Episode 19 – Environment: Mushrooms and Hypothermia

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.

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.

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 http://www.mindanews.com/buy-topamax/ with a GCS of 3.[polldaddy poll=8469565]

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

Question 3.

[polldaddy poll=8473489]

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

(ITUNES OR LISTEN HERE)

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:

10 Tips for Approaching Abdominal Pain in the Elderly – ALiEM
Ultrasound for SBO – The Short Coat
Euboxia – Not Necessary (Or Necessarily Normal) – The Short Coat
Abdominal Pain vs. Chest Pain in the Elderly – EMBlog Mayo Clinic

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:

The BEERS criteria is a good resource for risky medications but quite overwhelming – bottom line, nearly every medication is risky.
Don’t Trust Your Patient’s Med List – The Short Coat.

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. [polldaddy poll=8443367]

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. [polldaddy poll=8443380]

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.

Episode 18 – Falls and Geriatrics

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

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

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:

10 Tips for Approaching Abdominal Pain in the Elderly – ALiEM
Ultrasound for SBO – The Short Coat
Euboxia – Not Necessary (Or Necessarily Normal) – The Short Coat
Abdominal Pain vs. Chest Pain in the Elderly – EMBlog Mayo Clinic

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:

The BEERS criteria is a good resource for risky medications but quite overwhelming – bottom line, nearly every medication is risky.
Don’t Trust Your Patient’s Med List – The Short Coat.

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. [polldaddy poll=8443367]

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.

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:

Bonus. Up to one half.

FOAMcastini – SMACC

(ITUNES OR LISTEN HERE)

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 al, Thielle 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

(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, 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

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)

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

Also, the first 5 from 2013:

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

FOAMcastini – ACEP Round Up 1

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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. However, Jeremy and I both worked overnights so we got into town a little late. Our friends and ACEP luminaries, Drs. Justin Hensley, Howie Mell, and Todd Slesinger.

For updates, follow #ACEP14

A Few Council Pearls:

Opiates are a huge problem in the United States. A Town Council met and discussed this issue and the role of emergency physicians in this “epidemic.” There were a lot of opinions about how emergency departments may contribute to this problem and can possibly play a role in the solution. Further reading on this topic below and, look out for the December ALiEM Journal Club on this paper Lack of Association Between Press Ganey Emergency Department Patient Satisfaction Scores and Emergency Department Administration of Analgesic Medications.

Naloxone (Narcan) – The council approved resolutions in support of naloxone for everyone. There was also a resolution on developing a clinical policy for emergency physicians prescriptions of naloxone. Watch out for it.

Medical Marijuana – Apparently http://www.mindanews.com/buy-inderal/ every year brings some bickering about medical marijuana….and every year, the council defeats the resolutions. This year was no different…no support for medical marijuana from ACEP.

Emergency Department Pharmacists – These folks are indispensable in the ED (and in the FOAM world), and ACEP recognized this with the passing of Resolution 44 (what this means, clinically, not sure). And if you haven’t work with them – you’re missing out. We’re huge fans of EMPharmD and, naturally, Bryan Hayes (@PharmERToxGuy)

There’s also a lot of politics that goes into these bills, for that part, we got Dr. Kevin Klauer, Council Speaker on FOAMcast to explain.

But the real news… Dr. Kevin Klauer’s haircut.

Wow, Klauer got a haircut. Amazing. Still the same brain, just no bangs flip… pic.twitter.com/hmYtKKQyHc

— Stephen Anderson (@ACEPSteve) October 24, 2014

Also, congratulations to the new ACEP president-elect, Dr. Jay Kaplan and all others elected to new ACEP board positions.

And, of course, the conference is fun (and, it turns out, Dr. Seth Trueger (@MDaware) is actually the nice one).

ruh roh #ACEP14 pic.twitter.com/0PczJG4hN8

— Seth Trueger (@MDaware) October 26, 2014

Episode 17 – The Spleen!

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The Free Open Access Medical Education (FOAM)

We review Dr. Scott Weingart’s episode 133 on pre-hospital REBOA (resuscitative endovascular balloon occlusion of the aorta). Weingart interviews Dr. Gareth Davies about the encounter, underscoring the increasing use of REBOA.

For a quick REBOA refresher, check out Episode 121.

REBOA (Review of REBOA) – First described in 1954 in the Korean War, this is a form of hemorrhage control below the level of the chest without having to do a thoracotomy with aortic cross clamping, which has sparse mortality benefit and can be dangerous to providers. Most of the REBOA literature is from swine models and case-series, although there are currently larger trials underway.

