Eydawn

There are midwives who practice who are not RN's. There's a difference between a midwife and a certified nurse midwife... come to think of it, there's certified midwives (not RN), direct entry midwives (not RN), certified professional midwives (may or may not be RN) and certified nurse midwives. Just thought I'd throw that out there... This is some really excellent discussion! I would definitely agree that a lot of the misperception of nursing vs paramedicine comes from the attitudes that have developed within each specialty, with each disdaining the other through ignorance. Nurses are definitely independent thinkers (maybe not some of the SNF drones, but fortunately most of the ones I've met in that field so far have been very intelligent and good at what they do)and have to be in order to perform their job appropriately. Standing orders are standing orders, no matter what title you may happen to hold. I have standing orders to NOT EVER do CPR in my facility, because we're not a "skilled" facility. I also have standing orders to provide basic wound care since I have no nurse at night. Does that take all my thinking out of the equation? Certainly not, and if that holds true for me at the flunky level, it definitely holds true at higher levels. I think the perception that you are "autonomous" as a paramedic is one of the dumbest things I've encountered... it's where a lot of the cowboy medicine that is practiced without solid foundation comes from. Of *course* you need to make autonomous decisions based on the situation you are presented with... but at the end of the day you answer to the doc and if you gooned it up, the doctor will take away your ability to practice. Same holds true for nurses... you have to make critical decisions based on the information in front of you. Has anyone here been sick recently? What was your experience- who did you see? Who did the majority of your care? In my experience and that of close friends recently, it's been the nurse who does 90% of the care. The doctor may pop in to provide some of the puzzle pieces, but the nurse is providing care. That's autonomy if I've ever seen it... just autonomy with the awareness of physician involvement at the forefront instead of hidden away in the subconscious. Wendy CO EMT-B

Kiwi- how farking IGNORANT can you get? Just because you can't treat him doesn't mean you shouldn't try to figure out what's all going on and how it would be treated... what are you going to do if he develops complications during your transport? Say "Oh well, we just figured we were the taxi ride?" I thought you were against having to rely on physicians for everything. Get your story straight!! I'll puzzle through this and get back to you, have to get to my A&P lab... Wendy CO EMT-B

Ah hell you'd have to know my brother.. nvm

So Lady Gaga and Michael Jackson get together to discuss what they are. Michael: "I'm a little white girl!!" Lady Gaga: "Oh yeah? I'm a Christmas tree! NO, wait... I'm inside out! NO! I'm a Christmas tree!! No... I'm a telephone... telephone." ;-) Courtesy of my little brother... --Wendy

http://www.msnbc.msn.com/id/36077879/ns/world_news-europe/ Take a look at the pictures they've released so far... how the hell do you respond to something like this? I know we all have policies and procedures that tell us what to do... but I can't imagine actually being there and responding to it. Looks like they were just doing the best they could. I wonder what Russian EMS is normally like? My thoughts go out to all the victims and their families... Wendy CO EMT-B

See if there's a way you can make funny yet logical associations. Like, at 2 dollars (lpm) I can buy X amount of M&M's (% saturation)... at 3 dollars, I can buy X amount of Chips Ahoy... make it something that you're interested in instead of just plain old boring O2 % saturation. That random funny stuff is what your brain will remember come test time when you draw the blank. Or, find a mnemonic device... Google may be your friend here. For example, with oxidation-reduction reactions, I can't tell you how many times I've thanked my high school AP Chem teacher for "OIL RIG" (oxidation is loss, reduction is gain) and most of that within the last year. Good luck to you! Wendy CO EMT-B

Who says it FELL anywhere? And I'd much rather head into the hills and AWAY from the first blast... odds are shitty either way, but at least you've got people moving and doing something and you're more likely to be protected from another blast that's close to the first one. Wendy CO EMT-B

You're only 5 miles from the explosion- right in the worst radiation fallout zone. The citizenry are looking to you for what to do? GOOD! Take charge. Take your most dynamic and intelligent person and have them get up on top of the truck and start getting attention. If you can assume leadership right away, you may be able to avert a mass panic (or at least deaden its impact a little.) #1: Everyone needs to grab as much food and water and whatever armaments they have from their homes as they can carry and start heading AWAY from the blast. In an organized fashion, as much as possible. We're already exposed- no need to panic, but definite need to move fast. #2: You need to gut your ambulances and rescue rigs for as many medical supplies as you can. Each of your crew members needs to be outfitted with a pack containing food, water and medical supplies. #3: If there is a more sheltered location nearby (such as rock outcroppings in the foothills) that you can get into or behind (in case of another explosion) that's where everyone needs to go. #4: Expect the situation to turn into a riot quickly. You must be smart enough to protect yourself. Whoever is with you must take orders from the leader or get out. Be prepared to fend for yourself. Get away from the blast zone. Keep your head up and alert. Treat the injured as you can, but you're going to find yourself giving palliative care to radiation poisoning more than likely, and very probably among your own crew and crew's family, depending on how close they were to the blast. Start looking for ways to get communication out or in to figure out the scope of the incident. Prayer is definitely a must at this point... God, I hate post-apocalyptic thinking... (I was raised in such by my parents and given lots of post-apoc sci-fi to read, and it's taken me years to live fairly "normally" as a result without being afraid every time I turn around.) Wendy CO EMT-B

