Episode 17 – The Spleen!


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

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.  

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.



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



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


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


  • 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


  • 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.
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.
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

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.

FOAMcastini 3 – All About the Pearls


In this tiny episode, Jeremy reviews his favorite pearl from each episode, loooking at episodes 4-14.  Why the repetition?  Well, it turns out we learn better when information is spaced in small aliquots over time (spaced repetition).

Episode 4 – Transfusions and Ingested Foreign Bodies.

  • Most common infection from blood transfusion – Parvovirus B19

Episode 5 – Psychiatry and Increased ICP.

  • If re-initiating medications in the emergency department, some need to be titrated up slowly, such as quetiapine (Seroquel) and risperidone.
  • Figure out why patients stopped taking their medications.

Episode 6 – Hepatic Emergencies.

  • INR peaks after about 24-36 h in acute liver failure
  • AST>3000 suggests toxic or ischemic injury
  • ALT OR AST>300: Alk phos is useful.

Episode 7 – Heart Failure.

  • Right Ventricle MI: ST elevation in lead III greater than lead II – you know what to do (cath lab).  ST elevation in II greater than III – think pericarditee (pericarditis).
  • Right sided leads: elevation in V4R most specific but elevation in V3R-6R are indicative of RVMI.

Episode 8 – Acid-Base and Hyponatremia.

  • Strong Ion Difference (SID), which is the difference between the sums of concentrations of the strong cations and strong ions (typically Sodium minus Chloride). Small SID = acidic (example SID of 0.9% NaCl = 0)

Episode 9 – Pregnancy Emergencies.

  • The discriminatory zone is out.  Get ultrasounds in pregnant patients, regardless of the quantitative beta-hCG. A certain beta-hCG level can not be used to rule in or rule out ectopic pregnancy or viable intrauterine pregnancy (IUP), get the ultrasound and ensure you identify the uterus.

Episode 10 – Pediatric GI Emergencies.

  • Jaundice in the first 24 hours is NOT normal and is bad.

Episode 11 – Ebola and Transmission Precautions.

  • Airborne precautions recommended for: Measles (rubeola), Varicella, Tuberculosis.  Ebola is not airborne, but often we treat it as such.

Episode 12 – Anaphylaxis and Angioedema.

  • Biphasic anaphylaxis is extremely rare and prolonged ED observation does not really help as these reactions can occur up to 6 days later.  Rosenalli recommend observation 2-4 hours.

Episode 13  Tricyclic Antidepressants and Sodium Channel Blockade.

  • Tricyclic antidepressants can cause a rightward axis, in addition to prolonged QRS on an ECG.  This can resolve with treatment with sodium bicarbonate.

Episode 14 – Hand.

  • Flexor Tenosynovitis -Kanavel’s Cardinal Signs (look for words that start with “F”).
    • Pain on passive extension -happens early
    • Finger held in flexion – see above point..extension hurts!
    • Fusiform (uniform) swelling of finger – most common
    • Tenderness along flexor tendon sheath – happens later

Episode 15 – Atrial Fibrillation/Flutter

(iTunes or listen here)

The Free Open Access Medical Education (FOAM)

This week we review a post from Academic Life in Emergency Medicine, written by Brent Reed on selecting rate control agents in the management of atrial fibrillation.  This is a follow up post to Bryan Hayes’ summary of emergency department (ED) management of acute atrial fibrillation.  Both are high yield.

Acute Management:

  • No clear cut winner in the beta-blocker vs. calcium channel blocker battle

Long Term Atrial Fibrillation Management in General:

Avoid beta-blockers in:

  • Obstructive lung disease (asthma/COPD)
  • Peripheral vascular disease
  • Diabetics
  • Severe congestive heart failure (CHF)
  • Erectile dysfunction

Avoid calcium-channel blockers in:

  • Severe CHF and acute decompensated heart failure (ADHF)

Of note, in patients

The Maryland Critical Care Project has a great post with many of Dr. Amal Mattu’s key FOAM talks embedded on Tachydysrhythmias You Gotta Know.

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 280, 295 ; Rosen’s 8(e) Chapter  50 – a well written chapter, but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Atrial Fibrillation


Screen Shot 2014-09-16 at 3.57.07 PM


Unstable (hypotension, pulmonary edema, altered mental status, chest pain) – cardioversion.