Outline of procedure – Obtain arterial access through the common femoral artery, pass a vascular sheath, float a balloon catheter to the appropriate section of the aorta, and inflate the balloon to occlude blood flow. The aorta is divided into three zones so that balloon occlusion is performed in Zone 1 for abdominal injuries or Zone 3 for pelvic injuries, while Zone 2 is a proposed no-occlusion zone.

The Bread and Butter

Rosen’s Chapter 46, 134 and Tintinalli Chapter 260.

What DOES the spleen do?

Answer: More than most appreciate. The spleen filters the blood, removing abnormal or old red blood cells (RBCs), debris, and antibody coated bacteria from the bloodstream. It also serves as a reservoir for RBCs and platelets and synthesizes antibodies, opsonins, etc.

Splenic Trauma – EAST Guidelines (their podcast)

Diagnosis – suspect spleen trauma clinically, with hypotension, left upper quadrant abdominal pain, or even minimal trauma, especially after infectious mononucleosis.

CT with IV contrast (hemodynamically stable patients). While FAST and DPL can detect peritoneal free fluid, they can’t detect subcapsular bleeds.
Unstable patients – operating room versus interventional radiology

Grading – 1 is 1 (<1 cm laceration depth), 3 is 3 (>3 cm laceration depth). Everything else is somewhere in between. Higher grades typically result in more aggressive interventions. Historically these get operative intervention

Grade 1: < 1 cm laceration depth or<10% subcapsular hematoma
Grade 2: 1-3 cm laceration or 10-50% subcapsular
Grade 3: > 3 cm laceration depth or >50% subcapsular hematoma
- Grade 3 or higher should be considered for angiography with embolization (Level II, III – EAST)
Grade 4: partially devascularized spleen or contrast blush
Grade 5: a very battered, devascularized spleen

There’s slightly more to spleen grading, check out this post from Dr. McGonigal

Trivia: The punctate extravasation sometimes seen on angiogram after blunt trauma?

Answer: The Seurat Spleen (pubmed), named after the pointillist painter.

Treatment –

Unstable patients: Operating room or Angiographic Intervention (IR) (Level II – EAST)
- Note: Board exam? Send the patient to the OR. In reality, there is some practice variation. Many would still argue the patient belongs in the OR, some places have combined OR/IR suites, and some opt for IR.
- Post splenectomy patients will need immunizations for the encapsulated bacteria
Stable patients: Nonoperative management, which often comprises in-hospital monitoring, serial abdominal exams and hematocrits, etc is becoming increasingly common as first line for higher grade splenic injuries. The key here is that the team must be able to take the patient to the OR or IR should the situation change. Angioembolization has also gained momentum as management
- Benefits: Preserved immune function of the spleen/patient may get to keep their spleen (Banerjee et al)
- Cautions: Nonoperative management requires protocols, Complications of angioembolization

Post-Splenectomy Sepsis (Review)– Most common in the first years after splenectomy and in children.

Presentation – Patients may present with a vague flu-like illness or gastroenteritis but may go on to develop septic shock, DIC, and multiorgan dysfunction. In addition, meningitis without overwhelming infection or shock is a common presentation of pneumococcal infection in asplenic patients.

Etiology – encapsulated bacteria (Streptococcus pneumoniae, Haemophilus influenza, and Neisseria meningitidis), capnocytophaga canimorsus (dog bites), and parasites such as babesiosis (endemic in New England), malaria, and ehrlichiosis.

Management – Labs, blood cultures, antibiotics (typically ceftriaxone)

Splenic Sequestration – Second most common cause of death in kids with Sickle Cell Disease <5 years of age.

Classic presentation – LLL: LUQ, lethargy, lightness (pallor).

Labs: 3 point drop in hemoglobin, increased reticulocyte count, and thrombocytopenia.

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1. [polldaddy poll=8376275]

Question 2. A 23-year-old man presents with a stab wound to the abdomen. His vital signs are HR 132, BP 88/45. He has a positive FAST.[polldaddy poll=8376283]

References:

Chapter 46, 134. Rosen’s Emergency Medicine, 8e.

Chapter 260. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

Answers.

1. C. Splenic artery aneurysms are the most common type of visceral arterial aneurysms, accounting for up to 60% of cases. Etiologies include arterial fibrodysplasia, portal hypertension, and increased splenic AV shunting in pregnancy. Clinical presentation is vague with left upper quadrant pain with radiation to the left shoulder or subscapular area. Most of the aneurysms are <2 cm in diameter; only 2% result in life-threatening rupture. Treatment is surgical resection if the patient is symptomatic. Otherwise, asymptomatic patients can undergo transcatheter embolization. Of those aneurysms that rupture, up to 95% occur in young pregnant women.