Pt. went out to urgent care with her daughter this evening... bruising and swelling have both worsened, and she was diagnosed with another UTI... they gave her Keflex (cephalexin) both to treat the UTI and to treat for potential (non-confirmed) infection in her lower limb. So... still no final word, but it looks like I was closer by thinking infection of some sort... pt is in good spirits, but that leg is still looking wicked bad. Wendy CO EMT-B

Howdy folks... I guess it had to happen sooner or later, but I'm questioning my LPN's decision to chart something as a bruise when I think that it is cellulitis. I see this as a purely teachable moment; once I report something to nursing, it's their ball from there and I can't really challenge them... but I want to know if my thinking on this is reasonable, and if I'm wrong, why I'm wrong and why the nurse is right. Case: 65 y/o female with hx recurrent UTI's, recurrent skin yeast rash (turned bacterial a few weeks back and resulted in a hospital stay), pre-diabetic, obese, HTN, A-fib, depression, anti-coagulant therapy, lower extremity neuropathy. Pt has been on antibiotics off and on for UTI symptoms several times over last 2 months. Pt is prone to frequent falls and ambulates primarily with a power-scooter that she runs into stuff with all the time. Pt had a fall in her bathroom (unwitnessed) about 4 days ago. Her lower right leg has a very large dark bruise just below her knee surrounded by a swollen area roughly 4" across and elevated ~1" and her entire lower extremity is now swollen. The skin on the anterior part of her leg is red and very warm to the touch and has a shiny appearance. I reported this yesterday, and it has been charted as a bruise with swelling, tx is NSAIDs for pain PRN and ice packs. There are several things about this that are screaming cellulitis at me: The pt's lower leg neuropathy hx and recent infection issues, the fact that her entire lower leg is now displaying edema, the giant red blotch on her shin surrounding the swollen area that is shiny and hot... Correct me if I'm wrong, but can't cellulitis begin after a traumatic injury, especially in someone who's pre-diabetic with circulation issues? I'm documenting what I see as I see it, as my charting is separate from my LPN's, and I can't "diagnose" (aka put that I suspect cellulitis) anywhere in my written documentation, but I have a sinking feeling that my LPN (who is fairly new as a nurse) is missing something here. Teach me! Is my LPN right? Could this just be a bruise with swelling? Am I over-thinking this? I feel so bad for this lady, she's had so much stuff happen (and some things get missed thru bad communication) that I'd hate for us to miss budding cellulitis... but I'm also hoping that my assessment is wrong. Wendy CO EMT-B

This is why the ratings system is SO STUPID!! The guy asked a question. Just because you don't like the question doesn't mean you should hit him with a negative point!! It's supposed to be QUALITY OF POST... everything was spelled correctly, and this is a grand teachable moment if the idiots who knee-jerk would give us a little space and not goon it up... Please, anyone reading this, take a moment to give the kid some positive points to bring him back up to neutral rating... he's only got one post in here. Let's not run him off before he even gets started... Wendy CO EMT-B

Not seeing anything. As the phrase seems to be ubiquitous on facebook sites and so forth, you could print it yourself on a shirt at zazzle.com OR you could forgo the whacker-shirt and spend your money on something useful instead, like an anatomy atlas! ;-) That's just my thinking... Seriously, the shirts are funny to a point, but it detracts from the overall image... Wendy CO EMT-B

