Episode 20 – Anticoagulation

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The Free Open Access Medical Education (FOAM)

We review Dr. Rory Spiegel’s, A Case of Identity Part Two, post on EMNerd which is essentially a take down of dual antiplatelet therapy (DAT) in acute coronary syndrome (ACS).  The bottom line?  There’s no demonstrable and clinically significant benefit from DAT as demonstrated in the trials below.

CURE trial – composite endpoints of questionable clinical significance and an enormous sample size.

  • 2.1% absolute decrease in cardiovascular death and myocardial infarction (MI), completely powered by the 1.5% absolute difference in MIs. Almost all of these MIs were Type IV and peri-procedural. Mortality between groups was identical at 30 days and end of follow up (1.0% vs 1.1% and 2.3% vs 2.4%, respectively).

ACCOAST – RCT of prasugrel or placebo prior to angiography

  • No difference in cardiovascular death, myocardial infarct, stroke, urgent revascularization or glycoprotein IIb/IIIa rescue therapy (10.8% vs 10.8%)
  • Approximately 1% increase in major bleeding

CREDO – RCT with placebo or clopidogrel 3-24 hours prior to urgent cardiac catheterization

  • No statistical difference  in the rates of death, stroke or MI at 28 days
  • Statistical significance of a secondary endpoint of the 1-year outcomes with a 2% absolute reduction in the rate of death, MI, and stroke, largely the result of a 1.9% reduction of MIs.
  • 1% increase in major bleeding events

Thienopyridine Meta-Analysis

  • In patients with non-ST elevation ACS, pretreatment with thienopyridines is not associated with reduced mortality but comes at a cost of a significant excess of major bleeding.

Composite endpoints are problematic (see this post, “Would You Rather“) and statistical significance claimed in these trials is largely a product of composite outcomes rather than patient oriented measures.

The Bread and Butter

We summarize some key topics from the following readings, Goldfrank (10th ed) Chapter 60, EMPractice October 2013 (there’s almost nothing in Rosenalli on this topic) but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Aspirin

  • Irreversibly inhibits platelets (for the duration of platelet’s life)

Ibuprofen

  • Reversibly inhibits platelets

Novel Oral Anticoagulants (NOACs)

NOACs have gained increased popularity and are slowly supplanting warfarin for common anticoagulation indications such as non-valvular atrial fibrillation (NVAF) as well as treatment of venous thromboembolisms such as pulmonary embolism (PE) and deep venous thrombosis (DVT).

Direct thrombin inhibitor - dabigatran (Pradaxa).  This drug was the first to supplant warfarin for NVAF in the United States, billed as more patient friendly given the lack of purported need for routine monitoring.  Recent investigations by Cohen et al, however, demonstrate that monitoring may, in fact, be safer.  Further, in a real world, retrospective cohort of Medicare beneficiaries given either dabigatran or warfarin for atrial fibrillation, major bleeding of the dabigatran cohort was higher than in the warfarin cohort 9.0% (95% CI 7.8 – 10.2) versus 5.9% (95% CI 5.1 – 6.6) after propensity matching [Hernandez].  For more on the problems with dabigatran, check out Emergency Medicine Literature of Note.

  • Predominantly renal excretion
    • Caution with impaired renal function (can cause dabigatran to stick around longer)
    • Hemodialysis an option in acute overdose; however, most people would probably not want to put a dialysis catheter in a coagulopathic patient.
  • Half-life ~ 15 hours
  • Can elevate the PTT. If the PTT is normal, likely not coagulopathic secondary to dabigatran [Dager et al].
  • No reversal agent

Factor XA inhibitors – these have XA in the name….rivaroXAban, apiXAban, edoXAban.

Rivaroxaban – approved for NVAF and treatment of DVT/PE.  Half life approximately 6-9 hours.

Apixaban – approved for NVAF and treatment of DVT/PE. Half life about 12 hours.

Edoxaban – approved for NVAF. Half life about 10-14 hours.

Bleeding Duration from ACCP

Bleeding Duration from ACCP

  • Cleared by liver and kidneys.
  • Can elevate the prothrombin time (PT), but not reliably. Specific assays exist but are not widely available and are expensive.
  • No specific reversal agent although andexanet alfa is in the pipeline.  It’s a Factor Xa decoy (Andexanet Alfa) that binds up the F10A inhibitors like a sponge. Read more here.
  • In the setting of major bleeding, guidelines recommend 4 factor PCCs.  A recent study demonstrates reduction in bleeding using 4 factor PCCs on healthy patients given edoxaban [Zahir et al, EMLitofNote].  The benefit of 4 factor PCCs is predominantly based on improvement in numbers, not patient oriented benefit and is discussed in these posts by Dr. Spiegel The Sign of Four, The Sign of Four Part 2.