  • Pads in either an anterior-lateral (AL) or anterior-posterior (AP) position followed by synchronized cardioversion at 100-200 J biphasic.  Current literature shows no significant difference in pad placement [1]
  • If cardioversion fails, try amiodarone load or diltiazem. Check out EMCrit on Crashing A Fib


  • Rate control. A target of <120 beats per minute is acceptable in the ED [2-3].  First line agents are nodal blocking agents such as diltiazem and metoprolol
    • Diltiazem 0.25 mg/kg IV over 2 minutes with a peak effect in 2-7 minutes. Can repeat at 0.35 mg/kg IV over 2 minutes.
    • Metoprolol 5-10 mg IV.
  • Rhythm control with cardioversion.  While there’s no proven benefit to rhythm control, many patients would prefer to be in sinus rhythm and ED cardioversion of stable new-onset atrial fibrillation is appropriate in a select population, notably, when the onset is <48 hours (or <72 hours per Rosen).  The pooled literature suggests a thromboembolism rate <0.8% [4].
    • Note: A recent article in JAMA by Nuotio et al found a higher rate of embolic events in patients who were electively cardioverted after >12 hours in atrial fibrillation.The 30 day risk of thromboembolism when cardioverted between 12-48 hours was 1.1%, compared to the ~2% risk if cardioverted after 48 hours. While the risk is still small, it is higher than the ~0.3% risk of thromboembolism with anticoagulation on board.
  • Treat the underlying cause (ex: sepsis, pulmonary embolism, hyperthyroidism, etc)
  • May also consider Amiodarone, Digoxin (mean >11 hours to rate control) [3]

In atrial fibrillation with pre-excitation (WPW), an often wide and irregular rhythm with different/changing morphologies to the QRS do NOT treat with an AV Nodal blocking agent as this may result in death (Adenosine, Beta-blocker, Calcium-channel blocker, etc). Treat with procainamide or shock

Disposition – Admit patients that present unstable, with underlying co-morbidities, or those that are not rate controlled.  Depending on the patient’s follow up and local practice patterns, the

Atrial Flutter

How to Avoid Misdiagnosing Atrial Flutter – Dr. Amal Mattu

Management – same as atrial fibrillation

  • More sensitive to electrical cardioversion, less sensitive to chemical cardioversion

Multifocal Atrial Tachycardia

Irregular narrow complex tachycardia with p waves of at least 3 morphologies (this can be difficult to see, so look in multiple leads, particularly V2)

 Etiology -often seen in advanced pulmonary disease

Management  – Treat the underlying cause, do NOT cardiovert MAT

 Learn from the master ECG educator, Dr. Amal Mattu

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  A 72-year-old man with a history of hypertension, diabetes, and congestive heart failure presents to the ED with heart palpitations for the past 4 days. He denies any chest pain, shortness of breath, abdominal pain, or history of similar palpitations. In the ED, his vital signs are BP 135/75, HR 138, RR 14, and oxygen saturation 98% on room air. His ECG is seen below. Which of the following is the most appropriate next step in management?

Rosh Review

Rosh Review

A. Chemical cardioversion

B. Rate Control

C. Synchronized cardioversion

D. Warfarin

Question 2.  When do you worry about giving calcium channel blockers, beta-blockers, or digoxin in a patient with atrial fibrillation?

Question 3. An 18-year-old woman presents with palpitations and near syncope. Her vitals are T 98.7F, HR 199, BP 113/66, RR 32, and oxygen saturation 94%. Her ECG is shown below. What treatment is indicated?

Rosh Review

Rosh Review

A. Administer adenosine 6 mg IV

B. Administer diltiazem 10 mg IV

C. Administer lopressor 10 mg IV

D. Administer procainamide 100mg IV


1.  Kirkland S, Stiell I, AlShawabkeh T, Campbell S, Dickinson G, Rowe BH. The Efficacy of Pad Placement for Electrical Cardioversion of Atrial Fibrillation/Flutter: A Systematic Review. Acad Emerg Med. 2014;21(7):717–726.