Taken from Medscape... who knew that NSAIDs could increase fracture risk and interfere with fracture healing (especially COX-2 inhibitors like Celebrex)... think about all the fractures we see and how people self-medicate, and the potential for complications in the hip fracture geriatric population... To see Figure 1, you'll have to click this link: http://www.medscape.com/viewarticle/587888 and click through the article. For those who prefer the forum format, here it is below... Treating Skeletal Pain: Limitations of Conventional Anti-inflammatory Drugs, and Anti-neurotrophic Factor as a Possible Alternative Cory J. Xian; Xin-Fu Zhou Authors and Disclosures Posted: 02/10/2009; Nat Clin Pract Rheumatol. 2009;5(2):92-98. © 2009 Nature Publishing Group Summary Inflammatory and injury-induced skeletal pain are common conditions, and both conventional nonselective NSAIDs and the newer cyclo-oxygenase-2-specific inhibitors are widely used as post-traumatic and post-surgical analgesics. However, new research suggests that these drugs, particularly the cyclo-oxygenase-2 inhibitors, have a negative effect on the healing process in fractured bone and within orthopedic surgical sites, thus highlighting a need to develop new approaches for managing skeletal pain. Various experimental studies have revealed that locally upregulated neurotrophic factors, especially nerve growth factor, have a major role in mediating injury-induced or inflammatory pain. Nerve growth factor inhibitors, therefore, might be an effective alternative modality for post-traumatic and post-surgical analgesia, without impairing bone healing. Introduction Chronic pain is a leading cause of morbidity worldwide, with a prevalence of 50% in Europe—a figure that is likely to rise in elderly patients with chronic disorders, such as rheumatoid arthritis or osteoarthritis.[1] Nonselective NSAIDs, which inhibit cyclo-oxygenase (COX)-1 and COX-2, and the newer COX-2-specific inhibitors are commonly used in the management of post-traumatic or post-operative skeletal pain. However, studies have demonstrated a strong association between these agents and impaired bone healing, highlighting the need for new approaches to skeletal pain management. Data from the past few years indicate that neurotrophins—growth factors that are required for the survival, development and maintenance of neuronal cells—might be involved in the pathophysiology of injury-induced or inflammatory skeletal pain. This Review discusses the inhibitory effects of NSAIDs (particularly COX-2-specific agents) on bone healing, and the potential role of neurotrophic factors as mediators of skeletal pain and as targets for the treatment of skeletal pain. NSAIDS as Post-traumatic or POST-operative Analgesia Conventional, nonselective NSAIDs, which inhibit COX-mediated production of prostaglandins, are widely used to treat pain and reduce inflammation in patients with chronic inflammatory or autoimmune disorders.[2] The management of acute post-operative pain, however, remains suboptimal, despite the increasing use of clinical acute pain services; furthermore, there are disparities in opinion, both between clinicians and in the clinical practice guidelines, regarding the use of the newer modalities in this setting.[3,4,5] Conventional NSAIDS have become an important component of both post-traumatic and post-operative analgesia, and are used frequently in the treatment of acute athletic injury.[6,7,8,9] The proven efficacy of these agents in the management of post-operative pain, together with their opioid-sparing role in multimodal analgesia, have led to significantly reduced levels of opioid-related side effects.[10] The therapeutic effects of nonselective NSAIDs are mediated by inhibition of injury-induced or inflammation-induced COX-2 expression.[11] Clinical studies have shown that, as a result of inhibition of the physiological enzyme, COX-1, NSAIDs can be associated with an increased risk of fracture in patients with rheumatic disease.[12] In addition, their use has been called into question following concerns about the associated increased risks of gastrointestinal and cardiovascular adverse events, increased bleeding, impaired wound healing, and increased bone nonunion rates.[3,13,14] Furthermore, evidence from experimental research conducted over the past two decades suggests that NSAIDs have an inhibitory effect on fracture repair.[11] The newer NSAIDS, which specifically inhibit COX-2, are as effective as classical NSAIDs and are associated with a lower risk of gastrointestinal adverse events, as well as a lack of inhibitory effects on platelet function and, therefore, a reduced risk of blood loss.[1,3,9] Large-scale studies, however, have shown that these newer agents can increase the risk of adverse cardiovascular events.[1,15,16,17] Effects of COX-2-specific Inhibitors on Bone Fracture Healing Bone healing is a complex process that involves the coordinated actions of various cell types. The initial hematoma formation and inflammatory response result in the release of cytokines and growth factors that are important in regulating subsequent healing events, such as infiltration of progenitor cells. In the reparative and remodeling phases, bone formation and remodeling involve angiogenesis and the formation and functions of bone-forming cells (i.e. osteoblasts) and bone-resorptive cells (i.e. osteoclasts). It is now clear that all these events are regulated by prostaglandins, the products of COX enzymes.[11] When COX-2 is induced during the inflammatory response, increased prostaglandin expression upregulates various inflammation mediators and regulates the formation and activities of osteoblasts and osteoclasts.[18] Given the central role of prostaglandins in the bone healing process and the widespread use of NSAIDs in the management of post-injury and post-surgery orthopedic pain, the possible adverse effects of these agents in bone healing, particularly the COX-2-specific inhibitors, are concerning. Blockade of COX-2 function has been associated with variable outcomes in experimental models of bone, ligament and tendon repair.[19] One clinical study showed that short-term use of the COX-2 inhibitor celecoxib had no effect on rates of nonunion following spinal fusion surgery;[20] however, another clinical study indicated that longer-term COX-2 inhibition could increase the risk of fracture and delay healing.[11] Experimental studies suggest that COX-2 inhibitors can impair tissue repair and recovery of mechanical strength following acute skeletal injury, which could have important clinical implications for the rates of ongoing morbidity and future susceptibility to injury.[21] Accumulating evidence suggests that COX-2 activity in the early stages of bone healing is critical for efficient bone repair. Indeed, fracture healing was shown to be impaired in mice with mutated COX-2.[22] Furthermore, administration of celecoxib during the early stages of fracture repair in rats (but not before or 14 days after fracture) significantly reduced the mechanical strength of the fracture callus and often caused bone nonunion.[23] Similarly, early post-operative administration of COX-2 inhibitors in rodent bone fracture models resulted in increased fibrous tissue at fracture sites, limited blood flow across the fracture, delayed remodeling of calcified cartilage, and reduced bone formation in the fracture callus, or delayed allograft healing and incorporation.[24,25,26,27] Interestingly, it has been shown that COX-2-specific drugs inhibit fracture healing to a greater degree than classical NSAIDS.