More FOAM on Anticoagulation Reversal

Generously Donated Rosh Review Questions 

Question 1. A 65-year-old man with a metal aortic valve presents with hematemesis. His vitals are BP 95/50 and HR 118. The patient is on warfarin and has an INR of 7.3. 

Question 2. A 66-year-old woman with atrial fibrillation on warfarin presents with dark stools for 2 days. Her vitals are T 37.7°C, HR 136, BP 81/43, RR 24, and oxygen saturation 94%. Her labs reveal a hematocrit of 19.4% (baseline 33.1%) and an INR of 6.1. 

 

Answers.

1. D.  The patient presents with life-threatening bleeding and an elevated INR from warfarin use requiring immediate anticoagulant reversal regardless of the indication for anticoagulation. Warfarin acts by inhibiting vitamin K recycling thus limiting the effectiveness of vitamin K dependant clotting factors (factors II, VII, IX and X). The effect of warfarin can be measured using the prothrombin time or the INR. Warfarin is indicated for anticoagulation for a number of disorders including the presence of a metal valve. Patients with metal valves are at a higher 1-year risk of clot formation around the valve and subsequent embolic stroke. The therapeutic goal of warfarin in a patient with a metallic valve is usually between 2.5 –  3.5 or 3.0 – 4.0. Despite the increased stroke risk, patients with life-threatening bleeding should always have their warfarin reversed by administration of vitamin K and fresh frozen plasma (FFP). Alternatively, prothrombin complex concentrates can be given instead of FFP.

Warfarin is not amenable to hemodialysis (A) for removal or reversal. Although patients with a mechanical valve are at an increased stroke risk (increased 1 year risk) reversal should not be delayed (B), as the patient is more likely to die in the immediate situation from their gastrointestinal bleed. Platelet transfusion (C) will not help, as warfarin does not inhibit platelet function.

2. C.  The patient has a life-threatening gastrointestinal bleed in the setting of anticoagulation with warfarin, a vitamin K antagonist. Warfarin acts by inhibiting the synthesis of vitamin K-dependant factors in the coagulation cascade (II, VII, IX, X, protein C, and protein S). The anticoagulant effect of warfarin should be reversed as part of the patient’s emergent treatment. Fresh frozen plasma (FFP) contains all factors in the coagulation cascade and should be given in patients with major bleeding and elevated INR. Vitamin K should be given IV in critically ill patients with elevated INR because it shortens the time to effect.

Vitamin K should not be given intramuscularly (B) because absorption via this route is highly variable. Vitamin K should also not be given orally (D) in critically ill patients because the onset of action will be delayed. Additionally, absorption in patients with gastrointestinal bleeding may be variable. Vitamin K should be given along with FFP (A) because the factors inhibited rely on vitamin K for function.

Episode 19 – Environment: Mushrooms and Hypothermia

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The Free Open Access Medical Education (FOAM)

We review the Tox Talk podcast, Episode 23 – Mushrooms.  Our favorite pearls:

Clitocybe, Inocybe – contain muscarine which stimulates muscarinic receptors (acetylcholine/parasympathetic), causing a cholinergic toxidrome. Think SLUDGE (salivation, lacrimation, urination, defecation, gastric emptying/emesis) and the Killer B’s (bradycardia, bronchorrhea, bronchospasm) or DUMBELLS (diarrhea/diaphoresis, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation). Basically, cholinergic toxidrome: SMALL, WET, SLOW.

  • Memory aid: these mushrooms end in -yBE, akin to the “killer B’s” that make cholinergic toxicity deadly.

Gyromitra – (false morel) contains gyromitrin which can cause seizures, in addition to gastrointestinal upset and liver failure.  Treatment: pyridoxine (B6).

  • Memory aid: gyromitra named because they look like the gyri of the brain and, conveniently, make the brain seize through depletion of GABA.

Amanita phalloides – contains amatoxins which cause delayed gastrointestinal symptoms and liver failure., echoing acetaminophen toxicity.

  • Caution: this is different than the amanita muscaria ‘mushroom, which is tricky because that amanita muscaria has neither muscarinic properties nor the toxicity of amanita phalloides.

Bonus pearl: Coprinus species can cause a disulfiram like reaction.

FOAM article on mushrooms by Jo et al

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter  ; Rosen’s 8(e) Chapter  – but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Hypothermia starts at 35°C and then is categorized based on severity.