Hepatic artery aneurysms (A) represents 20% of visceral artery aneurysms and are caused by atherosclerosis, infection, and abdominal trauma. Clinical presentation can mimic cholecystitis. Inferior mesenteric artery aneurysms(B) are uncommon. Superior mesenteric artery aneurysms (D) are the 3rd-most common visceral aneurysms. IV drug abusers are at increased risk.

2. D. This patient presents with hemorrhagic shock from a penetrating abdominal trauma and should be immediately transferred to the operating room for an exploratory laparotomy. Stab wounds are the most common form of penetrating trauma. About 70% of anterior stab wounds penetrate the peritoneum. It is difficult to predict the specific organ injured based on the external location of the wound. Initial management should focus on securing the airway, assessing and supporting the patients breathing and circulation. IV access and supplemental oxygen should be provided. In hypotensive trauma patients, early blood transfusion should be initiated and consideration should be made for massive transfusion protocol. Concomitant with the primary and secondary survey, a Focused Assessment with Sonography for Trauma (FAST) exam should be performed. The speed and accuracy of the FAST has almost completely replaced the need for diagnostic peritoneal lavage. In a FAST exam, images are obtained of the splenorenal space, hepatorenal space (Morrison’s pouch), heart and bladder (pouch of Douglas). A FAST exam has high sensitivity in detecting as little as 100 ml of fluid. A FAST examination showing free fluid in any of the abdominal views in the presence of hypotension should lead to the patient being transported to the operating room for exploratory laparotomy according to the Advanced Trauma Life Support (ATLS) algorithm. Angiographic embolization (A) is useful in patients with pelvic fractures and bleeding from pelvic vessels. CT scan of the abdomen and pelvis (B) can be performed in trauma patients who are stable to further assess for injuries.Diagnostic peritoneal lavage (C) does not play a role in management of penetrating trauma patients with hypotension and positive FAST examination.

Episode 16 – Headaches

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The Free Open Access Medical Education (FOAM)

This week we review a post from Dr. Rob Orman’s ERCast, Is it really a sinus headache?

POUND- 4 criteria is very indicative of migraine (+LR 24), 3 criteria also likely (+LR 3), although most of this comes from the outpatient literature [1].

Pounding headache
hOurs: headache lasts 4-72 h without medication
Unilateral headaches
Nausea
Disabling: disrupts daily activities

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 159 ; Rosen’s 8(e) Chapter 20, 103 – but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself!

In Emergency Medicine, our job is to investigate and think about the life and limb threatening causes, even to mundane problems. Things such as intracranial bleeds, meningitis, masses – these are huge deals and are covered well and hammered into our heads. For FOAM core content on this, check out the St. Emlyn’s podcast. On this episode, we’re running a mini-ophthalmology headache special and focusing on headaches that treatment may render “sight saving.”

Temporal Arteritis – often in patients older than 50 years of age and more common in those with a history of polymyalgia rheumatica. May be accompanied by visual changes including the “classic” amaurosis fugax or “curtain” of unilateral vision loss. If not treated, these patient can lose vision permanently.

Unilateral or localized headache, often in the temporal or retro-orbital area
Jaw claudication (pain with chewing) – most specific sign
Decreased pulse in temporal artery or tenderness
Sedimentation Rate (ESR) >50

Treatment

Prednisone 40-60 mg if thinking about diagnosis
Temporal artery biopsy within 48 hrs

Acute Angle Closure Glaucoma – Classically, these patients present with unilateral mid-dilated pupils and severe nausea, vomiting, and headaches. The history can, naturally, be less classic and more vague. Also, if not treated, this can lead to vision loss.

Elevated intraocular pressure (>20 mmHg)
Decreased visual acuity
Fixed irregular semidilated (midposition) pupil
Slit lamp — shallow AC (closed angle), injected conjunctiva; corneal microcystic edema (cloudy)

Treatment –

Ophthalmology consult stat
- They may want topical b-blocker, cholinergic, alpha-2 agonist, eye drops or administration of acetazolamide

Idiopathic Intracranial Hypertension (Pseudotumor Cerebri) – Common in young, overweight women or those on oral contraceptives. Untreated, they can suffer vision loss.