[27] Moreover, the magnitude of this effect seems to be related to treatment duration, as the inhibitory effect was reversible after discontinuation of short-term treatment.[27] Up to 10% of bone fractures can result in delayed union or nonunion;[28] however, the extent of the contribution of COX-2 inhibitors to this rate of delayed union or nonunion remains to be investigated. Guidelines on the use of NSAIDS in Fractures and Orthopedic Surgery As NSAIDS are known to inhibit bone healing,[29] and opiates cause cognitive dysfunction and respiratory depression, the available treatment options for pain related to bone fractures or surgery remain limited. Based on animal and clinical studies, practical management guidelines have been generated to assist orthopedic surgeons and sports physicians with regard to the use of NSAIDS for analgesia. Clinicians are advised to carefully evaluate individual patient risk factors and the pharmacokinetics of individual NSAIDS when assessing the risks and benefits of discontinuing NSAID therapy in the perioperative setting.[14] NSAIDS can be used appropriately in the management of acute ligament sprains, muscle strains, tendinitis, and eccentric muscle injury, with the length of treatment being kept as short as possible. However, these agents are not recommended, or should be used with caution or only for a short duration,[6,27] in the treatment of fractures and stress fractures, which are associated with higher risks of nonunion or delayed union due to osseous, vascular, or patient-related factors,[25] or in the treatment of chronic muscle injury.[8] Neurotrophic Factors in Injury-induced or Inflammatory Pain Neurotrophins are a family of proteins that are essential for the proliferation, differentiation and survival of primary sensory neurons[30] and, as shown in recent studies, participate in the development of pain states. Each neurotrophin binds with high affinity to a specific receptor tyrosine kinase (Trk), and all bind to the common receptor p75. In adult animals, approximately 40–50% of primary sensory neurons express the nerve growth factor (NGF) receptor TrkA, 20–30% express the brain-derived neurotrophic factor (BDNF) receptor TrkB, and 20–30% of neurons express the neurotrophin 3 (NT3) receptor TrkC. Neurotrophins are expressed in sensory target organs and tissues, such as skin, blood vessels and visceral tissues;[31] BDNF is also highly expressed by a subpopulation of sensory neurons.[32] Neurotrophins released from their targets act on and maintain normal functioning of sensory neurons. In pathological conditions, such as trauma and inflammation, neurotrophins are upregulated by injured tissues,[33] and sensory nerve terminals are activated by target-derived neurotrophins, which participate in tissue healing and the development of pain. Neurotrophins in Wound and Tissue Repair and Fracture Healing Apart from its known biological effects on neuronal cells, NGF might also be an important component of the wound healing and tissue repair process. Early studies reported a therapeutic role for NGF in tissue repair, particularly in otherwise untreatable ulcers in patients with diabetes and in patients with severe pressure ulcers.[34] In addition, NGF accelerated the rate of wound healing both in normal mice and in healing-impaired diabetic mice.[35] Interestingly, NGF administered after injury was associated with the promotion of wound healing and increased numbers of fibroblasts and blood capillaries in granulation tissues in mice.[36] While NGF can be detected in periosteal osteoprogenitor cells in intact bone, NGF protein has also been detected in osteoprogenitor cells, marrow stromal cells, osteoblasts, some chondrocytes, endothelial cells, the periosteal matrix of the fracture callus, and skeletal muscle, suggesting that NGF and all these entities participate in fracture repair and re-innervation.[37] In a mouse model of fractured ribs, immunoreactivity of NGF, BDNF and NT3, and the receptors TrkA and TrkC, was observed in osteoblasts and/or hypertrophic chondrocytes in the bone forming area at the fracture callus.[38] In addition, mRNA levels of these neurotrophins were elevated during the healing process. Localized, intense ingrowth of new sensory nerve fibers containing the neuropeptide CGRP (calcitonin gene-related peptide) was also observed at the fracture callus in rats.[39] As CGRP immunoreactivity coincides with the amount of new bone formation, this finding suggests an association between CGRP-positive innervation and fracture healing. These findings indicate that neurotrophins might be involved in bone or nerve healing as autocrine and/or paracrine factors during fracture repair. Although treatment with anti-NGF antibodies did not seem to interfere with the bone healing process, as assessed by mechanical testing and histomorphometric analysis,[40] the potential role of neurotrophins and their mechanisms of action in bone fracture healing require further investigation. Neurotrophins in Injury-induced or Inflammatory Pain Various studies have shown that neurotrophins, mainly NGF, are involved in the pathophysiology of injury-induced pain in nerve tissues, peripheral tissues and intervertebral discs. Neurotrophins have an established role in neural survival, collateral sprouting of sensory axons,[41,42] and regulation of nociceptive sensory neurons.[43] Increased expression and secretion of NGF, NT3 and BDNF have been implicated in injury-induced neuropathic pain after axotomy of the sensory system or the motor nerve.[44] Interestingly, tibial fracture in rats induced upregulation of NGF in hindpaw skin and tibia bone, as well as sciatic nerve neuropeptide content.[45] NGF is secreted by target tissues (such as macrophages and Schwann cells following nerve injury, and by basal keratinocytes in the skin), and regulates the excitability of nociceptor fibers by altering the expression of key sodium channels, receptors and neuropeptides involved in the transmission of pain stimuli.[46] Local or systemic administration of NGF in rodents has been shown to induce acute thermal hyperalgesia and delay mechanical hyperalgesia, suggesting that NGF itself is sufficient to elicit hyperalgesia.[47,48] In addition, injection of NGF into the neck muscles of mice evoked neuronal activation in areas of the brainstem and cervical spinal cord that are involved in the processing of deep noxious input,[49] indicating that NGF has a role in the pathophysiology of neck muscle nociception. In humans, intravenous or intramuscular injection of low-dose NGF (1 μg/kg) resulted in widespread pain in deep tissues and hyperalgesia at the injection site.[50,51] Systemic or local blockade of NGF bioactivity, however, inhibited the effects of inflammation on the sensitivity of sensory neurons.[48] Nociceptive nerve ingrowth into the usually aneural inner parts of painful lumbar intervertebral discs is a known cause of discogenic back pain; accumulating evidence suggests that NGF-induced nerve growth could have a key role in the pathophysiology of inflammatory back pain. A localization study showed a causal link between substance-P-positive, CGRP-positive nociceptive nerve ingrowth into the painful disc and NGF produced by blood vessels growing into the disc from adjacent vertebral bodies.[52] In addition, inflammatory back pain in the lumbar facet joints has been associated with increased numbers of BDNF-positive neurons and the phenotypic switch to large neurons innervating these joints in rats.