Pearls:

  • Ethanol + hypothermia = bad news.  Ethanol is the most common cause of excessive heat loss in urban areas as people tend to not take warming measures, may be homeless or without heat, and have impaired thermoregulation.  Hypothermia also slows alcohol metabolism, making people drunker for longer.
  • Elderly patients are more susceptible to hypothermia, particularly as they may not sense the cooler temperatures.  Some may also have impaired thermoregulation.
  • Have a low threshold

Diagnostics:

  • Get a temperature, on all patients.  This applies to patient’s “found down” as well as the chronic alcoholic who just seems really drunk.
  • If patients aren’t rewarming 1°C/hr and they’re above 32°C, consider: sepsis, cortisol deficiency, myxedema, ethanol.
  • The J wave or “Osborn” wave is found in many cases of hypothermia, often quoted at ~80%.  However, it is not pathognomonic for hypothermia.

From the Rosh Review

Treatment: Warm the patient.  Don’t call the patient dead until they’re warm and dead, which means their temp is above 30-32°C.

Screen Shot 2014-11-22 at 9.30.13 PM

Passive Rewarming - effective when the patient can still shiver (33-35°C).

  • Generates ~1.5°C of heat/hr

Active Rewarming - direct transfer of heat to the patient.

  • Indications: Cardiovascular instability, temp ≤30-32° C, inadequate rate of rewarming or failure to rewarm, endocrine problem, trauma, tox, secondary hypothermia impairing thermoregulation
  • Can be external or internal (which can be minimally invasive like IV fluids or quite invasive with things like bypass or pleural lavage).

Outcomes -

  • Unlikely survival with a potassium > 12 mmol/L and recommendations are to terminate resuscitation for potassium >12 mmol/L and consider cessation for potassium between 10-12 mmol/L

FOAM Resources:

EBM Gone Wild on Prognostication

ScanCrit on ECMO in Accidental Hypothermia

EMCrit on Severe Accidental Hypothermia

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  A 40-year-old man with a history of substance abuse is brought in by EMS after being found unconscious outside of a nightclub in the middle of winter. It is unclear how long he was outside. He is unresponsive with a GCS of 3.

Question 2.  What is the most common cause of death in hypothermic patients after successful resuscitation?

Question 3.

Question 4. What abnormal rhythm is common with temperatures below 32°C?

References:

Danzl DF, Zafren K. Accidental Hypothermia, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2013, (Ch) 140: pp 1883-1885.

Brown D JA, Brugger H, et al. Accidental Hypothermia. N Engl J Med 2012;367:1930-1938.

Mair P, Kornberger E, et al. Prognostic markers in patients with severe accidental hypothermia and cardiocirculatory arrest. Resuscitation 1994;27:47-54.

Answers:

1. D. When the serum potassium is greater than 12 mmol/L resuscitative efforts should be halted as the patient is unlikely to survive and further efforts constitute futile care. Accidental hypothermia is not an uncommon occurrence particularly in colder climates. It may occur in conjunction with substance abuse when an individual becomes impaired and is subsequently exposed to the outdoors. It can also occur as a result of drowning, avalanche and other trauma. Bio-makers other than potassium have been studied including serum lactate (B), pH (C) and clotting time. None have been proven prognostically reliable and therefore should not be used as a guide to determine if resuscitation should be continued. Hypothermic patients that present in cardiac arrest should be warmed to a minimum of 32°C (A) preferably via ECMO or cardiopulmonary bypass. However, if a hypothermic patient is warmed to 32°C and remains in asystole, recovery is unlikely and resuscitative efforts should be terminated. Other indications to cease resuscitative efforts include: obvious signs of irreversible death (e.g. major trauma), valid DNR order, conditions that are unsafe for the rescuer or provider, and an avalanche burial > 35 minutes in which the airway is packed with snow and the patient is asystolic.

