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 The Written Summary of the EM:RAP Monthly Audio Program Editor: Marlowe Majoewsky MD September Volume 12 Issue 9 EMRAP.ORG Standard laryngoscope is dead! Darren Braude MD interviews Ron Walls MD There is a new edition of the Manual of Emergency Airway Management. What are some of the changes? • The difficult airway algorithm has been modified. How do you think through the key decisions once you have made the decision to intubate? Also, identify the difficult airway and treat it differently. o The decision is made to intubate… o Is this a crash emergent airway i.e. a peri-­arrest situation? In that case just begin intubating. o If not a crash airway, is this going to be a difficult airway? If a difficult airway is not anticipated, you can proceed to rapid sequence intubation. o But what do you do when the patient is a 350 lb 5’7” man with recent neck surgery presenting with status asthmaticus and in severe respiratory distress, oxygen saturation in the 80s on a non-­
rebreather mask, diaphoretic and agitated or any other difficult airway? The old difficult airway algorithm didn’t include paralysis unless you were confident you could intubate and oxygenate them. What do you do when you can’t do an awake technique, you can’t do any temporizing measures, you can’t do a surgical airway on a patient flailing around and you need to paralyze the patient? o Some new techniques/approaches for the difficult airway. 1) Intubating LMA. 2) Flexible endoscopy, either fiberoptic or video scope. For example, the Ambu aScope, which is a disposable single use, flexible video bronchoscope and costs about $200 each. Instead of paralyzing the patient, you can use while keeping the patient awake with some light sedation, topical anesthesia, possibly a drying agent such as glycopyrrolate and use the endoscope through either the mouth or nose to pass the endotracheal tube through the difficult anatomy into the trachea. This a great option in the difficult airway such as severe angioedema, supraglottic swelling, smoke inhalation, disruption to the upper airway, a post-­‐surgical or traumatic hematoma, etc. Increasing in availability and expertise. • Increased emphasis on video laryngoscopy. “It is wrong for people to practice direct laryngoscopy in 2012”. Say what? o Well, maybe not “wrong”, but there is now unassailable evidence that video laryngoscopy, regardless of device, is superior to direct laryngoscopy. The only studies where direct laryngoscopy approached the performance of video laryngoscopy used truly expert intubators. Many of these studies have excluded difficult airways and focus on routine intubations. They perform even better in difficult airways. o Sakles et al. A Comparison of the C-­MAC Video Laryngoscope to the Macintosh Direct Laryngoscope for Intubation in the Emergency Department. Ann Emerg Med. 2012 May 4. Compared the C-­‐MAC video laryngoscope to the Macintosh direct laryngoscope. Found an odds ratio of 12.7 for successful intubation with video laryngoscope over direct, which is a big difference. o Why are we still using direct laryngoscopy? Element of resistance to new technologies. Why are we still teaching direct laryngoscopy? Fear that residents will go work in an Emergency Department without video laryngoscope is a weak argument. This is similar to the argument against using ultrasound guidance to place central lines. Do we want to start training residents without ultrasound in case they go to an ill-­‐equipped ED in the future? Which patient do you want to teach them on? How do you consent that patient? o We need to move on to video laryngoscopy. If someone needs to know direct laryngoscopy for their work in Africa for example, they can learn it. Would you work in a place with no capnography, EM:RAP Written Summary September 2012 Volume 12 Issue 9 pulse oximetry, electrocardiogram, etc? What if it is your child that needs to be intubated? Standard laryngoscope is dead… ALTE Ilene Claudius, MD and Joel Tieder, MD ALTE or Apparent Life Threatening Event is vaguely defined as an episode that is frightening to a caregiver involving some combination of apnea, change in tone or color, choking or gagging. What do you do when a child presents with a frightening episode but looks well? There is not a lot of good literature or clear recommendations on what to do. • The Society of Hospital Medicine convened an expert panel to perform a systematic review and develop evidence-­‐
