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Date: April 14th, 2015

Guest Skeptic: Dr. Alan Chiem is an assistant clinical professor and the director of ultrasound at UCLA Olive View.

Case: 78-year-old man with a history of diabetes, hypertension and coronary artery disease presents with a two day history of increasing shortness of breath. He does not have any chest pain or fever. You have been doing more and more with ultrasound and wonder whether you can make the diagnosis of acute pulmonary edema before getting the standard CXR, ECG and lab tests.

Background: Acute heart failure is a condition where the heart cannot pump well enough to meet the demands of the body. It can be due to a number of different causes including: myocardial infarction, arrhythmias, valvular dysfunction, pneumonia, uncontrolled hypertension, anemia, hyperthyroidism and many other causes.

The diagnosis of heart failure before the 1990’s was fairly grim with 60-70% of patients dying within five years of diagnosis.

Things have improved tremendously over the last couple of decades with respect to mortality but heart failure is still the most common re-admission diagnosis within one month for patients over 65 years of age. In the U.S. we spent roughly 25 billion every year on acute heart failure hospitalizations alone.

The diagnosis of acute heart failure can be challenging because the signs and symptoms are insensitive and/or non-specific.

Clinical gestalt alone is moderately specific, but not sensitive (LR+ 4.4, LR- 0.45). Chest x-rays have been used for years to diagnose heart failure, but is also imperfect. For example the presence of interstitial edema has LR+ 17.1 but LR- only 0.7. In addition, chest x-ray interpretation agreement between radiologist and emergency physician can be less than 50%. This could result in many patients with acute heart failure being missed.

Serum markers of BNP and ProBNP sometimes help diagnose patients with acute dyspnea. A systematic review by Lam et al in Ann of Intern Med 2010 demonstrate ED testing may decrease hospital LOS by a day, and possibly reduce admission rates, but they did not really affect mortality rates. http://pmid.us/22123173

In 2012, BEEM and Dr. Peter Rosen published a review of 5 diagnostic RCTs that explored ED physician awareness of BNP or not (J Emerg Med). This study noted no consistent differences in any measurable outcome (diagnostic accuracy, ED length of stay, hospitalization rates, length of hospital admission, etc.)

POCUS is now part of the core curriculum for emergency medicine residents. Identifying B-Lines on thoracic ultrasound can be used to identify interstitial fluid.

Clinical Question: Can novice emergency medicine resident physician sonographers accurately identify B-lines in undifferentiated dyspnea patients to diagnose acute heart failure after a 30-minute training course?

Reference: Chiem AT, et al. Comparison of expert and novice sonographers’ performance in focused lung ultrasonography in dyspnea (FLUID) to diagnose patients with acute heart failure syndrome. AEM April 2015

* Population: Sixty-six EM resident physicians from one inner-city ED with over 100,000 annual visits assessing patients >18 years old presenting with chief complaint of dyspnea.

* Exclusions: Attending physician perspective that dyspnea due to cause other than CHF, incarcerated individuals, patients who were pregnant, on dialysis, on positive pressure ventilation, or receiving nebulizer treatment, or too ill to provide written consent. Non-English speaking patients were also excluded.

* Intervention: Bedside ultrasound by EM resident assessing for three or more B-lines using eight-zone thoracic ultrasound on thora...

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Date: April 29th, 2015

Guest Skeptic: Dr. Kerstin deWit did an Internal medicine and EM training in the UK. Since then she has worked in Thrombosis research and received a doctorate in the UK and a Masters in Epidemiology from the University of Ottawa. Kerstin currently works as a Thrombosis physician and Emergency Physician at McMaster University and member of Best Evidence in Emergency Medicine (BEEM).

Case: An 84-year-old woman presents to the ED with vague symptoms of shortness of breath and mild chest discomfort for the last two days. She does not say “pain” but rather just an ache when taking a deep breath. Her past medical history includes hypertension, dyslipidemia, type-2 diabetes and osteoarthritis. Her vital signs are normal. She is Well’s low but PERC positive due to her age. You do not want to order a D-dimer because of the high false positive rate but pulmonary embolism (PE) is on your differential.