2. Pulmonary edema.

2. C. Hypothermia. The ECG demonstrates the presence of J waves or Osborn waves which are seen in hypothermia. One of the first cardiac effects of hypothermia is bradycardia secondary to decreased firing of the cardiac pacemaker cells in cold temperatures. Osborn waves may appear at any temperature below 32°C. The waves are an upward deflection at the terminal portion of the QRS complex. They may represent abnormal ion flux in cold temperatures along with delayed depolarization and early repolarization of the left ventricular wall. As temperatures continue to drop, the ECG will demonstrate prolonged intervals: PR, followed by QRS and then QTc. Both diabetic ketoacidosis (A) and digoxin toxicity (B) may lead to hyperkalemia. In diabetic ketoacidosis, hyperkalemia develops as a result of the acidic pH in the blood and the transport of hydrogen ions intracellularly in exchange for a potassium ion. Digoxin toxicity poisons the cellular Na+/K+ ATPase resulting in elevated extracellular levels of potassium. The ECG manifestations of hyperkalemia begin with peaked T waves. Multiple other findings eventually develop including a shortened QT interval, ST depression, bundle branch blocks, widened QRS, prolonged PR interval, flattened T wave and ultimately a sine wave. Hyperparathyroidism (D) may lead to hypercalcemia. In hypercalcemia, the ECG shows a shortened QT interval, flattened T waves and QRS widening at very high levels.

4.  Atrial fibrillation.

Episode 18 – Falls and Geriatrics

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The Free Open Access Medical Education (FOAM)

We review Dr. Ken Milne’s podcast, The Skeptic’s Guide to Emergency Medicine Episode #89,  special episode on falls in the geriatric.  This episode is the first in the HOP (Hot Off the Press) series in which Dr. Milne has paired with Academic Emergency Medicine and the Canadian Journal of Emergency Medicine to review a paper, with the author, the same week the paper is published.

Why HOP is special:

  • Reducing the knowledge gap by disseminating hot-off- the press
  • Concurrent peer review from global audience.  Peer review is a flawed process and in this way, Dr. Milne takes his skeptical perspective to the paper and the author.
  • Key comments from social media will then be published in these journals, reaching the traditional academic readership.

Pearls from the Carpenter et al systematic review

Fall Statistics:

  • Fall Rates – > 65 y/o – 1 in 3 people fall per year; > 80 years old – 1 in 2 people fall per year
  • Elderly patients who fall and are admitted have a 1 year mortality of ~33% [1,3]. So, geriatric falls are bad, it seems logical to wish to predict who is going to fall.

Predictors of Falls:

  • The best negative likelihood ratio (-LR) was if the patient could cut their own toenails –LR 0.57 (95% CI 0.38-0.86) (remember, the target for a -LR is 0.1). This outperformed traditional assessments like the “get up and go test.”
  • Previous history of falls is a big predictor of falls.  Of elderly patients who present to the ED with a fall, the incidence of another fall by 6 months later is 31%.  Of those patients who present with a fall as a secondary problem,14% had another fall within 6 months.
  • The Carpenter instrument has a promising -LR of 0.11 (95% CI = 0.06-0.20) but has not been validated
    • Carpenter instrument: Nonhealing foot sores, self-reported depression, not clipping one’s own toenails, and previous falls

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (6e) Chapter 307 (This chapter was removed from the seventh edition) ; Rosen’s 8(e) Chapter 182 – but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Abdominal Pain Abdominal pain in the elderly is much higher risk than the younger cohort. This is complicated by vague presentations.  Abdominal pain in the elderly often causes one to raise an eyebrow and ponder chest pathology such as an atypical presentation of ACS.  However, the converse can also be true.  Chest discomfort may really reflect intra-abdominal pathology.  Bottom line – presentations are vague and badness is common.

Geriatric abdominal pain stats:

  • Fever and WBC unreliable.  Per Rosen’s “Elders with potentially catastrophic intra-abdominal processes may not present with a fever or an elevated white blood cell count.”
  • Much higher risk than younger patients – 2/3 patients admitted and 1/5 go directly to the operating room.
  • Most common serious pathologies:  Biliary pathology (cholecystitis), small bowel obstruction, appendicitis.
  • Vascular pathologies such as abdominal aortic aneurysm (AAA) and mesenteric ischemia also have an important place in the differential given increased incidence in the elderly.

FOAM resources:

Polypharmacy  Elderly patients are often on a host of medications but have physiologic alterations that make them susceptible to increased adverse events.