based guidelines. Identified 37 relevant articles. All were observational, none were randomized and only a few were prospective. • Key questions for the clinician. o Which criteria should we use to admit the child to the hospital? o What laboratory studies/tests would be most helpful in identifying risk? o What historical or exam features are most helpful in identifying risk? • High risk infants. 1) Age under two months and a history of prematurity are higher risk of having another event or a significant underlying condition that may require treatment. Example: a six week old with bronchiolitis may not look like bronchiolitis upon presentation but instead have apnea or feeding difficulties. Similar to pertussis. 2) Risk factors for child abuse or maltreatment. In studies, the risk of abuse in children with ALTEs was about 2-­‐3%. • In these studies, a comprehensive history and physical identified these children and led to observation or further testing. • None of the studies addressed what makes a patient low risk and a candidate for discharge. But once you’ve excluded the high risk group, you can be relatively reassured that most others are low enough risk to outweigh the risks of hospitalization (ex. nosocomial infections, anxiety due to testing, pain, etc.). • For the patient who might not have the above risk factors but is admitted for observation, what testing should be performed in the Emergency Department? No single test was helpful in the literature. The most commonly performed test was a CBC. While it may be positive, it contributed to the determination of a diagnosis less than 5% of the time. Are these children at risk of serious bacterial infection? Unlikely in the absence of fever or other signs of infection. There are no routine tests indicated in the evaluation of an ALTE although specific testing may be performed on a case-­‐by-­‐case basis depending on findings on history and physical exam. • The 24 hour observation period can be helpful, especially if there are social issues. • In the ALTE patient who seems low risk and will likely be discharged, how long should they be observed in the ED prior to discharge? They need to be kept in the ED long enough to take a good history and physical, especially looking for risk factors for child maltreatment. May need social work screening. • Differential diagnosis in ALTE. Includes abuse, bronchiolitis, pertussis, gastrointestinal reflux, sepsis, urinary tract infections, other serious bacterial infection, seizure, toxic ingestion, metabolic disorders, airway abnormalities especially associated with the facial structure, etc. Sickle Cell Disease Update Part Two Jeff Glassberg MD interviewed by Scott Weingart MD The critically ill sickle-­cell patient. Acute Chest Syndrome • Pathophysiology. Not fully understood. Kills a lot of people with sickle-­‐cell disease but clinically is indistinguishable from pneumonia. • Definition. Pulmonary infiltrate and symptoms of pneumonia; shortness of breath, fever, chest pain, etc. Why not just call it pneumonia? Pulmonary infiltrates with chest pain and fever are not necessarily infection. Fat embolism, pulmonary infarction, sickle cell crisis in the pulmonary parenchyma are examples of things that can present with pulmonary infiltrates. When the patient is critically ill, it is considered acute chest syndrome but the actual pathophysiology (embolism vs infection etc) may not be known. • The patient should be considered acute chest syndrome if they have two out of five features; chest pain, fever >38.5, infiltrate, respiratory symptoms or hypoxemia. Treat as if they are going to develop acute chest syndrome, even if they do not look critically ill at this point. • Antibiotics and supportive care is not enough, these patients need exchange transfusion. If unavailable, simple transfusion is an option but not preferred. EMRAP.ORG EM:RAP Written Summary September 2012 Volume 12 Issue 9 •
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What is an exchange transfusion? Patients may not know if they have had acute chest syndrome in the past. You can ask them if they have ever been admitted to the intensive care unit where a large machine with rotating cylinders took their blood out, washed it and put someone else’s blood back in. Goal is to decrease percentage of sickled hemoglobin below 50% (or 30% or less with acute chest syndrome). Why is this better than a simple transfusion? Too much blood leads to viscosity problems and strokes. If exchange transfusion is unavailable and you have to give a simple transfusion, how much should you transfuse? Be gentle. If their hemoglobin is above 8, do not transfuse more than one unit at a time (wait 6 hrs unless the patient is rapidly decompensating). If the hemoglobin is 5 and they are normally at 8, you could transfuse two units. How do you treat acute chest syndrome in the community ER? Give oxygen if they are hypoxemic. Start antibiotics such as ceftriaxone and azithromycin to cover pneumonia. More than 50% of acute chest syndrome patients eventually grow mycoplasma or strep pneumoniae from bronchial washings. If you have a sickle-­‐cell hematologist available, call them. If you are going to transfer the patient, you can transfuse one unit. Pain control is important (they have so much pain that they are often splinting). Use incentive spirometry. If they have a history of asthma and they look like they are having an asthma attack; treat them as usual with bronchodilators and steroids. There is not a role for routine steroids however (these have association with bounceback painful crisis and weak association with intracranial hemorrhage). Dispo to the ICU or high-­‐level monitored bed. This is the leading cause of death for adults with sickle cell disease. •