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

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

4. Cohn BG, Keim SM, Yealy DM. Is Emergency Department Cardioversion of Recent-onset Atrial Fibrillation Safe and Effective? J Emerg Med. 2013;45(1):117–27.


1.  B. Atrial fibrillation is caused by chaotic, disorderly firing from a second focus within the atria, resulting in uncoordinated atrial contractions. Patients with atrial fibrillation may present with palpitations, chest pain, shortness of breath, or they may be asymptomatic. Atrial fibrillation can be classified as chronic or paroxysmal, with paroxysms lasting minutes to days. On ECG, there are irregularly irregular narrow QRS complexes. In addition, no discernible p-waves are noted, rather fibrillatory waves are seen. Unless the patient is hemodynamically unstable, the mainstay of therapy is rate control. This is achieved through medications that act on the AV node such as calcium channel blockers (eg diltiazem or verapamil), beta-blockers, or digoxin. Due to digoxin’s slow onset of action and side effects, it is considered a second line medication.

If atrial fibrillation has been present for >48 hours, there is an increased risk of atrial thrombus formation. An echocardiogram should be obtained in these patients to exclude thrombus formation prior to rhythm control. Patients with chronic atrial fibrillation usually are placed on warfarin (D) or a similar anticoagulant to prevent thromboembolism.Chemical cardioversion (A) (amiorodone, procainamide or flecainide) can be attempted in patients with paroxysmal atrial fibrillation for less than 48 hours. Synchronized cardioversion (C) is used in patients who are hemodynamically unstable. This can be achieved by administering 50 – 100 J of electricity in synchronization mode.

2.  If a patient has an accessory pathway, such as Wolff-Parkinson-White Syndrome.

3. D. This patient presents with near syncope in the setting of atrial fibrillation with abberant conduction most likely secondary to Wolff-Parkinson-White (WPW) syndrome and should be chemically or electrically cardioverted. WPW syndrome refers to the presence of an accessory pathway between the right atrium and right ventricle. This accessory pathway has a shortened refractory period and can bypass normal conduction down the AV node. Because of the shortened refractory time, the accessory pathway in WPW can conduct atrial impulses much faster than the AV node can allowing for a ventricular rate between 150 and 300 beats per minute. Any tachycardia greater than 200 beats per minute in an adult should raise suspicion for an accessory pathway.

Patients with WPW can be asymptomatic or may present with severe tachydysrhythmias. The most common presenting dysrhythmia is reentrant tachycardia (70-80%) and second is atrial fibrillation (10-30%). In these tachydysrhythmias, the patient can conduct orthodromically (down the AV node and back up the accessory pathway), antidromically (down the accessory pathway and up the AV node) or in both directions. Patients who have any antidromic conduction will present with wide complex tachycardias. In patients with irregularly irregular wide-complex tachycardias, atrial fibrillation with WPW is the most common diagnosis. If the patient is unstable, electrical cardioversion should be pursued immediately as these patients run the risk of degrading into ventricular tachycardia and ventricular fibrillation. If the patient is stable, procainamide can be administered for chemical cardioversion. Procainamide is a class Ia anitdysrhythmic agent. The dose of procainamide (D) is 18-20 mg/kg administered at a rate of 20-30 mg/min.

In patients with WPW, antidysrhythmic agents that block the AV node are contraindicated. Blocking the AV node causes unopposed electrical conduction down the accessory pathway. This can lead to ventricular dysrhythmias. Additionally, the accessory pathway in WPW responds paradoxically to AV nodal blocking agents by further decreasing its refractory time. Adenosine (A), beta-blockers (C), calcium-channel blockers (B) and digoxin all block the AV node.

Episode 14 – Hand

(iTunes or listen here)

The Free Open Access Medical Education (FOAM)

This week we review EM in 5’s episode on the Neuro Exam of the Hand.

All 3 motor nerves (median, ulnar, radial) in one motion:

  • Make the “ok sign” and try to break the ring formed by the thumb and index finger – median
    • Memory aid: The median is “ok.”
  • Spread 3-5 fingers apart and adduct against resistance – ulnar
    • Memory aid: The intertriginous areas between abducted fingers make a “U” for ulnar
  • Dorsiflex wrist – radial
    • Memory aid…if you look really hard, the the dorsiflexed hand and arm appear to be a sideways, lower case “r”

…all in one

Motor Exam of the Hand

Motor Exam of the Hand

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 280, 295 ; Rosen’s 8(e) Chapter  50 – a well written chapter, but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Flexor Tenosynovitis

Kanavel’s Cardinal Signs (look for words that start with “F”).