  • 12-30% of admitted elderly patients have adverse drug reactions or interactions as a primary or major contributing factor to their admission and 25% of these drug reactions or interactions are serious or life-threaten
  • Garfinkel et al demonstrated that reducing medications in elderly nursing home patients may actually be better for their health.
  • Some of the highest risk medications, in general, for our elderly patients: diuretics, nonopioid analgesics, hypoglycemics, and anticoagulants.  A patient’s presentation (syncope, fall) may be a manifestation of a medication side effect.
  • There are many high risk pharmaceuticals in the ED, but be very cautious of: narcotics, nonsteroidal anti-inflammatory agents, sedative-hypnotics, muscle relaxants, and antihistamines.
    • NSAIDS – patients may have reduced renal function and due to loss of lean muscle mass, creatine may not be accurate and NSAIDs may tip the patient into renal insufficiency. These drugs may also worsen hypertension and congestive heart failure as a result of salt retention.  NSAIDs are also associated with gastrointestinal bleeding.  Be cautious – acetaminophen is the safer bet.
    • Narcotics – may predispose patients to falls (which are bad in the elderly).  These drugs may also constipate patients, which can cause abdominal pain.  Give guidance and make sure the patient has a solid bowel regimen.
  • Start low and go slow.  It’s much easier to add doses of medications than clearing excess medications.
  • Cautiously start new medications. Furthermore, as drugs may be responsible for the patient’s symptoms that brought them to the ED, review the medication list. If possible, consider discussing discontinuation of medications with the patient’s PCP.

FOAM resources:

Delirium – Delirium in the elderly ED patients is associated with a 12-month mortality rate of 10% to 26% [5].  Be wary of chalking up alterations in mental status to dementia or sundowning.

 

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.

Question 1. An 87-year-old woman presents to the ED after her caregiver witnessed the patient having difficulty swallowing over the past 2 days. The patient is having difficulty with both solids and liquids. She requires multiple swallowing attempts and occasionally has a mild choking episode. She has no other complaints. Your exam is unremarkable. 

Bonus Question: What proportion of elderly patients with proven bacterial infections lack a fever?

References:

1.Carpenter CR, Avidan MS, Wildes T, et al. Predicting Geriatric Falls Following an Episode of Emergency Department Care: A Systematic Review. Acad Emerg Med. 2014 Oct;21(10):1069-1082.

2. “The Elder Patient.” Chapter 182.  Rosen’s Emergency Medicine, 8e.

3.  “The Elderly Patient.” Chapter 307.  Tintinalli’s Emergency Medicine: A Comprehensive Review, 6e.

4. Garfinkel D1, Zur-Gil S, Ben-Israel J. The war against polypharmacy: a new cost-effective geriatric-palliative approach for improving drug therapy in disabled elderly people.  Isr Med Assoc J. 2007 Jun;9(6):430-4.

5. Gower LE, Gatewood MO, Kang CS. Emergency Department Management of Delirium in the Elderly. West J Emerg Med. May 2012; 13(2): 194–201.

Answers:

1.D.  Physiologic changes of aging affect virtually every organ system and have many effects on the health and functional status of the elderly. Compared to healthy adults, elderly patients have a decreased thirst response that puts them atincreased risk for dehydration and electrolyte abnormalities. Cell-mediated immunity (A) is decreased, which increases susceptibility to neoplasms and a tendency to reactivate latent diseases. Peripheral vascular resistance (B) is increased contributing to development of hypertension. Sweat glands (C) are decreased in the elderly, which puts them at risk for hyperthermia.

2.B.  Dysphagia can be divided into two categories: transfer and transport. Transfer dysphagia occurs early in swallowing and is often described by the patient as difficulty with initiation of swallowing. Transport dysphagia occurs due to impaired movement of the bolus down the esophagus and through the lower sphincter. This patient is experiencing a transfer dysphagia. This condition is most commonly due to neuromuscular disorders that result in misdirection of the food bolus and requires repeated swallowing attempts. A cerebrovascular accident (stroke) that causes muscleweakness of the oropharyngeal muscles is frequently the underlying cause.
Achalasia (A) is the most common motility disorder producing dysphagia. It is typically seen in patients between 20 and 40 years of age and is associated with esophageal spasm, chest pain, and odynophagia. Esophageal neoplasm (C)usually leads to dysphagia over a period of months and progresses from symptoms with solids to liquids. It is also associated with weight loss and bleeding. Foreign bodies (D) such as a food bolus can lead to dysphagia, but patients are typically unable to tolerate secretions and are often observed drooling. These patients do not have difficulty in initiating swallowing.

Bonus. Up to one half.

FOAMcastini – SMACC

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FOAMcast will be back shortly with regular core content-cutting edge mash ups.  However, we would be remiss not to take a moment to focus on a conference that inadvertently created FOAMcast…and is coming to Chicago in June 2015.  SMACC – Chicago (#smaccUS) June 23-26, 2015.

The etiology:  FOAMcast was dreamed up whilst milling around the exhibition hall at SMACC, discussing how even core content and “basic” medicine seemed cutting edge and important here.  These projects can be dreamed up via Twitter or e-mail but I think there’s something special engendered by the propinquity of Free Open Access Medical education (FOAM) mixed with the physical conference. Our fate was sealed when Dr. Victoria Brazil happened to stop by to say “hi” while we were hyped up on “long blacks” and blabbering away about what we would call our project.  For better or worse, FOAMcast was born.