Background: A negative D-dimer has been shown to safely rule out pulmonary embolism in patients who are not high risk. It has a high sensitivity but low specificity. This means that there is a high false positive rate.

The false positive rate increases with age. This is because normal D-dimer levels increase with age. The result is older patients are subjected to more diagnostic image testing to rule-out PE.

There is a worldwide epidemic of over-testing with the downstream consequences of over-diagnosis and over-treatment. The problem of over-testing is complex. It stems from an imperfect mix of incomplete and flawed diagnostic evidence, constant malpractice threats (worse in some parts of the world than others), and clinicians struggling to balance clinical care (our day job) with maintaining awareness of the ever-evolving research landscape.

PE is a prime target to reduce over-testing and there have there have been a number of studies looking at age adjusting the D-dimer. The derivation study was done by Douma et al 2010. They suggested using a new cut off for patients over the age of 50 years of age.

The formula was patient’s age x 10. So in our case it would be 84×10=840 μg/L

* Conclusion: “The age adjusted D-dimer cut-off point, combined with clinical probability, greatly increased the proportion of older patients in whom pulmonary embolism could be safely excluded.”

The concept of age-adjusting the D-dimer to rule-out PE was validated in two trials (van Es et al 2011 and Penaloza et al 2012). Both of these studies demonstrated the clinical usefulness of this approach.

In 2013, Schouten et al in the BMJ published a systematic review and meta-analysis. It had over 12,000 patients and compared conventional D-dimer cut off of 500 μg/L vs. age-adjusted D-dimer.

* Conclusion: “The application of age adjusted cut-off values for D-dimer tests substantially increases specificity without modifying sensitivity, thereby improving the clinical utility of D-dimer testing in patients aged 50 or more with a non-high clinical probability.”

There were some concerns about this meta analysis expressed by some including Dr. Brent Thoma from Boring EM. His concerns seemed to focus on the heterogeneity of the studies and combining DVT studies with PE studies in the meta analysis.

Theme Music: Good Riddance by Green Day performed by Ethan Milne

Another turning point, a fork stuck in the road. Nurse grabs you by the hand, directs you where to go.

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Date: April 24th, 2015

Guest Skeptic: Meghan Groth (@EMPharmGirl). Meghan is the emergency medicine pharmacy specialist at the University of Vermont Medical Center in Burlington, Vermont and an adjunct professor of pharmacy at the Albany College of Pharmacy and Health Sciences.

Case: A 58-year-old male presents to your emergency department complaining of a warm, painful, reddened area on his left thigh. His past medical history is only significant for generalized anxiety disorder and he has no known drug allergies. On exam, you find no evidence of an abscess, and you find his labs and vital signs are within normal limits. You confidently give him a diagnosis of uncomplicated cellulitis and need to determine an antibiotic regimen. You’d like to send him home with a five day course of cephalexin, but are thinking about giving him an intravenous (IV) dose of cefazolin before he leaves.

Background: In certain infectious disease conditions, such as meningitis or septic shock, we know that rapid administration of antimicrobials in adequate doses is associated with improvement in patient outcomes.

Septic shock is a time dependent emergency. It has been demonstrated for every hour delay in providing antibiotics to patients with septic shock mortality increased by almost 8%.

However, in patients who are well enough to be discharged home, this same relationship has not been demonstrated.

We all know that antibiotic associated diarrhea (AAD) is a common side effect of antibiotic therapy. The incidence in the literature has been reported to be between 5% and 39%. One of the most concerning types of AAD is Clostridium difficile (CDI). This has been on the increase.

There is such concern about C.diff that it has been one of the patient safety quality indicators in many organizations/jurisdictions.

There have been a number of factors that increase the risk of AAD/CDI including the type of antibiotic prescribed and the duration of use. While almost all antibiotics can cause AAD and CDI the cephalosporins, broad-spectrum penicillins and clindamycin are more often the cause.

Patient factors are also thought to be involved: age greater than 65 years, co-morbidities and having a history of AAD.

Clinical Question: What is the risk of getting antibiotic associated diarrhea with an IV dose of antibiotics prior to discharging patients home with an oral course?

Reference: Haran et al. Factors influencing the development of antibiotic associated diarrhea in ED patients discharged home: risk of administering IV antibiotics. Am J Emerg Med 2014

* Population: Adult patients from three emergency departments (2 large urban and 1 small community site).