  • Pain on passive extension -happens early
  • Finger held in flexion – see above point..extension hurts!
  • Fusiform (uniform) swelling of finger – most common
  • Tenderness along flexor tendon sheath – happens later [3]

Treatment – serious surgical emergency and failure to treat adequately can result in necrosis, proximal spread, and loss of use of hand.

  • IV Antibiotics – penicillinase resistant penicillin (ampicillin-sulbactam, piperacillin-tazobactam) + vancomycin (if suspect MRSA)
  • Consult hand surgery
  • Admit

Hand Pearls

Mallet Finger:  Disruption of the distal extensor tendons, often caused by a jamming injury, hyperextension, or crush.  Look for bruising at the distal interphalangeal joint. Closed injury –  immobilization. Open- extensor tendon repair.

High pressure injection injuries (paint gun, on the job stuff): Worse than they look.  Tetanus, IV antibiotics, consult hand.

Digit amputation storage: Cover the stump with saline gauze and wrap amputated digit in saline soaked gauze.  Put the saline soaked gauze covered digit in airtight plastic bag and place that bag in a bag on ice.

Amputations have best success of reimplantation if they are:

  • Clean cut (saw, etc) versus a crush injury
  • Distal (distal finger > proximal finger > hand)

Learn to Splint Like a Pro (via ERCast) and document a thorough neurovascular exam pre and post-splinting.

Bonus Rosenalli Myth Buster:  Common teaching prevails that epinephrine should not be used with anesthesia of the fingers, nose, toes, penis, etc.  FOAM has debunked this (SMART EM podcast), as well as peer reviewed literature: Waterbrook et alTruth, and epinephrine, at our fingertips: unveiling the pseudoaxioms.

  • Use of epinephrine in finger, nose, etc IS Rosenalli approved [Ch 40, Tintinalli 7e; Ch 3 Rosen's 8e].

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  Which of the following is classically seen in flexor tenosynovitis?

A. Extended position of the involved digit

B. Fusiform swelling of the digit

C. Tenderness over the extensor sheath

D. Vesicular eruption over the flexor surface

Question 2. A 42-year-old man presents to the ED with an amputation of his left thumb just proximal to the interphalangeal joint. The injury occurred 1 hour ago at a rural construction site while the patient was operating a power miter saw. The thumb is brought in, in a sandwich bag, along with the patient. Which of the following is true regarding predictors of successful replantation?

A. Crush injuries have a high success rate of replantation

B. Digits have better tolerance for ischemia than limbs have

C. The amputated part should be kept cold and dry

D. The patient’s social history adds little value to the success rate of replantation


1. Chapters 3, 50.  Rosen’s Emergency Medicine, 8e.

2.Chapters 40, 280, 295.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

3. Draeger RW, Bynum DK Jr. Flexor tendon sheath infections of the hand. J Am Acad Orthop Surg. 2012 Jun;20(6):373-82. doi: 10.5435/JAAOS-20-06-373.


1. B.  The flexor tendons of the fingers are covered by a double layer of synovium to promote gliding of the tendon underneath. Infections in the synovial spaces in the hand tend to spread along the course of the flexor tendon sheaths and may extend proximally to the hand. Infections are usually due to penetrating trauma involving the sheath but occasionally from hematogenous spread. Four cardinal signs of acute flexor tenosynovitis are usually present to help distinguish tenosynovitis from other hand infections. These criteria are referred to as the Kanavel’s signs. Flexor tenosynovitis is a surgical emergency. Consultation with a hand surgeon is warranted along with intravenous antibiotics. The affected digit is held in a flexed (A), not extended, posture. The tenderness is over the flexor (C) sheath, not extensor. Vesicles (D) are not commonly associated with flexor tenosynovitis. A localized herpes simplex infection may cause vesicles to form on a digit