[53] BDNF-positive small dorsal root ganglion (DRG) neurons have an important neuromodulatory role in inflammatory conditions; therefore, the presence of BDNF immunoreactivity in DRG neurons innervating the intervertebral disc suggests that, under physiological conditions, these DRG sensory neurons can transmit inflammatory pain from the intervertebral disc.[54] Furthermore, constitutive NGF expression in cultured human intervertebral disc cells was increased in the presence of the proinflammatory cytokines interleukin-1β and tumor necrosis factor.[55] Similarly, cultured lumbar NGF-sensitive DRG neurons exhibited increased axonal growth potential in response to neuronal injury in the presence of tumor necrosis factor.[56] These studies suggest that, apart from being involved in the pathophysiology of neuropathic pain following nerve and peripheral tissue injury, neurotrophins have an important role in the development of injury-induced or inflammation-induced back pain. Possible Mechanisms of Action of NGF in Bone-Injury-Induced Pain Although the potential pathophysiological mechanisms of NGF in bone-injury-induced pain remain unclear, the studies discussed above suggest that the ensuing inflammation triggers a cascade of proinflammatory cytokine upregulation, which in turn increases NGF synthesis in macrophages, chondrocytes, fibroblasts and osteoblasts at the site of injury (Figure 1). NGF released from these cells might then directly or indirectly act on sensory neurons, resulting in pain. NGF activates TrkA on sensory nerves, upregulating the expression of pronociceptive molecules, such as capsaicin receptor (TRPV1), BDNF, and neuropeptides (substance P and CGRP), in sensory neurons, which mediate nociception via peripheral and central mechanisms. NGF also causes pain indirectly by activating TrkA on mast cells, which release a variety of nociceptive activators such as neuropeptides.[47] Furthermore, NGF can activate TrkA on sympathetic neurons, which triggers sprouting of sympathetic nerves and the release of catecholamines, which interact with sensory neurons and cause ectopic nerve firing. Nociceptive activators produced from central or peripheral routes might act upon nociceptive sensory neurons, causing the release of neurotransmitters in the dorsal horn, which in turn sensitize spinal cord neurons and transmit pain after a bone injury. Bone-injury-induced pain might, therefore, be mediated by increased nociception due to the actions of NGF on both the peripheral and central nervous pathways. Figure 1. Potential functions and mechanisms of action of NGF in the development of post-injury pain. Inflammatory cells or bone healing cells at the fracture site upregulate NGF, which can act on sensory neurons directly or indirectly, resulting in pain. NGF activates its receptor (TrkA) on sensory nerves, which upregulates the expression of pronociceptive molecules, such as BDNF and neuropeptides (e.g. SP and CGRP) in sensory neurons, which mediate nociception via peripheral and central mechanisms. In addition, NGF can cause pain indirectly by activating TrkA on mast cells (which release a variety of nociceptive activators) and on sympathetic neurons. Abbreviations: BDNF, brain-derived neurotrophic factor; CGRP, calcitonin gene-related peptide; DRG, dorsal root ganglion; NGF, nerve growth factor; SP, substance P; TrkA, receptor tyrosine kinase A. Anti-NGF Therapy for Injury-INDUCED or Surgery-induced Pain Despite the development of new technologies to aid post-operative pain control,[4] safer and more effective modalities for pain management after skeletal trauma or surgery are still needed. As most of the CGRP-positive sensory nerve fibers innervating the bone express the NGF receptors TrkA and p75,[57,58] blocking the sensitization and activation of these fibers and nociceptors would represent an attractive approach to relieving musculoskeletal pain induced by trauma, injury or surgery. Increasing attention, therefore, has focused on evaluating the potential efficacy of anti-NGF therapy in pain management. In a mouse model of femur fracture, treatment with anti-NGF antibody on the first day after fracture resulted in a 50% reduction in pain-related behavior and did not seem to interfere with bone healing, as assessed by mechanical testing and histomorphometric analysis.[40] A similar study showed that administration of anti-NGF antibody reduced fracture-induced pain-related behaviors by over 50%, a level of reduction also achieved with a dose of 10 mg/kg of morphine.[29] Moreover, bone healing was not impaired, as measured by callus formation, fracture site bridging or mechanical bone strength. This study also indicated that NGF is likely to be involved in the maintenance, but not the acute generation, of fracture pain. As CGRP-positive and TrkA-positive fibers constitute the majority of sensory fibers innervating the bone, the antihyperalgesic action of an anti-NGF antibody could be effective in attenuating pain resulting from bone fracture or bone surgery. However, although anti-NGF treatment reduced nociceptive sensitization and preserved some bone mass in a rat model of tibial fracture, it did not decrease hindpaw edema, warmth or cytokine production, suggesting that anti-NGF treatment reduced some, but not all, signs characteristic of the complex regional pain syndrome.[45] This finding might have been due to the complexities involved in the pathogenesis of injury-induced skeletal pain and NGF signaling.[45] Furthermore, anti-NGF therapy seems to be efficacious in reducing pain associated with spinal cord injury or bone cancer. Administration of anti-NGF antibodies attenuated mechanical hyperalgesia following spinal cord injury in rats, suggesting that anti-NGF therapy is a potential analgesic treatment for central pain.[59] In a mouse prostate model of bone metastasis, where significant bone formation and bone destruction occur simultaneously, NGF-blocking antibody produced a significant reduction in both the early and late stages of bone cancer pain-related behaviors.[57] Interestingly, this therapy did not influence tumor-induced bone remodeling, formation of osteoblasts and osteoclasts, tumor growth, or markers of sensory or sympathetic innervation in the skin or bone. In a similar mouse model of bone cancer, administration of an anti-NGF antibody was found to produce a profound reduction in both ongoing and movement-evoked pain-related behaviors.[58] Conclusions Both conventional and COX-2-specific NSAIDS are important components in the management of pain after skeletal trauma or surgery. The limitations associated with these agents, including a possible role in the impairment of fracture healing, highlight the need to develop new modalities of pain management. Neurotrophic factors, particularly NGF, have been shown to mediate injury-induced or inflammatory pain of the skeleton, and studies have demonstrated that anti-NGF therapy could represent an attractive and effective alternative to NSAIDs, without compromising bone healing and remodeling. Further studies are required to understand how NGF and other neurotrophic factors, and their receptors, mediate pain evoked by injury, surgery, chronic inflammation, or cancer of the skeletal system. Questions remain regarding the cellular sources of the neurotrophic factors at or near the pain epicenter, and the molecular mechanisms of pain development. In addition, future studies are needed to evaluate or develop more-effective analgesic agents, based on the neuropathic roles of neurotrophic factors with minimal interference of their normal physiological neurotrophic functions and their functions in tissue and bone healing. More preclinical and clinical studies are needed to determine the role of these potential new modalities in clinical practice.