* Excluded patients if they had diarrhea or Clostridium difficile in the previous 4 weeks, had received an antibiotic in the previous 4 weeks, or were admitted to the hospital.

* Intervention: IV antibiotics as part of their emergency department and discharged home with a new prescription for antibiotics.

* Comparison: Patients who were not given IV antibiotics as part of their emergency department care and discharged home with a new prescription for antibiotics.

* Outcome:

* Primary outcome was the development of AAD, which the authors defined as three or more loose stools per day for at least two days.

* Secondary outcome was the development of CDI, which the authors defined as AAD that led to a diagnosis of CDI confirmed by a positive C. difficlie toxin A assay.

Author’s Conclusions: “Intravenous antibiotic therapy administered to ED patients before discharge was associated with higher rates of AAD and with 2 cases of CDI. Care should be taken when deciding to use broad-spec...

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Date: April 15th, 2015

Guest Skeptics: Clay Odell. Clay is a paramedic and Executive Director of Upper Valley Ambulance, a regional EMS system covering nine communities in rural New Hampshire and Vermont. He’s been involved in EMS for over 30 years in a variety of roles including urban paramedic, flight paramedic, an emergency nurse, and Chief of the State EMS Office in New Hampshire. Clay is very interested in EBM for EMS and says he’s trying really hard to learn, but continues to procrastinate about actually taking a statistics course again.

Previous EMS/Pre-hospital Episodes on the SGEM:

* SGEM#54: Baby It’s Cold Outside (Pre-Hospital Therapeutic Hypothermia in Out of Hospital Cardiac Arrest)

* SGEM#59: Can I get a witness (Family Members Present During CPR)

* SGEM#96: Machine Head (NIPPV for Out of Hospital Respiratory Distress)

Case: Your rural EMS unit is dispatched to a call for a 65-year-old man with chest pain. On scene a 12 lead ECG is acquired in six minutes, revealing ST elevation in V3 through V6. The patient is given 324 mg of chewable aspirin, sublingual nitroglycerin which reduces his 9/10 chest pressure, oxygen by nasal cannula at 2 lpm to maintain his SaO2 above 94%. The patient is removed from the second floor of his home by stairchair, placed on the stretcher, loaded into the ambulance and transport is initiated to the closest PCI center. The EMS provider calls the hospital with a STEMI alert with a 30 minute ETA. Enroute the patient is monitored, serial 12 lead is done, another nitro is given when chest discomfort returns, but otherwise you settle in for the ride. You recall reading an article in a journal recently about remote ischemic conditioning, which is done by inflating a BP cuff on the patient’s arm to 200 mmHg for 5 minutes, then release the pressure for 5 minutes, and repeat three more times. The article said this technique reduces myocardial damage from reperfusion injury after the PCI. It’s not in your protocols so you call online medical control to discuss it.

Background: The phenomenon of ischemic preconditioning was reported almost 30 years ago in experiments done on dogs. These early studies looked at limiting infarct size. The technique involved a series of alternating periods of ischemia of a coronary artery with reperfusion sessions to render the myocardium more resistant to a subsequent ischemia event.

When a coronary vessel is occluded during an MI, myocardial cells distal to the occlusion suffer from ischemic injury. A reperfusion injury has been described once the flow has been restored via PCI that may increase the infarct size.

Unlike the dog experiments, the remote ischemic conditioning (RIC) involves placing a blood pressure cuff on an extremity. It typically is on the arm and inflated to 200 mmHg for 5 minutes, then released. This pattern is repeated three more times.

The exact mechanism behind remote ischemic conditioning (RIC) is not known. It is thought to be a neuroal and hurmoral interaction mediating the protective effect.

RIC has been investigated in a number of large cardiac surgery and PCI trials. These have reported benefit in improving cardiac markers and limiting infarct size.

Clinical Question: Does pre-hospital remote ischemic conditioning performed on STEMI patients decrease myocardial reperfusion injury and improve their long-term outcome?

Reference: Sloth et al. Improved long-term clinical outcomes in patients with ST-elevation myocardial infarction undergoing remote ischaemic conditioning as an ad...