2. B.  Ischemia time is one of the most important predictors of successful replantation. Digits have less muscle mass to oxygenate and tolerate ischemia better than amputations more proximally along the limb. Replantation of limbs must be completed within 4–6 hours, but digits can tolerate an ischemic time of up to 8 hours, given proper preservation.  Crush injuries (A) have a low success rate for replantation due to the significant destruction of neurovascular structures. The amputated body part should be irrigated with normal saline to remove gross contamination, wrapped insterile gauze moistened with saline (C), and placed in a sterile, watertight container. This container should be placed in ice water, but the digit itself should not be submerged. Research has repeatedly shown that tobacco use (D), especially smoking after surgery, will worsen the chance of successful replantation. Obtaining a social history is important in these cases.

Episode 13 – Tricyclic Antidepressants and Sodium Channel Blockade

(iTunes or listen here)

The Free Open Access Medical Education (FOAM)

We review Dr. Amal Mattu’s episode, Why You Should Care When Things are Totally RAD, on his fabulous weekly ECG video series.  This week’s episode reviews Rightward Axis Deviation (RAD) and the two “can’t miss” causes in the Emergency Department (ED): Sodium channel blocker toxicity (tricyclic antidepressants and cocaine) and pulmonary hypertension (pulmonary embolism).

Causes of Rightward Axis Deviation – Lead misplacement, Hyperkalemia (can do anything on the ECG)
Ventricular ectopy (VT), Lateral MI (Q-waves in lead I), Left posterior fascicular block, Right ventricular hypertrophy, Dextrocardia

Sodium Channel Blocker Toxicity ECG clues: 

  • Tachycardia (most common)
  • Right Axis Deviation
  • Tall R wave in aVR
  • Tall R in V1
  • Prolonged QRS
  • Prolonged QTc

EMCrit Episode 98 - Dr. Scott Weingart reviews the treatment of tricyclic antidepressant (TCA) toxicity.   Top pearls

  • When using sodium bicarbonate (NaHCO3) to treat TCA toxicity, the pH doesn’t seem to rise above 7.5 (but you still have to check it). Ventilate these patients appropriately (given breakdown of NaHCO3 to CO2).
  • When infusing NaHCO3, check a VBG every hour to follow the pH and the potassium.
  • Calcium can be critically low in these patients, replete and check accordingly.

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 171 ; Rosen’s 8(e) Chapter  151, Goldfrank’s Toxicology Chapter 73 but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Tricyclic Antidepressants

Includes drugs like amitriptyline, nortriptyline and work on a variety of receptors. Other drugs, such as carbemazepine and cyclobenzaprine demonstrate TCA-like properties, albeit with different toxicologic properties (ALiEM post) Properties include anticholinergic, antihistamine, and alpha-1 adrenergic blockade in addition to sodium channel blockade and inhibition of the reuptake of norepinephrine and serotonin.

Clinical Presentation

  • Anticholinergic Symptoms predominate early on – tachycardia, flushed/dry skin, mydriasis, altered mental status, urinary retention (Mad as a Hatter, Hot as a Hare, Dry as a Bone, Blind as a Bat)
  • Mumbling speech
  • Seizures and ventricular dysrhythmias typically occur within the first few hours after ingestion.

Diagnosis – serum TCA levels and urine drug screens have no value in acute treatment (that’s per Rosen) [2].  In addition to history and physical examination, the ECG may be helpful:

  • QRS >100 ms*
  • Tall R wave in lead aVR (>3mm), R/S(avr) > 0.7
  • T40-ms axis between 120° and 270° (difficult to measure)

*It is widely taught, included in Rosen’s, Tintinalli, and Goldfrank, that seizures occur with a QRS >100 ms and ventricular dysrhythmias occur with a QRS >160 ms [1-3].  A 2004 meta-analysis demonstrated operating characteristics that were less than favorable, with the following characteristics:

  • QRS duration >100 ms to predict seizure: Sensitivity 69% (CI 57-78), +LR 3.18, -LR 0.38
  • QRS duration to predict ventricular dysrhythmia: Sensitivity 79% (CI 58-91), +LR 1.77, – LR 0.39
    • Note: It appears the studies in this analysis used a QRS of 100 ms whereas traditional teaching references 160 ms as the threshold for most ventricular dysrhythmias
  • Most predictive of ventricular dysrhythmia: R/S waves ratio (+LR 15.67) but this was evaluated in only one study (Sensitivity 47%)



In acute overdose with an ingestion < 1 hour prior, activated charcoal may be given if no contraindications exist.