My condolences to everyone impacted by this LODD... Stay safe out there folks, remember, it's never when you expect it that catches you... Wendy CO EMT-B

It is a serious pity that you can't upvote a post made by a chat moderator... What Mike said. Everything he said. He speaks the truth. Wendy CO EMT-B

Let me clarify our modus operandi for you a bit. Team members carry their own personal gear (climbing harnesses and gear, search packs, medical small-kits for those of us who are EMT's) in their vehicles along with uniforms. When something requiring a very quick response goes down (eg missing child, missing Alzheimer's, rescue) we respond TO THE SCENE in our personal vehicles. Nobody will EVER run hot to the shed to go get the truck. Some people have bumper stickers, some of us use these handy little magnetic panels that come off and on with our team's logo on them... but all of us in some fashion try to identify our vehicles when we get to a scene. The local PD tends to argue a lot less with the search leader who gets there if the search leader has a vehicle with emblems and lights on it (sometimes there isn't time to change into uniform prior to arriving on scene and sometimes city PD or rural folks are kind of dense and not really sure who we are even though they requested us...) so that's another function of why we have members with lights... everyone who has lights, to my knowledge is a rated leader of some sort on our team. All our important gear, including our various baskets, large basket wheel, rescue kits, ropes, medical kits, O2, avi beacons, probe poles, shovels, winter sled, etc. is in one of our primary response vehicles; one looks like a big ambulance that's just full of shit, while the other is more of a truck with boxes model. Those vehicles are ONLY driven emergent by individuals certified by our sheriff's office. I drive them non-emergent, as that is what I am qualified for. Both these trucks also have additional lighting, with the best lighting coming from our primary truck, not our backup (our primary is the ambo style with a light tree you could make toast with on the roof). Sometimes, there is no good place to park onscene, so you end up stuck halfway off the road. Lights are a good thing for this, and we try to sandwich vehicles without lights in between vehicles WITH lights when that happens. Different countries, different modes of operation. This seems to work pretty well for us. Nobody said this guy has a ton of lights, and nobody has yet to prove to me that he's a whacker and deserves to have a SIMPLE QUESTION hit with a bunch of negatives. This whole reputation system was supposed to be based on quality of post, rather than whether or not your opinion was popular. Since threads in the damn FUNNY SECTION can be upvoted or downvoted, there goes that idea... Drives me nuts to see everyone who's got an issue with POV lights downvoting someone for asking a friggin' question. If he were arguing that it just looks cool and he's got to run hot to everything, I'd understand... but he just asked how to install the lights he's got. OP- my hubby suggests you visit a Dodge truck forum, as there's bound to be threads on that kind of thing with which wires to splice, etc. Wendy CO EMT-B