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Date: April 11th, 2015

Guest Skeptics: Dr. Bret Batchelor. Bret is a general practitioner with Enhanced Surgical Skills currently working in Vanderhoof, BC. He is the host of the newly created podcast that can be found on iTunes called Really Rural Surgery.

Case: A 35-year-old man presents to the emergency room with right lower quadrant pain for approximately 18 hours. You assess the patient and find that his Alvarado Score is 7. You then ask for an ultrasound, as his body mass index is in the normal range. The ultrasound shows that he has an enlarged appendix >6mm that is not compressible and there is no intraperitoneal fluid present. You make a presumptive diagnosis of uncomplicated acute appendicitis. You relay this finding to the patient and he turns to you and asks, “Hey doc, I heard that you can treat appendicitis with antibiotics now. Is that true?”

Background: Claudius Amyand did the first appendectomy in 1735.  The standard treatment for acute appendicitis ever since Charles McBurney described it in 1889 has been appendectomy.

Omar et al (2008) showed just how safe laparoscopic appendectomies have become. They found in a study of over 230,000 UK patients under the age of 49 there were no deaths. Kluiber et al (1996) demonstrated the incidence of post-operative intra-abdominal wound infection to be about 2-5%.

Being that there are doctors out there without scalpels, and that diverticulitis has often been treated successfully with antibiotics (this also being an infection based on the same theory), some have put two and two together and postulated that perhaps acute appendicitis could be treated successfully with antibiotics.

Two meta-analyses have been done recently and interestingly enough; they looked at nearly the same studies on “uncomplicated” acute appendicitis and came up with two opposite conclusions. This is an example of why things in evidence-based medicine can be “complicated”.

Clinical Question: Are antibiotics in non-complicated acute appendicitis an effective and safe alternative to appendectomy?

Reference #1: Varadhan et al. Safety and efficacy of antibiotics compared with appendectomy for treatment of uncomplicated acute appendicitis: meta-analysis of randomised controlled trials. BMJ 2012

* Population: 4 RCTs of adult patients (n=900)

* Intervention: Antibiotics

* Comparison: Appendectomy

* Outcome:

* Primary Outcome: Complications (wound infection, perforated appendicitis, peritonitis)

* Secondary Outcomes: Length of stay, readmissions, efficacy of treatment, perforation, pain and body temperature.

Authors’ Conclusion: “Antibiotics are both effective and safe as primary treatment for patients with uncomplicated acute appendicitis. Initial antibiotic treatment merits consideration as a primary treatment option for early uncomplicated appendicitis.”

Quality Checklist for Therapeutic Systematic Reviews:

* The clinical question is sensible and answerable. Unsure. Sensible question but the definitive diagnosis is pathology. That will always limit the group assigned to antibiotics to know whether they truly had uncompli...

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Date: March 25th, 2015

Guest Skeptic: Dr. Steve Carroll. Steve is an Emergency Medicine Physician and EM Core Faculty with the US Army at San Antonio Military Medical Center in San Antonio, Texas. He also does an awesome podcast called EM Basic that is your “boot camp guide to emergency medicine”. EM Basic reviews common EM topics at the level of a medical student or intern.

Case: A 40-year-old male comes to the Emergency Department with a dislocated shoulder while playing football. He’s a weekend warrior and has never had any shoulder dislocations in the past. It took him about an hour to get the Emergency Department. After some pain control, you try the Cunningham and scapular manipulation to get the shoulder back in but they are not working. You decide that he needs procedural sedation. One of your residents asks you “I’ve heard about ketofol thing, can we try it in this patient?”

Background: Ketofol’s use has been rising in popularity in the EM and pediatric EM community. Ketofol refers to a combination of ketamine (which we talked about using in a sub dissociative dose for pain control recently) and propofol. It is often mixed in the same syringe but people some choose to give it separately. The theory is that the two medications can make a procedure go right by canceling out the bad effects of the other.

Propofol tends to cause hypotension and sometimes apnea whereas ketamine usually raises the blood pressure and doesn’t affect the respiratory drive. On the flip side, ketamine tends to cause vomiting when emerging from its effects whereas propofol has some antiemetic properties.