Transient red cell aplasia • Infection with parvovirus stops production of red blood cells for several days. Not a problem in normal patients, but causes anemia in sickle cell patients with high red blood cell turnover. • In a sickle cell patient with anemia (defined as a drop in their baseline hemoglobin, for example, from 7 to 4), consider all of the causes as you would in a normal patient, as well as transient red cell aplasia, splenic sequestration and hemolytic crisis. Perform guaiac in the patient. A reticulocyte count tells you if they are not making cells. • If the patient has a reticulocyte count of zero, you know they have transient red cell aplasia due to parvovirus. Do two things: 1) isolate the patient with droplet precautions because they have parvovirus (it can cause fetal hydrops in pregnant women) and 2) call a hematologist. Treatment is IVIG. • The patient can usually wait for transfusion unless unstable. Splenic sequestration • Not just a problem in pediatrics, can also affect adults. There is no upper age limit. If the patient has hemoglobin SS, the most common and severe form, these patients usually infarct their spleen by puberty. However, there are multiple case reports of patients with hemoglobin SC presenting with splenic sequestration as adults. • Transfuse first and ask questions later. These patients are critically ill and need to go to the ICU. • How can you diagnose splenic sequestration? Send a reticulocyte count to rule out transient red cell aplasia. The reticulocyte count should be high in hemolytic crisis and splenic sequestration (ex. 5-­‐12). There are several things you can do to differentiate between hemolytic crisis and splenic sequestration. On physical exam, the spleen should be huge in sequestration. Look for markers of hemolysis on labs; LFTs (AST and indirect bilirubin will increase) and LDH. Can be tricky because these patients have baseline hemolysis; compare to previous lab results to look for an increase from the usual. If it is not hemolysis or transient red cell aplasia, it is probably splenic sequestration. • Clinical presentation. Rapid progression of symptoms; become anemic quickly. These patients are sick. • Treatment. Transfuse two units to start. It doesn’t matter what their hemoglobin is to start; these patients die from their anemia. Don’t wait for serial hemoglobins. Dispo to the ICU. • Disease course is in two phases. Initially critically ill because they are basically bleeding to death into their spleen. After receiving transfusions, eventually the blood will remobilize and they are risk for hyperviscosity and strokes. Hemolytic crisis • Treatment. Usually indolent course. The patient will be admitted for a transfusion. You can transfuse in the ED for symptomatic anemia but otherwise there is really nothing to do. What type of blood should you transfuse? Preferably cross-­‐matched and leukocyte-­‐depleted and irradiated. But don’t delay in splenic sequestration. Hyphema. Is a big deal in sickle cell patients or patients with sickle cell trait. If they have trauma to their eye, you need to measure their intraocular pressure. A hyphema is an emergency. You can get vaso-­‐occlusion of the eye, leading to acute angle closure glaucoma and vision loss. Patients may not have a visible hyphema but a micro-­‐hyphema that needs to be treated the same way. If you have a patient with a hyphema, send a sickle cell prep. Consider sending a sickle cell prep in any patient with significant blunt trauma to the eye. Treatment? Elevate the head of bed. Call EM:RAP Written Summary September 2012 Volume 12 Issue 9 ophthalmologist. Beta-­‐blockers and clonidine are ok. Don’t give acetazolamide (Diamox) or other diuretics, mannitol or topical beta-­‐agonists like epinephrine (avoid medications that can cause sickling). Admit the patient. Sudden death after exercising. Patients with sickle cell trait may experience sudden death at high altitude or exhausting exercise. Unknown etiology. Priapism • 89% of sickle cell patients will have an episode of priapism by age 20. • How does the treatment of priapism differ in sickle cell? If less than two hours, give analgesics and IV fluids. However, most patients will present after two hours. Intracavernosal injection of epinephrine (1:1,000,000 dilution) or phenylephrine. If that doesn’t work, you can do two other things. 1) Exchange transfusion – but there is an association with stroke-­‐like symptoms 2) Epidural anesthesia. • If they detumesce, do you send them home or admit them? Usually send home after period of observation in the ED. Chest Pain History Again Amal Mattu MD • Classic ACS presentation. Typically midsternal or left-­‐sided chest pain described as pressure, squeezing, tightness, provoked by exertion, more concerning if at rest, radiates to left arm/neck/jaw, associated with shortness of breath, nausea/vomiting, diaphoresis, lightheadedness. • If a patient presents with symptoms other than a classic presentation, we tend to call it atypical chest pain. However, an atypical presentation does not mean it is not cardiac. For example, 20% of patients with proven MI will present with upper abdominal pain instead of chest pain. Or may have isolated pain to the left arm (especially women), anterior neck or back (upper or left trapezius). 