You'll have more luck in a fire forum getting an honest answer to your question. I can't help you, I only know Toyotas as far as that kind of vehicle goes. Two questions for the OP: Are you required to have these? If not, think about whether you really want/need that visibility... only you know your area, but know that lights bring risks along with benefits. Are you going to be running "emergent" driving with these on? If so, what training requirements do you have to do so, and are you aware that driving fast while running emergent drastically increases your likelihood of an accident? To all of you folks in here bashing this poor guy for asking how to install his lights, why the hell did you assume off the bat that he was a whacker and didn't have a legit purpose for lights on his vehicle? Some of my SAR team (search managers, rescue leaders, etc.) have lights that are hidden on their POV until in use, and let me tell you, it DOES enhance your safety as you're parked in a wonky spot along a road because the unfortunate guy you're rescuing went through the guardrail there... people can see you from a lot further off, especially at night. They're also a godsend as you're trying to fight your way up the Thompson or Poudre canyons- people get out of your way in *safe spots* and you can make it to the scene faster. (I don't have lights on either my vehicle or my husband's, but I know the people who do run with them- safely, I might add. You drive like an asshole, you get your sheriff's understanding and certification for lights/siren yanked immediately.) My team, having operated since 1979 officially as a nonprofit organization with a memorandum of understanding with the local sheriff, has YET to have an incident with a member running hot. EVER. The worst that happens to us is someone falling asleep at the wheel as they head home from a search... thank God nobody's wrecked... Not everyone with lights is a whacker. Not everyone asking about lights is a whacker. Since this guy mentioned green for rescue and blue for fire, I'm betting he's not running hot with them, especially as he doesn't have reds and a siren. It may be policy where he is to have lights on his response vehicle based on his qualifications. Ya'll are knee-jerk reacting to something, and guess who looks the fool for it? Wendy CO EMT-B

That was seriously funny!!! Holy shit! And yeah. Babs would kick his butt, no questions asked... ;-) Wendy

Ok, at the risk of sounding stupid, what are the diagnostic criteria for Adult Respiratory Distress Syndrome? I actually know of a former classmate who died of this in MI but I never fully understood exactly what it is and how it differs from acute respiratory failure or a bacterial infection that goes completely wonky... I know I could JFGI, but I like Vent's explanations and references ;-) I would agree that airway suctioning seems to be indicated here. Any time there is vomit, aspiration must be suspected, and the best thing you can do is get as much gunk out of there as possible. I'm particularly interested in the link between pneumonia and ARDS, as one of my residents got returned to us with a positive diagnosis of pneumonia (confirmed via CXR) and a scrip for Levaquin... what is the link, and where does a severe case of pneumonia differ from ARDS? Wendy CO EMT-B

Hey, at least they weren't at the titty bar. They were freakin' grocery shopping for crying out loud... within a reasonable distance from the fire house. I bet they waste a whole lot less diesel getting groceries than they do needlessly responding to EMS calls. I personally am totally OK with this. This kind of break promotes mental well-being; companies with closed-campus lunch and strict "clock in and out for all your meals" stuff have poor morale and often worse performance than their looser counterparts. I would rather see them out in the community than twiddling their thumbs at some station where nobody ever sees them, personally... at least this way they're walking around and getting some exercise, right? This is much less a waste of taxpayer money than other issues in the fire service and I think this is missing the forest for the seedlings... Wendy CO EMT-B