Clinical Question: How does propofol compare to ketofol mixed at 1:1 ratio compared to ketofol mixed at 4:1 (propofol to ketamine) for adults requiring procedural sedation in the Emergency Department?

Reference: Miner et al. Randomized, Double-Blinded, Clinical Trial of Propofol, 1:1 Propofol/Ketamine, and 4:1 Propofol/Ketamine for Deep Procedural Sedation in the Emergency Department. Annals of Emerg Med 2014

* Population: Adults 18 and over presenting to the ED requiring procedural sedation for a painful ED procedure

* Intervention: Propofol/ketamine at 1:1 ratio or 4:1 ratio

* Comparison: Propofol alone

* Outcome:

* Primary Outcome: Number and proportion of subjects experiencing airway or respiratory adverse events leading to an intervention.

* Secondary Outcomes: Lowest oxygen saturation during the procedure, success of the procedure, recovery agitation, patient’s pain scale, memory of the procedure by the patient, and patient satisfaction with the procedure

Authors’ Conclusions: “We found a similar frequency of airway and respiratory adverse events leading to intervention between propofol alone and either 1:1 or 4:1 ketofol.”

Quality Checklist for Randomized Clinical Trials:

* The study population included or focused on those in the ED. Yes

* The patients were adequately randomized. Yes

* The randomization process was concealed. Yes

* The patients were analyzed in the groups to which they were randomized. Yes

* The study patients were recruited consecutively (i.e. no selection bias). Yes– 24/7 enrollments with trained research assistants

* The patients in both groups were similar with respect to prognostic factors. Yes

* All participants (patients, clinicians, outcome assessors) were unaware of group allocation. Unsure?- syringes all looked the same, prepared ahead of time

* All groups were treated equally except for the intervention.

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Date: March 26th, 2015

Guest Skeptics: Dr. Suneel Upadhye (BEEM Group) and Dr. Tiffany Osborn (ProMISe Author)

Suneel is an Associate Clinical Professor Emergency Medicine at McMaster University and Associate Member of Clinical Epidemiology and Biostatistics. He is also the Chair CAEP standards committee and a sepsis researcher.

Tiffany is the second author on the ProMISe Trial. She is an Associate Professor in the Department of Surgery and the Department of Emergency Medicine at Washington University, St. Louis.

Case:  You see a 62 year-old man sent from a nursing home with a three day history of a productive cough, intermittent fevers and today is a bit confused. The transfer notes include a history of congestive heart failure, chronic obstructive pulmonary disease, gout, hypertension, type 2 diabetes, and mild dementia. His emergency department vitals are as follows: Temperature 39.1C, heart rate 103, blood pressure 115/100, respiratory rate 26, oxygen saturation is 92% on room air, and capillary blood sugar is normal.

Question: Does an emergency department patient with septic shock need aggressive EGDT or is “usual” resuscitation just as good?

Background:  Sepsis can be defined as a “clinical syndrome complicating severe infection characterized by inflammation remote from the site of infection. Dis-regulation of the inflammatory response can lead to multiple organ dysfunction.”

* Systemic Inflammatory Response Syndrome (SIRS) Criteria:

* A temperature over 38C or less than 36C

* A heart rate over 90 beats/min

* A respiratory rat e over 20 breaths/min or PCO2 less than 32mmHg

* A WBC count less than 4,000 or over 12,000 or greater 10% immature forms

* Sepsis: At least two of the four SIRS + infection.

* Severe Sepsis: Sepsis + hypotension and end organ failure

* Hypoxia, renal failure, hepatic failure, coagulopathy, hypotension, lactate greater than 2 mmol/l

* Septic Shock: Severe sepsis and hypotension refractory to fluid treatment or lactate greater than 4 mmol/l

Previous SGEM Episodes on Sepsis:

* SGEM#44: Pause (Etomidate and Rapid Sequence Intubation in Sepsis)

* SGEM#69: Cry Me A River (Early Goal Directed Therapy) ProCESS Trial

* SGEM#90: Hunting High and Low (Best MAP for Sepsis Patients)

* SGEM#92: ARISE Up, ARISE Up (EGDT vs. Usual Care for Sepsis)

Reference: Trial of Early, Goal-Directed Resuscitation for Septic Shock. NEJM March 2015.