1/3 of patients will describe the pain as pressure, but many will describe mild ache or sharp, stabbing, burning. 20% will use the term indigestion. Only 1/3 of patients report pain came on with exertion. 7% of patients report the pain came on with emotional stress (don’t disregard this; screaming at your spouse is a stress test). 8% reported the pain came on with eating. Pain radiating to the right side occurs in up to 40% and may be more specific. And patients may not even present with pain; about 1/3 have no pain (especially diabetics, elderly and women). ACS can and does present atypically. You can’t rule out ACS based on absence of typical features. • Three articles that you should know about: 1) Panju et al. The rational clinical examination. Is this patient having a myocardial infarction? JAMA 1998 Oct 14;280(14):1256-­‐63. 2) Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA 2005 Nov 23;294(20):2623-­‐9. o These two articles reviewed all the literature on ACS presentations and assigned likelihood ratios for various presenting features to determine which signs and symptoms were useful for both increasing and decreasing the likelihood of ACS. o Only four features significantly increased the likelihood of ACS rule-­in. 1) Pain that radiates bilaterally or to the right. 2) Pain associated with exertion. 3) Pain associated with diaphoresis. 4) Pain associated with nausea/vomiting. All of the other typical symptoms such as chest pressure did not increase the likelihood. o Factors that decrease the likelihood of ACS include pleuritic pain, positional, sharp pain, pain at rest and pain that is reproducible with palpation. Even though these factors decreased the risk, there is no single or combination of factors that should obviate your concern about ACS. 3) Body et al. The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes. Resuscitation. 2010 Mar;81(3):281-­‐6. Included 796 patients, with 148 of those ruling in for MI, and looked at the factors that increased or decreased the risk of MI. They found four things that increased the risk of ruling in for MI; pain that radiates bilaterally or to the right arm, pain with vomiting, pain with sweating and central location of the pain. This was similar to the previous two articles. Pressure, squeezing and tightness were not associated with any increase or decrease in likelihood. • You need to assess and document the presence or absence of these concerning factors of pain radiating bilaterally or to the right side, pain with vomiting or sweating and exertional chest pain. Remember, patients with MI often can and do have atypical presentations. • These factors might be useful when the EKG is non-­‐diagnostic; for example, a left bundle branch block that does not meet Sgarbossa criteria but does have these concerning factors. EM:RAP Written Summary September 2012 Volume 12 Issue 9 Procedural Sedation – Go Deep! Clay Josephy MD • We don’t do conscious sedation in the ED, we do deep sedation. The continuum is moderate, deep, anxiolysis and analgesia. What we mainly do is deep sedation, but regulatory agencies view deep sedation as monitored anesthesia care. It has been difficult for Emergency Medicine physicians practicing in small hospitals to secure this privilege. • The FDA considers the drugs that we use to be general anesthetics; etomidate, brevital, propofol, ketamine. The Centers for Medicare & Medicaid Services (CMS) had a revision of their interpretive guidelines in December of 2009 that stated these need to be administered by professionals trained in anesthesia, without defining it further. • After work by ACEP, CMS revised this in January 2011, stating that EM physicians have a very specific skill set to manage airways and ventilation in patients requiring rescue and are “are uniquely qualified to provide all levels of analgesia/sedation and anesthesia (moderate to deep to general)”. In addition, we are supported by an increasing body of peer-­‐reviewed literature as well as ACEP sponsored practice policy guidelines. • It is time to come out of the closet and openly confess that you are an expert in management of ED sedation. • Suggest an Emergency Department procedural sedation policy, a single privilege, including all levels of sedation and analgesia in adults and children. • Note: the CMS revision of the revision has two caveats that can be difficult to get around. First, they require that there be a hospital service called Anesthesia Services and directed by a single individual. This falls under anesthesiology by proxy. Although not required, it is recommended that the anesthesia policies and procedures are developed by a committee including other hospital disciplines so that all practice environments and patient needs are met. Also, different departments in the hospital can use different guidelines for their