  • Note: Please do not blame Dr. Brazil for our off-beat humor or the podcast.  She had no idea what we were up to and does not endorse FOAMcast or Drs. Jeremy Faust and Lauren Westafer.

The talks at SMACC were unparalleled.  The speakers inspiring, the slides clean, the material relevant, and the audience questions thoughtful.  We learned from social workers (Liz Crowe’s hilarious talk), nurses, medics, and doctors from around the globe.  In fact, we became friends, even the pre-med university student.  We learned from them all.

The Core Content – There were a cornucopia of excellent core content talks; for example, Natalie May’s pediatric pearls, Aortic Catastrophes, and the Meaning of Acidosis by Dr. David Story.  There are too many to list and they’re all worth a listen and can be found on iTunes or via the Intensive Care Network.  Even the sonowars were brilliant.  For example, Drs. Matt Dawson and Mike Mallin taught us to visualize cardiac view using humans.  The awkward apical 4 chamber view for cardiac ultrasound:

Apical 4 Chamber View - Cardiac Ultrasound

Awkward (Apical) 4 Chamber View – Cardiac Ultrasound

In this episode, we only had time to hit just a few heavy hitters that haven’t made it onto our other podcasts.

Dr. Haney Mallemat – The Art and Science of Fluid Responsiveness

  • Dr. Mallemat beautifully describes various methods of assessing fluid responsiveness – from IVC ultrasound (used alone, approximately equal to CVP), stroke volume variation, to passive leg raise and more advance ultrasound techniques.
  • Use dynamic markers rather than static numbers, which seemed to be universally lousy.  Trend the patient’s response in order to give them “as much fluid as they need, and not one drop more.”

Dr. Scott Weingart – Sepsis in New York: Our First 15,000 Patients

  • Source control is key in sepsis.  If a patient has an infected gallbladder, obstructing kidney stone, etc – call surgery. Advocate for these patients.
  • ProCESS (and now ARISE) have demonstrated that protocols don’t necessarily have to be followed in order to reduce mortality in sepsis.  We have become increasingly good at identifying and treating sepsis since the original EGDT trial.  In his words – you don’t have to do sh*t, you just have to give a sh*t (Note: you still have to provide basic resuscitation, antibiotics, etc; you just don’t have to do the fancy stuff).
  • He had more pearls about lactate – such as in his collaborative, the number predicted badness but trends mattered less.

Dr. Cliff Reid – Resuscitation Dogmalysis

  • One cannot predict blood pressure based on the presence or absence of a pulse in various anatomic locales (i.e. if there’s a pulse at the radial artery, then their systolic blood pressure is at least >80 mmHg).  This myth was taught for years and still persists in some trauma bays; however, even the evidence and the two most recent iterations of ATLS agree with Dr. Reid [Deakin et al]

Dr. Rob Mac Sweeney – ARDS: An Evidence Based Update

  • The Berlin definition of ARDS [ARDS Definition Task Force]:
    • Acute worsening of respiratory failure (< 1 week)
    • Edema not solely due to hydrostatic pulmonary edema (i.e. should not be due to heart failure or fluid overload)
    • Bilateral infiltrates on CT/CXR *(subjective)
    • PaO2/FiO2 ratio <300 mmHg with at least 5 cm H20 of PEEP
  • The premise of Dr. Mac Sweeney’s talk; however, is that we ARDS is problematic because:
    • ARDS is a disease we can’t diagnose –  Many of the criteria, although seemingly helped by the Berlin definition, are still subjective (ex: CXR Sensitivity 0.73; specificity, 0.70 [Figueroa-Casas]
    • The diagnosis of ARDS is of limited clinical utility.  What he means by this is that the definition doesn’t really affect management and nearly all drugs targeted towards ARDS fail to show benefit consistently.  The ARDS care that does work, like lung protective ventilation and fluid balance, these are just good critical care.  Proning may work, but doesn’t seem to pan out in everyone [Guerin].  Dr. Mac Sweeney is also a little sweet on ECMO, awaiting future studies.
    • People don’t typically die from ARDS even though ARDS is associated with a 40-50% mortality rate.  Yet, only 10% of people with ARDS die of ARDS or respiratory failure. Most people with ARDS die because they’re super sick.
    • Most people with ARDS don’t have ARDS.  Autopsy studies have demonstrated that ~50% of people who met Berlin criteria for ARDS didn’t have the pathognomonic feature of ARDS, diffuse alveolar damage (DAD). The other half of the patients had pneumonia, abscesses, COPD, or other processes [Pinheiro et alThielle et al].
  • The crux of the ARDS issue per Dr. Mac Sweeney -It seems that ARDS is a fairly diverse spectrum with some subjectivity to the criteria.  If approximately half of the people diagnosed with ARDS don’t have ARDS, then it’s no surprise that the therapies don’t benefit them.  He leaves better identification in the hands of researchers.