Elevated opening pressure (>20-25 cm H20) on lumbar puncture

Treatment

Neuro follow up
Acetazolamide +/- furosemide
Therapeutic lumbar punctures

Cerebral Venous Sinus Thrombosis – may present as atypical headache with stroke like symptoms in patients without known vascular risk factors. The neurological findings may be transient. Often associated with post-partum patients, patients with hypercoaguable states (Factor V mutations, protein C or S deficiency, antithrombin III deficiency, etc), patients on OCPs.

Diagnosis – CTV or MRV (magnetic resonance venography) after CT scan, which may be normal.

Treatment – Anticoagulation, although this is somewhat controversial

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1. A 73-year-old woman with a history of hypertension presents with a unilateral headache for 3 weeks. She states that she has a throbbing pain at her right temple and has pain in her jaw with opening and closing. The vision in her right eye has worsened over the previous day. Her blood pressure is 173/100.

[polldaddy poll=8340282]

Question 2. A 71-year-old woman presents to the ED with daily headaches for 2 months. She describes the headache as a dull pain that is most intense in the morning and resolves by the afternoon. On exam you note 4/5 motor weakness of the left upper and lower extremity.

[polldaddy poll=8340292]

References:

1. Detsky ME,McDonald DR, Baerlocher MO, Tomlinson GA,McCrory DC, Booth CM. Does this patient with headache have a migraine or need neuroimaging? JAMA. 2006 Sep 13;296(10):1274-83.

2. Chapter 20, 103. Rosen’s Emergency Medicine, 8e.

3.Chapter 159. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

Answers

1. D. This patient presents with a unilateral, subacute headache with associated jaw claudication and vision change; symptoms consistent with temporal arteritis. Temporal arteritis or giant cell arteritis is a systemic inflammatory process of small and medium-size arteries. The most commonly involved vessels are the ophthalmic vessels and the extracranial branches of the aortic arch. The disease typically affects patients over 70 years of age and is more common in women than in men. Patients present with a subacute headache that is throbbing in nature and may be present for weeks to months. Often, patients will have symptoms for more than 2 months. Patients may also report jaw claudication secondary to vascular insufficiency of the masseter and temporalis muscles. Physical examination may reveal tenderness over the temporal artery. Systemic symptoms may also be present including fever, joint pains, and weight loss. Diagnostic testing in the Emergency Department generally begins with an erythrocyte sedimentation rate (ESR) with a cutoff of 50 mm/hour although the level may be >100 mm/hour. However, the ESR will be normal in 10-25% of patients. The gold standard diagnostic test is a temporal artery biopsy. In patients with a high-clinical likelihood of temporal arteritis, treatment should be initiated regardless of initial diagnostic testing as delay can lead to permanent visual loss. Prednisone should be started at 60 – 120 mg/day.

Carbamazepine (A) is the treatment of choice for trigeminal neuralgia, not temporal arteritis. The patient does not present with symptoms consistent with hypertensive emergency requiring emergent antihypertensive treatment withlabetalol (B). A non-contrast head CT scan (C) is not helpful in temporal arteritis as the disease does not involve the intracranial contents.

2. B More than half of patients diagnosed with a brain tumor complain of headache. However, the headache associated with brain tumor is highly variable. Patients may describe it as continuous or intermittent, unilateral or bilateral, sharp or dull. It is associated with neurologic deficits less than 10% of the time. However, in the setting of aneurologic deficit and chronic headache (as in this scenario with motor weakness), a mass lesion should be strongly considered as the cause. Patients may also complain of nausea, vomiting, visual change, and gait disturbance. Headaches due to brain tumors are classically associated with pain that is worse in the morning (as in this case). However, this is rare.

Central venous thrombosis (A) results from hypercoagulable states and is associated with acute to subacute headaches with vomiting and sometimes seizures. Risk factors include the use of oral contraceptives, postpartum or postoperative states, and any hypercoagulable state such as factor V Leiden mutation, antithrombin III deficiency, protein S or C deficiency, or polycythemia. The diagnosis is usually made by MRI venogram. Migraine headache (C) is classified as a primary headache and can be quite variable in presentation. These headaches can be associated with nausea, vomiting, photophobia, and phonophobia. The headache may also be preceded or accompanied by an aura that develops gradually over minutes, usually lasts 60 minutes, and is reversible. Auras may include neurologic symptom but commonly include scintillating scotomas (dark spots) or flashing lights. Temporal arteritis (D) occurs almost exclusively in patients older than 50 years and is much more common in women. Headache is the most common symptom of temporal arteritis and usually occurs over the frontotemporal region. It is strongly associated with a history of polymyalgia rheumatic. It is not associated with focal neurologic deficits, but it can lead to vision loss due to ischemic optic neuritis.