departmental practices and policies (such as ACEP guidelines for the Emergency Department). • Some pitfalls: go gingerly, have bargaining power, anesthesia often feels they are granting the ED privileges, watch out for language such as “pushing medication” versus “administering” medication because the CMS states RNs are unable to administer anesthesia. • Contact Clay Josephy at [email protected] for a copy of his generic policy that you can use as a starting point at your hospital. Mini-­Journal Club -­ Power David Newman, MD Selker et al. Out-­of-­hospital administration of intravenous glucose-­insulin-­potassium in patients with suspected acute coronary syndromes: the IMMEDIATE randomized controlled trial. JAMA. 2012 May 9;307(18):1925-­‐33. Context Laboratory studies suggest that in the setting of cardiac ischemia, immediate intravenous glucose-­‐insulin-­‐
(GIK) reduces ischemia-­‐related arrhythmias and myocardial injury. Clinical trials have not consistently shown potassium these benefits, possibly due to delayed administration. To test out-­‐of-­‐hospital emergency medical service (EMS) administration of GIK in the first hours of suspected Objective acute coronary syndromes (ACS). Design, S etting, and Participants Randomized, placebo-­‐controlled, double-­‐blind effectiveness trial in 13 cities (36 EMS from December 2006 through July 31, 2011, in which paramedics, aided by electrocardiograph (ECG)-­‐based agencies), decision support, randomized 911 (871 enrolled) patients (mean age, 63.6 years; 71.0% men) with high probability of ACS, Intervention Intravenous GIK solution (n=441) or identical-­‐appearing 5% glucose placebo (n=460) administered by in the out-­‐of-­‐hospital setting and continued for 12 hours. paramedics Main Outcome Measures The prespecified primary end point was progression of ACS to myocardial infarction (MI) hours, as assessed by biomarkers and ECG evidence. Prespecified secondary end points included survival at 30 within 24 days and a composite of prehospital or in-­‐hospital cardiac arrest or in-­‐hospital mortality, analyzed by intent-­‐to-­‐treat and by presentation with ST-­‐segment elevation. Results There was no significant difference in the rate of progression to MI among patients who received GIK (n=200; 48.7%) v s those who received placebo (n=242; 52.6%) (odds ratio [OR], 0.88; 95% Cl, 0.66-­‐1.13; P=.28). Thirty-­‐day was 4.4% with GIK vs 6.1% with placebo (hazard ratio [HR], 0.72;95% Cl, 0.40-­‐1.29; P=.27). The composite of mortality cardiac a rrest or in-­‐hospital mortality occurred in 4.4% with GIK vs 8.7% with placebo (OR, 0.48; 95% Cl, 0.27-­‐0.85; P=.01). A mong patients with ST-­‐segment elevation (163 with GIK and 194 with placebo), progression to MI was 85.3% with GIK vs 88.7% with placebo (OR, 0.74; 95% Cl, 0.27-­‐1.49; P=.29). The composite outcome of cardiac arrest or in-­‐ EMRAP.ORG EM:RAP Written Summary September 2012 Volume 12 Issue 9 hospital mortality was 6.1% with GIK vs 14.4% with placebo (OR, 0.39; 95% Cl, 0.18-­‐0.82l P=.01). Serious adverse events occurred in 6.8% (n=28) with GIK vs 8.0% (n=41) with placebo (P=.26). Conclusions Among patients with suspected ACS, out-­‐of-­‐hospital administration of intravenous GIK, compared with glucose placebo, did not reduce progression to MI. Compared with placebo; GIK administration was not associated with improvement in 30-­‐day survival but was associated with lower rates of the composite outcome of cardiac arrest or in-­‐hospital mortality. • Earlier studies suggested cardioprotective effect of glucose-­‐insulin-­‐potassium (GIK). Thought to reduce bad outcomes of ACS including progression to MI, possibly death or ventricular arrhythmias. However, these early studies were mostly observational or non-­‐blinded. • A randomized controlled trial in 2008 showed no benefit; however, in that study the drug was administered 60% of the time to patients who had already had a reperfusion intervention so a cardioprotective effect for actively ischemic tissue might not have been seen. The IMMEDIATE trial was designed to provide the glucose-­‐insulin-­‐
potassium earlier in the prehospital setting rather than waiting until after MI was diagnosed in the hospital. • This study enrolled 911 patients from the prehospital EMS setting. 54,579 patients were screened. Who was included? Patients received a 12-­‐lead EKG in the field. The 12-­‐lead EKG had software embedded in it that provided an ACI-­‐TIPI (Acute Coronary Ischemia Time-­‐Insensitive Predictive Index) score that tells you how likely it is that the patient is having acute coronary syndrome. This study included patients who were 75% or more likely to have ACS per ACI-­‐TIPI. About 40% of patients had STEMI when they were enrolled. The study was double-­‐blinded and the patients received either IV glucose-­‐insulin-­‐potassium (GIK) or placebo. • The primary outcome was reduction of progression to myocardial infarction. If the ECG and enzymes performed later at the hospital showed an MI; that was considered progression to MI (even though 40% of these patients started out as a STEMI). It