Symptomatic treatment and observation for at least six hours.

Hypotension – crystalloid intravenous fluids, vasopressors if needed (norepinephrine)

Seizure – Most seizures are self-limiting and spontaneously terminate within 3 minutes but benzodiazepines and standard seizure treatment can be used .

Prolonged QRS (>100 ms) or Dysrhythmia

Sodium Bicarbonate – 1-2 mEq/kg bolus.  Each amp of NaHCO3 has 50 mEq so the average 70 kg patient can get 1.5-2.5 amps.  An infusion of NaHCO3 may be used (3 amps of NaHCO3 in 1 L of D5W).

  • Caution: must follow pH (can titrate as high as 7.5-7.55) as well as potassium.

If the NaHCO3 pushes the patient’s pH to the 7.5-7.55 limit and the QRS remains wide, 200 mL of hypertonic saline (3%) can be used.

Lidocaine, a class IB sodium channel blocker/antiarrhythmic can also be used although it may seem counterintuitive.

Magnesium may also be used


Asymptomatic patients six hours after ingestion (no sinus tachycardia) can be medically cleared.

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  A 24-year-old man presents to the ED via the police because of altered mental status and violent behavior. The patient reportedly had been on a drug binge, using amphetamines and cocaine for the last 2 days. On arrival, he is afebrile, his heart rate is 140 beats per minute, blood pressure is 180/110 mm Hg, and he is respiring at 22 breaths per minute. He is agitated and combative, but there is no evidence of traumatic injury. His pupils are dilated, and he is diaphoretic. Which of the following statements is true regarding the treatment of amphetamine and cocaine toxicity?

A. Antipsychotics are the preferred initial therapy for agitation and psychosis

B. Beta-adrenergic blockers are safe for managing tachycardia and dysrhythmias

C. Body packers with leaking packets should receive whole-bowel irrigation

D. Vasodilators are first-line therapy for treating amphetamine-induced hypertension

E. Wide-complex tachydysrhythmias should be treated initially with sodium bicarbonate

Question 2.  A 27-year-old man is brought to the ED by EMS after being found wandering in the street. His BP is 155/70, HR 115, T 37.5°C, RR 16, pulse ox 99% on room air, and finger stick glucose 98. On exam, the patient is confused with mumbling speech. His pupils are 7 mm and reactive. His face is flushed. Mucous membranes and skin are dry. Which of the following toxidromes is this patient exhibiting?

A. Anticholinergic

B. Cholinergic

C. Sedative-hypnotic

D. Sympathomimetic

More FOAM:

Life in the Fast Lane TCA case

Life in the Fast Lane TCA ECG


1. Chapter 151.  Rosen’s Emergency Medicine, 8e.

2.Chapter 171.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

3.Chapter 73.  Goldfrank’s Toxicologic Emergencies, 9e, 2010

4.  Bailey B, Sc M. A Meta-Analysis of Prognostic Indicators to Predict Seizures , Arrhythmias or Death After Tricyclic Antidepressant Overdose . 2004;42(6):877–888. doi:10.1081/CLT-200035286.  

Episode 12 – Back to Biphasics

(iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Episode 1 of Dr. Salim Rezaie’s REBEL Cast covering exposing the dogma behind biphasic anaphylaxis reactions.

Traditionally, we’re taught to observe patients in the Emergency Department (ED) for 4-6 hours to watch out for biphasic reactions, as the rate of biphasic reactions can approach 20%.

Grunau BE et al. Incidence of Clinically Important Biphasic Reactions in Emergency Department Patients with Allergic Reactions or Anaphylaxis. Ann of EM 2014; 63(6): 736 – 44.

  • Retrospective chart review of 430,000 visits
  • Anaphylaxis n=496 (2 had biphasic reactions, Allergic reactions n=2323 (3 had biphasic reactions)
  • No deaths, biphasic reactions occurred anywhere from 16 minutes into the ED stay to 6 days later

Rohacek M et al. Biphasic Anaphylactic Reactions: Occurrence and Mortality. Eur J All Clin Imm 2014; 69(6): 791 – 7.