http://www.msnbc.msn.com/id/35519187/ns/health-aging/ I think the article itself puts it best, so I'll just copy and paste here. Is this something you've considered while treating elderly patients, especially those with chronic pain? Has it ever come up in your area? What's your opinion on it? Pot use among seniors goes up as boomers age Gray-haired stoners turn to marijuana to relieve many problems of aging Perry Parks Chuck Burton / AP MIAMI, Florida - In her 88 years, Florence Siegel has learned how to relax: A glass of wine. A copy of The New York Times, if she can wrest it from her husband. Some classical music, preferably Bach. And every night, she lifts a pipe to her lips and smokes marijuana. The use of the U.S.'s most popular illicit drug is growing among retirees as the massive generation of baby boomers who came of age in the 1960s and '70s grows older. The number of people aged 50 and older reporting marijuana use in the prior year went up from 1.9 percent to 2.9 percent from 2002 to 2008, according to surveys from the Substance Abuse and Mental Health Services Administration. Story continues below ↓advertisement | your ad here The rise was most dramatic among 55- to 59-year-olds, whose reported marijuana use more than tripled from 1.6 percent in 2002 to 5.1 percent. Observers expect further increases as 78 million boomers born between 1945 and 1964 age. For many boomers, the drug never held the stigma it did for previous generations, and they tried it decades ago. Some have used it ever since, while others are revisiting the habit in retirement, either for recreation or as a way to cope with the aches and pains of aging. Siegel walks with a cane and has arthritis in her back and legs. She finds marijuana has helped her sleep better than pills ever did. And she can't figure out why everyone her age isn't sharing a joint, too. "They're missing a lot of fun and a lot of relief," she said. Relieves problems of aging Politically, advocates for legalizing marijuana say the number of older users could represent an important shift in their decades-long push to change U.S. laws. "For the longest time, our political opponents were older Americans who were not familiar with marijuana and had lived through the 'Reefer Madness' mentality and they considered marijuana a very dangerous drug," said Keith Stroup, the founder and lawyer of NORML, a marijuana advocacy group. "Now, whether they resume the habit of smoking or whether they simply understand that it's no big deal and that it shouldn't be a crime, in large numbers they're on our side of the issue." Each night, 66-year-old Stroup says he sits down to the evening news, pours himself a glass of wine and rolls a joint. He's used the drug since he first went to university, but many older adults are revisiting marijuana after years away. "The kids are grown, they're out of school, you've got time on your hands and frankly it's a time when you can really enjoy marijuana," Stroup said. "Food tastes better, music sounds better, sex is more enjoyable." The drug is credited with relieving many problems of aging: aches and pains, glaucoma, macular degeneration, and so on. Patients in 14 states enjoy medical marijuana laws, but those elsewhere buy or grow the drug illegally to ease their conditions. Among them is Perry Parks, 67, of North Carolina, a retired Army pilot who suffered crippling pain from degenerative disc disease and arthritis. He had tried all sorts of drugs, from Vioxx to epidural steroids, but found little success. About two years ago he turned to marijuana, which he first had tried in college, and was amazed how well it worked for the pain. "I realized I could get by without the narcotics," Parks said. "I am essentially pain free." But older users could be at risk for falls if they become dizzy, and smoking marijuana increases the risk of heart disease and can cause cognitive impairment, said Dr. William Dale, chief of geriatrics and palliative medicine at the University of Chicago Medical Center. He said he'd caution against using it even if a patient cites benefits. "There are other better ways to achieve the same effects," he said. Pete Delany, director of applied studies at the Substance Abuse and Mental Health Services Administration, said boomers' drug use defied stereotypes, but is important to address. "When you think about people who are 50 and older you don't generally think of them as using illicit drugs — the occasional Hunter Thompson or the kind of hippie dippie guy that gets a lot of press maybe," he said. "As a nation, it's important to us to say, 'It's not just young people using drugs it's older people using drugs.'" In conversations, older marijuana users often say they smoke in less social settings than when they were younger, frequently preferring to enjoy the drug privately. They say the quality (and price) of the drug has increased substantially since their youth and they aren't as paranoid about using it. Dennis Day, a 61-year-old attorney in Columbus, Ohio, said when he used to get high, he wore dark glasses to disguise his red eyes, feared talking to people on the street and worried about encountering police. With age, he says, any drawbacks to the drug have disappeared. "My eyes no longer turn red, I no longer get the munchies," Day said. "The primary drawbacks to me now are legal."

This particular lady has excellent quality of life, so as long as she friggin' wants to fight for is my vote!! She told us the other day she's got to make it to a hundred and one because "Her Name 101" sounds like a "college basket weaving course!!" She's absolutely one of the most amazing women I've ever had the chance to meet. I will be very sad when she finally makes her exit. I wish she was a DNR, personally, so that they wouldn't have to work her when she does code... but it's her choice and I respect that. She apparently had some elevated cardiac enzymes, but not to the point that would indicate an MI (got this second hand from a nurse, so not sure if I got the full picture or not.) They were in fact thinking cardiac, as most of the rest of her labs came back within normal limits (or normal for her I guess I should say.) She was given the amoxicillin due to having developed a slight abscess related to an extraction. The amoxicillin was maintained throughout her hospital stay and still administered upon return to our facility, so I think we can mostly rule that out. She's normally hypertensive but is on beta-blockers (found that out digging through her computerized chart) at a very low dose to maintain her more within a "normal" range. No real evidence of sepsis according to what they did for her in hospital. As far as having her self ambulate, I certainly wouldn't have... but that's me... Thanks all for your responses!! She was definitely a puzzler, but she's back up and running and seems no worse for the wear! Wendy CO EMT-B

Give DwayneEMTP a PM- he used diphenhydramine in Afghan-land when he was over there working with some Aussie docs and clued me in to its use when I was talking to him about some nasty food poisoning my husband was going through. Worked like a freakin' *charm* in concert with some dramamine... Dwayne will have access to some actual protocols, probably. Wendy CO EMT-B

Sorry, Kiwi, my post was directed at the OP. And yeah, I say it is a wholly different assessment based on what you gain from doing it. You can teach a 10 year old to perform a NREMT assessment, doesn't mean they're doing the same assessment as an EMT-P... Wendy CO EMT-B

This is a workplace liability issue. Anywhere that has these signs has designated employees who have been trained as CPR/AED responders at company expense and they are responsible for getting to the patient and using the AED's. It doesn't mean that nobody else can use them, what it really means is that the company has provisions in place and is now covered if Larry the Mail Room R-Tard (thinking Larry the Cable Guy here) goes for the AED and uses it, the company's not liable if he fries himself or someone else. This is exactly how it works at my hubby's workplace, and he is one of the AED/CPR responders there. Wendy CO EMT-B