was thought that GIK might abort an MI in progress or take a patient with ACS and prevent them from going on to full occlusion. This is interesting because the cardioprotective effect of GIK was not thought related to platelets or preventing occlusion but rather making the myocardium better able to tolerate ischemia and preventing arrhythmias. • The study researchers hoped to find a 12% difference in progression to MI. They estimated 56% of patients in the placebo group and 44% of patients in the GIK group would progress to MI. And they powered the study to be able to determine if there was a 12% difference between the placebo and GIK. • What did they find? There was not a statistically significant difference in progression to MI. There was only a 4% difference. The P value was 0.28. • So why are we talking about this study? There was a secondary outcome of cardiac arrest and in-­‐hospital mortality. 4.4% in the GIK group had cardiac arrest or in-­‐hospital mortality compared to 8.7% in the placebo group. The P value was 0.01. This was a secondary outcome. It can generate a hypothesis about something that should be studied as a primary outcome but it can’t give you a definitive answer about whether something reduces an outcome. It is not proof that GIK reduces cardiac arrest or in-­‐hospital mortality. • So why is it that you can have 4% difference in cardiac arrest or in-­hospital mortality with a P value of 0.01 and a 4% difference in progression to MI with a P value of 0.28? It is all about the power. • Power is the statistical ability to detect a difference. If differences are really small between two groups, you will need more patients to detect the difference. Increasing the power means increasing the number of patients in your study. In this study, there was adequate power to detect a 12% difference in progression to MI. • When you are trying to determine whether a P value is important, you need to know whether an adequate number of patients, interventions, etc was enrolled in the study. Why? It is always possible that there are going to be random fluctuations that affect events. For example, if you flipped a coin five times and got heads all five times, you would probably assume it was a random event rather than a rigged coin. The likelihood of getting five heads in a row is about 4% with a P value of 0.04 – making it appear statistically significant. While it may be statistically significant, this is not a sufficient number of times flipping the coin to determine if it is rigged. If you flipped the coin 100 times and got heads every single time, you would think about it differently. To get 100 heads in a row would happen 1 in a billion times or less. Finding low P values is easy. You are not powering a study to find a difference but to show you can have enough confidence that when you find a difference and a low P value, you have flipped the coin or administered the drug enough times to know that the difference is real and not an anomaly. • The problem with the above study is that they powered the study to find a 12% difference in progression to MI. This is a big difference. Because big differences are less likely to be due to random fluctuations, they needed to enroll only 900 subjects. If a 12% difference was found after 900 subjects, it was less likely a random fluctuation and more likely a genuine difference. • If they had wanted to power the study to detect a 4% difference between GIK and placebo in cardiac arrest and in-­hospital mortality, they needed thousands of patients. Remember that smaller differences are EM:RAP Written Summary September 2012 Volume 12 Issue 9 •
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more likely to happen due to random fluctuations so you need more patients to be confident the difference is real. When this trial was originally planned, they had wanted to enroll 15,000 patients in the study to find a difference in cardiac arrest and in-­‐hospital mortality. However, because they were doing this study in the prehospital environment, they found they did not have enough resources to enroll 15,000 patients. They changed their primary outcome when they realized that they could only enroll 900. This is why the primary outcome of progression to MI is such a weird outcome (especially when 40% had STEMI from the beginning). The secondary outcomes in this study raised interesting questions. While this was supposed to be the definitive trial on GIK, it is apparent that these issues will have to be examined with cohorts that include enough subjects to detect whether cardiac arrest or in-­‐hospital mortality changes as a result of GIK. Power is about having enough subjects to show that any difference you find is not a random fluctuation. It is not about finding a P value that looks good. It is about flipping the coin or giving the intervention enough times that you can be confident that any difference is not due to random fluctuation. And remember, studies that have too much power are able to find statistically significant differences that may not be clinically relevant. Pain Management