word against yours or put them in individual incident reports. I for one would end this relationship right now and refuse to work with this partner.

Excellent excellent replies Now a follow up question Since we all do diagnose, what if any training courses should we invest in or provide to our students/employees to aid them in their ability to diagnose someone and give the receiving ER or facility their best diagnosis.