* Population: Adult patients presenting to the emergency department with early septic shock (SIRS 2+ criteria with refractory sBP<90mmHg despite fluid resuscitation 1L within 6 0minutes, or hyperlactatemia >4mM). Patients recruited from 56 hospitals (approximately 25% of total hospitals) in England (29% teaching hospitals).

* EXCLUDED if age<18yo, pregnant, primary acute diagnosis (stroke, acute coronary syndrome, congestive heart failure, status asthmaticus, arrhythmia, seizure, over-dose, burn/trauma), unstable GIB, need immediate surgery, history of AIDS, do not resuscitate/other advanced directives restricting resuscitation,

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Date: March 7th, 2014

Guest Skeptic: Dr. Anthony Crocco. Associate Professor, McMaster University, Medical Director and Division Head McMaster Children’s Hospital Emergency Department.

Case: 11-year-old snowboarder fails to land epic jump. She was wearing helmet. There was a brief loss of consciousness and she is amnestic to the event. The only complaint is a mild headache. Her examination is normal and a shared decision is made to observe her rather than getting a CT scan. She is ultimately diagnosed with a concussion. When leaving the department she wants to know when can she go back shreddin’ the gnar?

Background: Pediatric traumatic brain injury (TBI) is a leading cause of death and disability. The Center for Disease Control (CDC) has called it a national health problem. TBIs are responsible for close to 500,000 ED visits, over 35,000 hospitalizations and more than 7,000 deaths/yr in the USA. TBI is considered mild 75% of the time. Most patients with TBI are discharged from the ED with active concussive symptoms.

TBI represents a challenging situation to emergency physicians. We do not want to miss a significant intracranial lesion while at the same time want to avoid ionizing radiation.

So how do you decide when to get neuroimaging? The best clinical decision instrument and the one we use at McMaster Children’s Hospital is PECARN (Pediatric Care Applied Research Network). It has been externally validated and found to be better than the CHALICE Tool and the CATCH Tool (Easter et al Annals Emergency Medicine).

PECARN has been collecting data on patients with head trauma since 2004.

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Date: March 11th, 2015

Guest Skeptic: Billy Sin is an Assistant Professor of Pharmacy Practice Arnold & Marie Schwartz College of Pharmacy and Health Sciences, Long Island University, Clinical Pharmacy Educator Emergency Medicine, The Brooklyn Hospital Center

Case: 27-year-old woman presents to the emergency department again with severe back pain radiating to her legs. She has tried analgesics, anti-inflammatories, narcotics and even trigger point injections. You have been reading more and more papers suggesting a sub dissociative-dose of ketamine (SDDK) could work.

SGEM-HOP Process:

* We pick a manuscript in conjunction with AEM’s Editorial Board that has been submitted, peer-reviewed, and ultimately accepted for AEM but not published yet.

* The SGEM then put a skeptical eye upon the manuscript using a modified BEEM critical appraisal tool.

* One of the authors of the paper is invited to discuss the strengths, weakness, limitations and clinical application their study.

* A SGEM Hot Off the Press podcast is posted the week the manuscript gets published.

* The SGEM audience gets a chance to respond via the blog, twitter or on Facebook.

* A summary of the SGEM critical appraisal gets published in a subsequent issue of AEM including the top social media feedback.

Background: Ketamine was developed more than 50 years ago and been used mainly as an anesthetic agent. It has a number of other medical uses including procedural sedation in the ED as well as chronic pain syndromes like neuropathic pain or cancer pain.

Ketamine is a N-Methyl-D-aspartate (NMDA) receptor antagonist that exerts sedative, amnestic, and analgesic effects as a dissociative anesthetic.

Ketamine also has some other non-medical uses. It is used as a street drug and goes by some other names such as Special K and cat valium. If recreational users take too much they referred to it as heading down the K-hole.

Ketamine historically had a bad reputation of raising intracranial pressure. EM Pharmacist, Meghan Groth debunked that myth on SGEM#93. The bottom Line from that episode was: “Ketamine seems to be a reasonable alternative induction agent for undifferentiated patients requiring RSI in the ED. Evidence to show that ketamine has negative effects on neurologic outcomes is weak and has been largely extrapolated from non-ED patients. This systematic review found no compelling evidence that ketamine worsens ICP, CPP, or neurologic outcomes as measured.”