Algorithm Mark Jaben MD Problems with pain management; we don’t treat people who should be treated and we prescribe medications to people we shouldn’t. How do we de-­‐stress these interactions? Developed an algorithm to assist in management of these patients. #1. Is this an opiate-­naïve or opiate tolerant person? The people who are not used to daily opiates and come in with a painful condition should be treated. How do you know? Review the med list, look at the number of and reason for visits, controlled substances database. #2. For opiate tolerant patients, is this an acute problem on top of their chronic problem? These are the most difficult patients. If they have an acute problem, they fall into the same category of opiate-­‐naïve patients and will be treated for their pain via rapid control of their pain in the Emergency Department followed by a short outpatient program. Some talking points for these patients (especially the chronic low back pain patients): explain what we know about the effects of opioids, how long it takes someone to get hooked, if they have any personal or family history of abuse (consider looking at the database), what they can realistically expect from these medications, how to get off them quickly and why they shouldn’t be on them for more than a few days. #3. The opiate tolerant patient does not have an acute problem but has an exacerbation of their chronic problem. Two options; are they in a pain program or not? o If they are in a pain program, are they in violation of their program by being in the ED? What contract have they made? What part of the program they are involved in is not working for them? Are they not getting to see their doctor? Is their doctor not prescribing enough for them? Can lead to discussion with the patient and coordination with the primary care physician. Review patient responsibilities; if they are running out of their medication, they need to address it beforehand rather than showing up in the ED. o If they are not in a pain program, have a frank discussion with them about the difference between fixing acute pain and chronic pain. They are not going to get the sort of the relief that you might get in an acute situation. Talk about the risks of long-­‐term opioid use and the importance of being in a program. Controlling chronic pain takes more than pills. Ask if they are diverting: are they using it recreationally or other people are using their medications? •
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EM:RAP Written Summary September 2012 Volume 12 Issue 9 Pain Management Algorithm Review med list Review medical record for # of visits, reason for visits, amount opioids given Opiate Tolerant Opiate naïve Pain management Acute problem 1) Rapid control 2) Short outpatient program 3) Avoid schedule 2 drugs Exacerbation of chronic problem In pain program Risk for addiction-­‐ previous personal or family substance abuse issues; check controlled substances database Data about long term risk 1) 2x greater risk of prolonged disability from low back pain with > 100-­‐150 mg Morphine equivalent (10-­‐15 Percocet 10) 2) 90% can’t get off meds after 90 days of 50-­‐100 mg equivalent per day Realistic expectation of opioid effects What patient should and should not expect How to get off quickly 1) In violation by being in ED? 2) What about your program is not working for you? 1) Coordinate with PCP 2) Review patient responsibility 3) Consider few pills until next day or by plan with PCP 4) Consider limiting future care 1) Categorize patient properly 2) Treat when appropriate 3) Respect every patient by defining their problem, defining success for each person and yourself, form a plan. Our only obligation is to listen earnestly, articulate what is doable and articulate a plan acceptable to you, especially if not what that the patient wants. If they don’t agree, have them contact the ED director 4) No replacements for lost or stolen meds, if scheduled drugs 5) No refills if under another doctor’s care for this acute problem without verification 6) Photo ID required for dispensed meds, photo to be taken if no photo identification Not in pain program 1) Agree with patient there is a problem with chronic pain, and with the way patient is getting care 2) Not appropriate use of the ED -­‐ risk being labeled and losing this source 3) Every therapy has risk of benefit and risk of harm, especially with long term opioid use and uncoordinated care 4) Importance of a program and PCP -­‐ Best chance is to avoid risk of harm -­‐ Controlling chronic pain takes more than just opioids 5) Public health risk – Recreational use, overdose, diversion and abuse -­‐ Prescribed meds are a major source ‘I have to ask since I don’t know your situation especially with chronic use outside a program’ ‘I hope you understand my responsibility to do no harm’ 6) Realistic expectations of opioid effect –decrease pain by 30-­‐50% 1) Referral 2) Consider few pills to avoid withdrawal (2/day) 3) Consider limiting future care EDITOR: Marlowe Majoewsky MD EMRAP.ORG EM:RAP Written Summary September 2012 Volume 12 Issue 9