  • Retrospective study in Europe of presentations to one hospital from 2001-2013 of n=1334 allergic reactions, n=524 anaphylaxis reactions
  • 2.3% (n=12) met criteria for clinically important biphasic reactions

Additional FOAM on the topic: The SGEM

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 27 ; Rosen’s 8(e) Chapter  119 but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!


Diagnosis -

Two or more systems involved after likely allergen exposure (within hours):

  • Skin – generalized hives, itch-flush, swollen lips-tongue-uvula
  • Pulmonary – dyspnea, wheezing, bronchospasm, stridor
  • Cardiovascular -hypotension or associated symptoms (syncope, incontinence)
  • Gastrointestinal symptoms- crampy abdominal pain, vomiting

Hypotension after exposure to known allergen for that patient (minutes to several hours)also qualifies

Differential Diagnosis -vasovagal (most common mimicker), myocardial ischemia, status asthmaticus, epiglottitis, angioedema, foreign body, carcinoid, vocal cord dysfunction, drug reactions, psychogenic

Treatment -

Epinephrine. Commit the dose to memory and look up if, needed as this is a huge source of medication errors [Gaeta et alBenklefat ].

  • Adults: 0.3mg, Pediatrics 0.01mg/kg of 1:1000 epinephrine intramuscular (IM) to lateral thigh (pediatric patients >30kg get the adult dose).
  • If repeated doses of IM epinephrine required and patient continues to remain hypotensive, start intravenous epinephrine. ALiEM’s post on making the dirty epi drip.


  • IV fluids for blood pressure/shock
  • Corticosteroids may help prevent recurrence although they take 4-6 hours to work, so are unhelpful in acute attacks [Choo et al].  Rosen recommends either prednisone 0.5-1mg/kg orally or methylprednisolone 80-125 mg IV. (You don’t have to give IV in all cases)
  • Histamine blockers (H1 and H2 such as diphenhydramine and famotidine, respectively) may help with the dermatologic symptoms and pruritis.
  • Glucagon in patients that aren’t responding or are on beta-blockers.  ALiEM post.
  • Give patients that are going home a prescription for an EpiPen (for pediatric patients, have one parent go fill the script during the observation period) and show them how to use the autoinjector.  These things are expensive and do expire, and there are some coupons out there to help out.

Disposition – Clearly patients with ongoing symptoms and/or shock should stay in the hospital. However, most patients can be discharged home once they are improved and the effects of the epinephrine have worn off.  Tintinalli recommends about 4 hours, referencing a study by Brady et al from 2007.  Interestingly, in this study there were 2 biphasic reactions that occurred at 20 hours and 46 hours after the initial ED visit.  So, not sure how they came up with 4 hours.

FOAM Pearls Supported by the Literature and Rosenalli – 

Iodine Allergy is not a thing.

Shellfish allergy does NOT put a patient at increased risk of contrast allergy more than any other allergen [Kaufman et al].

Cross-reactivity between penicillin and cephalosporins is often quoted at 10-20% but, in reality, is far less and a review demonstrates cross reactivity of 1% in patients reporting a penicillin allergy [Campagna et al]. Rosen’s agrees with this assessment and states that the overall cross reactivity is minimal.  ALiEM post on this myth

ACE-Inhibitor Induced Angioedema

Cause:  The vasodilation and non-pitting edema of the mucosal, dermal, and subcutaneous tissues thought to be mediated by the build up of bradykinin and substance P.  Non-allergic, often asymmetric.

Presentation: Swelling of the lips, tongue, airway most often although it can also involve the genitals and viscera.


  • Stop the ACE-Inhibitor.
  • Active, anticipatory airway management.  Perhaps, even an awake airway (The EMCrit Way, The Strayer Way).
  • Epinephrine, corticosteroids, and histamine blockers do not work.  While fresh frozen plasma may work for hereditary angioedema, but it doesn’t really work in ACE-inhibitor angioedema and there’s no proven therapy [Winters et al].
  • Investigations underway for icatibant (bradykinin 2 receptor antagonist) Bas et al, Schmidt et al and Ecallantide (reversible kallikrein inhibitor)

Question 1. A 55-year old man who is taking several antihypertensive medications presents to the ED with nausea, vomiting, shortness of breath, and a rash after eating a home-cooked Thai meal at a friend’s house about 1 hour ago. The symptoms began within seconds of the first bite of his meal. Despite the patient being administered 2 doses of intramuscular epinephrine, diphenhydramine, dexamethasone, and crystalloid fluids, his blood pressure remains at 75/38 mm Hg.Which other medication should be considered in this patient?