There are a group of doctors out there who like to combine ketamine with propofol into Ketofol. We have a podcast coming up on that topic with Steve Carroll from EM Basic. 

Clinical Question: Is the administration of subdissociative dose ketamine for acute pain control safe and effective compared with placebo?

Reference: Sin B, Ternas T, Motov SM. The use of subdissociative-dose ketamine for acute pain in the emergency department. Acad Emerg Med (in press)

* Population: English-language randomized controlled trials assessing adult or paediatric emergency department patients with acute pain (fracture, dislocation, abscess, burns).

* Exclusion criteria varied across studies, but included obesity, substance abuse, acute intoxication, psychiatric disorders, respiratory/renal/hepatic failure, pregnancy, severe shock,

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Date: March 7th, 2015

Guest Skeptic: Dr. Eric Schneider. Eric is a Community Emergency Medicine Physician in Kansas City, Missouri, who has a drive to bring the most pragmatic, evidence-based and cost-effective care to his patients at an inner city trauma hospital. He’s a father of three, married to a Pathologist, and an avid musician.

Case: 65yo African American male presents to emergency department complaining of swelling of the tongue/lips. It started when he woke at 08:30. He went to Urgent Care and was treated with intramuscular steroids, benadryl and epinephrine. The swelling did not get any better. The patient was referred to emergency department. Swelling started >4 hours ago when you see him. He states no change in the swelling. On examination is vital signs are normal, no stridor, no respiratory distress, no hypoxia but he does have a swollen tongue and slightly slurred speech. He has a history of hypertension and the only medication he takes is the ACE-Inhibitor Lisinopril.

Background: Angiotensin-Converting Enzyme Inhibitors (ACE-Inhibitors), such as Lisinopril, were approved by the FDA in the 1980’s. ACE-I are common medications used for hypertension, congestive heart failure, post myocardial infarction, chronic kidney disease and diabetic nephropathy.

They inhibit the renin-angiotensin-aldosterone system. Angiotensinogen is converted to Angiotensin I by renin. Angiotensin I is then converted to Angiotensin II by angiotensin converting enzyme (ACE) that is mainly produced in the lung.

Angiotensin II has many biological effects including:

* increased blood vessel resistance

* increased aldosterone

* increased thirst

* increased antidiuretic hormone (ADH)

* increased vascular hypertrophy

* increased noradrenaline

Angiotensin converting enzyme also breaks down bradikinin. So if you block ACE with an ACE-I you can get a build up of bradikinin.

ACE-I have side effects like all biologic agents. Because it causes lower blood pressure patients can get hypotension causing people to be weak/dizzy and even cause syncope.

Hyperkalemia is another well-recognized side effect of ACE-I. Urinary potassium excretion is stimulated by aldosterone and ACE-I decrease aldosterone. The estimated incidence of hyperkalemia secondary to ACE-I use is approximately 3%.

Then there is the classic ACE-I cough. This is thought to happen from in 5-35% of patients. This chronic dry could can start after the first dose but interestingly can not show up for weeks, months or even years.

No one knows the exact mechanism by which ACE-I cause cough but it is though to be due to the increased concentration of bradykinin, substance P, prostaglandins and thromboxane. Stopping the ACE-I is the treatment but the cough can persist for months in some patients.

The build up of bradykinin is also though to be the mechanism behind angioedema. The incidence of angioedema is seen in up to 0.7 % of users. It is usually self-limiting and has a very low fatality rate. The angioedema occurs in the mucosal tissue of the tongue, lips, eyelids, GI tract or genitalia that all have rich capillary blood supply.

An interesting fact is that angioedema is up to five times more common in those of African descent.

Angioedema can be divided up into two main types:

* Allergic-histamine-mediated Angioedema:

* Insect bites (bees), foods (peanuts/shellfish), drugs (many)

* Fast onset, pruritus, rash and potential systemic effects

* Responds to anaphylaxis therapy (antihistamines/steroids/epinephrine)

* Non-allergic Angioedema:

* Hereditary angioedema (HAE) and ACE-I angioedema

* Gradual onset,