Timing, Tribes, and STEMIs

  • In medicine we use teams or “tribes” to cope with stress, work together, and rally – Tribe Emergency Medicine, Tribe Anesthesiology, Tribe Surgery, etc.  While making snarky comments, if in jest, may boost the morale and confidence of our team, this may be detrimental to overall patient care
SMACC GOLD

SMACC – Built Friendships, Adventures, and Better Learners

FOAMcastini – ACEP Wednesday

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FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.  Weekend review, Monday review, Tuesday review

Scientific Assembly Wednesday Pearls

(there’s too much to choose from, so follow #ACEP14)

Debating Clinical Policies: Implications for tPA and Beyond – Drs. David Newman, David Seaberg, and Edward Sloan

  • The ACEP clinical policy on TPA is hotly debated, as it gives Level A evidence to TPA in acute ischemic stroke.  This policy is being reconsidered and big props to ACEP for doing this, most professional organizations aren’t that responsive.
  • TPA has a NNT of 8 and a NNH of 16.  The TPA supporters typically reference NINDS, ignoring the other RCTs.  They also reference large sets of registry data.
TPA in Stroke courtesy of Dr. Andy Neill

TPA in Stroke courtesy of Dr. Andy Neill

  • Check out his SMART EM podcast on the topic

Evidence-Based Approach to the “Other” Stroke – Dr. Jon Edlow

  • Prothrombin complex concentrate (PCCs) are all the rage, particularly since the 4 factor PCC was approved last year in the United States.  It improves patients numbers of coagulopathy, but not necessarily patient outcomes (Dr. Rory Spiegel on the topic).
  • Fresh frozen plasma, dosing is based on INR and the patient’s weight, it’s not an empiric “2 units.”
  • Blood pressure control may be safe in Intracerebral hemorrhage, but the studies such as INTERACT don’t show that it benefits patients (The SGEM).

Chest Pain in the ED: Is One Troponin Enough? – Dr. David Newman

  • The miss rate for MI is often quoted as 2%, but it’s more like 0.2% per the Pope et al study.  So, we’re pretty good at this.
  • ACEP has a policy stating that a single troponin after 8 hours of chest pain is sufficient
  • States that have tort reform have shown fewer lawsuits and less money without compromising patient outcomes.
  • See the SMART EM talk on this

Clinical Pearls From the Recent Medical Literature – Drs. Jerome Hoffman and Richard Bukata (#hofkata)

  • Topical analgesia for corneal abrasions – the FOAM world has been buzzing with the notion of using tetracaine for corneal abrasions (Rebel EM, The SGEM).  Hofkata reviewed this paper by Waldman et al that showed no difference in visual analog scores for normal saline compared with tetracaine for corneal abrasions.  Tetracaine was perceived more effective so there may be a role for dilute proparacaine but we’ll need some more studies.
  • Cough medicines don’t work, as demonstrated by Smith et al but honey might per Cohen et al (The SGEM)
EMRA award!

EMRA award! Thanks, y’all!

FOAMcastini – ACEP Tuesday

(ITUNES OR LISTEN HERE)

FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.  Weekend review, Day 1 review.

Scientific Assembly Day 2 Pearls

(there’s too much to choose from, so follow #ACEP14)

Simple Complaints in Patients with HIV – Dr. John Perkins

  • HIV is a risk factor for coronary artery disease (CAD) and these patients are prone to thrombotic complications [Boccara et al]
  • Dr. Amal Mattu has really championed this point, as in this videocast

Resuscitation Pearls – Dr. Scott Weingart 

  • REBOA and ECMO are exciting and coming…but most of us don’t have them.  Watch the literature.
  • “Normal” vital signs shouldn’t reassure us in trauma. Don’t wait for patients to become hypotensive (this is a danger of euboxia)
  • The Shock Index (Heart Rate/Systolic Blood Pressure) is one way to help detect badness amongst “normal” vital signs in these patients (See this post)
  • ACLS algorithms, they’re helpful for people who don’t specialize in resuscitation.  Think about the individual patient and target interventions accordingly.  Oh, and do good CPR.
    • The AHA supports this, for example, they recommend against the routine use of calcium and sodium bicarbonate [2010 Guidelines].