  • A. Cimetidine
  • B. Glucagon
  • C. Norepinephrine
  • D. Octreotide

Question 2. A 55-year-old woman presents to the ED for swelling of her tongue and lips.

Photo: Rosh Review

Photo: Rosh Review

She recently started a new antihypertensive medication. Which of the following is the direct mediator for her condition?

  • A. Angiotensin
  • B. Bradykinin
  • C. C1-esterase inhibitor
  • D. Histamine


1. B.  The patient is experiencing an acute anaphylactic reaction, most likely to peanuts that are commonly found in Thai cooking. Although uncommon, patients taking beta-blocking agents for hypertension may exhibit refractory hypotension despite being administered fluids and epinephrine. This is because epinephrine acts by binding to adrenergic receptors, which includes beta-receptors. To circumvent the beta-receptor, glucagon can be administered, which will bypass the beta-adrenergic second messenger system, potentiate the circulating epinephrine, and help restore vasomotor tone.

Cimetidine (A) is an antihistamine. Although it may help in mild allergic reactions, it will not treat hypotension in severe anaphylaxis. In addition, cimetidine prolongs the metabolism of beta-blockers. Octreotide (D) may be used in management of esophageal variceal bleeding control, treatment of carcinoid syndrome, and refractory hypoglycemia after sulfonylurea-induced hypoglycemia. There is no role in anaphylaxis. Norepinephrine (C) also binds adrenergic receptors that may be inhibited in patients who take beta-blocking medications.
2. B.  Angioedema is the clinical manifestation of transient, localized, nonpitting swelling of the subcutaneous layer of the skin or submucosal layer of the respiratory or gastrointestinal tracts. There are many cases of angioedema, but the condition is usually divided into hereditary, acquired, and drug-induced causes. Hereditary angioedema (HAE) is caused by deficiency or dysfunction of C1-esterase inhibitor and is usually precipitated by stress or trauma. Acquired angioedema is also due to deficiency or dysfunction of C1-esterase inhibitor, but is not due to a genetic cause; rather, it appears later in life. The exact etiology is unknown, but the condition is exceedingly rare. The most common cause of drug-induced angioedema is due to an adverse reaction from ACE inhibitors. When ACE is inhibited by medications, angiotensin I is not converted to angiotensin II, and bradykinin is not metabolized. It is thought that the increased level of bradykinin is responsible for angioedema induced by ACE inhibitors. Angioedema can result in severe airway compromise or, less commonly, compromise in the GI tract that is associated with abdominal pain. Evaluation should focus on ruling out laryngeal edema and airway compromise. Although direct visualization is best, asking the patient to phonate a high-pitched “E” is one quick way of assessing for laryngeal edema. If the patient is able to phonate a high-pitched “E,” then the presence of laryngeal edema is unlikely. Treatment is mainly supportive with special attention to airway protection. Angioedema caused by deficiency or dysfunction of C1-esterase inhibitor can be treated by replacing C1-esterase inhibitor with fresh frozen plasma or other recombinant agents.

Angiotensin (A) is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs (ACE inhibitors) that lower blood pressure. An elevated level of angiotensin is not responsible for angioedema. C1-esterase inhibitor (C) serves as the main regulator of the kallikrein-kinin system. As a result of decreased amounts of functional C1-INH, when the kallikrein-kinin system is activated, it is not kept in check. This leads to increased formation of bradykinin and the resultant increased vascular permeability and edema formation and is the cause of hereditary angioedema, not ACE-inhibitor induced angioedema. Histamine (D) has many roles in the body, but its primary role is within the immune system. Mast cells release histamine through a process known as degranulation when they have been sensitized with IgE antibodies and then come in contact with an appropriate antigen leading to the development of urticaria and pruritus.