End of Life/Palliative Care – Dr. James Adams

  • Hospice and palliative care are INTENSIVE. Listen to Dr. Ashley Shreves on the EMCrit podcast if you’re not convinced of this (actually, listen regardless, it’s worth it).
  • A Do Not Resuscitate (DNR) order only speaks to whether or not a patient wants CPR if they die.  No more, no less.  But, for more on this, check out this blog post.
  • In general, physicians don’t broach end-of-life topics with patients. Dr. Adams quoted a statistic “Approximately 50% of doctors don’t know their patient’s resuscitation wishes.”  The consensus in the room was that it really doesn’t take that much time to initiate these conversations but brief questions asking about a patient’s wishes, checking in to see if they have sufficient resources, or.  (Lauren’s take on the topic).

ACEP’s New Additions to Choosing Wisely

The cliff notes, courtesy of Dr. Seth Trueger

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Also, the first 5 from 2013:

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FOAMcastini – ACEP Round Up #2

(ITUNES OR LISTEN HERE)

FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.  Yesterday’s episode covered the council meetings.

Scientific Assembly Day 1 Pearls

Opening Session by Freakonomics hosts Steven Levitt and Stephen Dubner. Weird choice? It turns out that economists and physicians have a lot in common.  What’s that?  Probabilities.  As physicians we like to think of ourselves as diagnosticians, but we’re more like probalisticians.  We make predictions, hopefully based on the best evidence, our clinical expertise, and our patient’s values.  People don’t remember the little stuff, like extra testing but they do tend to remember the more outlandish things, like the “amazing saves” or awful “misses.”

  • See this post by Dr. Simon Carley, in which he describes the ways in which physicians are really playing the odds and gambling.

Cardiology Pearls from Dr. Slovis.

  • Post cardiac arrest – targeted temperature management to 35-36 Celsius is the new 33 Celsius [Nielsen].
  • Many patients should probably go to the cath lab after arrest, but it’s still not clear exactly who benefits the most.  STEMIs should probably go to the cath lab and, perhaps, non-STEMI ventricular fibrillation/tachycardia arrests.  Apparently, 10-30% of these are actually STEMIs “on the inside” [More skeptical takes on this from Dr. Radecki here and here]

Infectious Disease Pearls from Dr. David Pigott – When someone returns from a developing nation, say, West Africa, the cause of their fever is not necessarily ebola. It’s probably an unknown, regular virus.   It’s probably not ebola but it may be malaria which is quite common.

  • His thoughts on predictors of badness: Symptoms typically appear within 8-10 days although the “watch” period is 21 days.  If a patient is in their second week of symptoms and are hemodynamically stable, then the patient has a pretty good shot.

Tox Pearls from Dr. Tim Erickson

  • Calcium channel blocker toxicity – you can try fluids, calcium, atropine, and vasopressors.  For sick patients, however, insulin is the best bet (Note, FOAM is ahead of the curve: post on the lack of utility in glucagon from 2012).
    • Insulin bolus of 1 unit/kg followed by a drip of 1 unit/kg/h.  Add dextrose at about 0.5 mg/kg/h, depending on their glucose.
    • Check glucose and potassium every 30 minutes, with the goal to keep the potassium 2.8-3.2, per Goldfrank.
  • Cyanide toxicity (discussed here) – if you’re thinking about it, please do NOT wait on a cyanide level, or any labs.  Treat, with the current recommendation of intravenous hydroxocobalamin. There’s some discussion on the use of intramuscular cobinamide, which would be great in situations without IVs; however, this is largely untested in humans presently [Bebarta et al].
  • Beware of cognitive biases, such as anchoring. For example, lactic acidosis isn’t always sepsis, cyanide, or carbon monoxide.  Metformin associated lactic acidosis is also a thing.

Dr. Scott Weingart – Catch the CO2 Wave (podcast).  End tidal CO2 (ETCO2) – ETCO2 has become essential in monitoring patients in the ED.  With anything we monitor, we really need to understand what we’re looking at as well as the interventions.

  • ETCO2 does NOT = PaCO2.
  • In most patients, the PaCO2 will be ~3-5 mmHg higher than their ETCO2.
  • This is because ETCO2 is really a measure of: PaCO2 (or production) but also cardiac output and alveolar ventilation.  Thus, the ETCO2 may be falsely low in a patient with significant dead space, such as COPD, or with impaired cardiac output (heart failure).

For updates, follow #ACEP14

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