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.
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].
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).
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 .
hOurs: headache lasts 4-72 h without medication
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 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
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.
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.
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!
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 
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% .
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) 
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
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?
A. Chemical cardioversion
B. Rate Control
C. Synchronized cardioversion
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?
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.
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!
Two or more systems involved after likely allergen exposure (within hours):
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 –
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.
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?
Question 2. A 55-year-old woman presents to the ED for swelling of her tongue and lips.
She recently started a new antihypertensive medication. Which of the following is the direct mediator for her condition?
C. C1-esterase inhibitor
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.
We review Mount Sinai Emergency Medicine Residency’s blog post on Ebola. The Pearls:
Signs and symptoms of ebola: Fever (>101.5F, 41C), severe HA, myalgias, vomiting, abdominal pain, unexplained hemorrhage, hypotension plus an epidemiologic risk factor in the past 3 weeks.
Risk factors: contact with blood or other body fluids of a patient known or suspected to have ebola, residence or travel to endemic areas, and direct handling of bats, rodents, or primates from disease endemic areas.
CDC recommends screening in those with :
percutaneous/mucous membrane exposure or direct skin contact with body fluids of a person with a confirmed or suspected case of ebola without appropriate personal protective equipment
laboratory processing of body fluids of suspected or confirmed ebola cases without appropriate PPE or standard biosafety precautions
participation in funeral rites or other direct exposure to human remains in the geographic area where the outbreak is occurring without appropriate personal protective equipment.
Personal protective equipment is key in prevention of ebola spread. Ebola is not airborne but due to the case mortality rate, fear, and questionable history of aerosol transmission in the past, we treat it like it is. Recommended protection in the United States: fluid impermeable gown, N95 respirator, eye shield and in situations with large amounts of fluids -double gloving, disposable shoe covers, and leg coverings (CDC recommendations).
We summarize some key topics from the following readings, Tintinalli (7e) Chapters 157, 148 but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself! Airborne Precautions – used for patients known to be or suspected of being infected with organisms transmitted by airborne droplets and small particle residue (<5 micrometers) of evaporated droplets containing microorganisms that can be spread by air currents.
Require special, negative pressure rooms with special ventilation and filtration and the N95 respirators.
Limited movement of patient within the health care setting and in the ED they need to be in a room with the door closed.
Recommended for: Measles, Varicella, Tuberculosis
Droplet Precautions – used for patients known to have or suspected of having serious illnesses transmitted by large particle droplets (>5 micrometers) produced by the patient during talking, sneezing, or coughing or during procedures.
Use a mask and wash your hands. N95 respirator recommended for procedures like bronchoscopy, suctioning, etc.
Non Sterile gown if one anticipates substantial contact with the patient or if the patient is incontinent or has wound drainage not contained by dressings.
Limit transportation and movement of the patient – they should wear a mask when transported throughout the hospital.
Varicella – Herpes virus that causes chickenpox (primary infection) and a secondary reactivation (herpes zoster/shingles) as the virus may lie latent in dorsal root ganglia.
Use Airborne precautions as it’s spread via respiratory secretions but may also spread (although less infectious) from the fluid of the non-crusted vesicles.
Symptoms of chickenpox: fever, malaise, headache and a vesicular rash that appears in crops with lesions at varying stages, including papules, vesicles, and crusted lesions, predominantly on the torso and face.
Most infections are minor and self-limited but increased sequelae exist in the immunocompromised and elderly. These subgroups may benefit from antivirals
Immunizations now prevalent although individuals can still get mild chickenpox after immunization.
Varicella-zoster immune globulin exists but use as postexposure prophylaxis is essentially limited to non-immune pregnant women and the severely immunosuppressed. Healthy non-immunue individuals can be vaccinated after exposure and, if they are high risk and develop symptoms, they can get antivirals.
Generously Donated Rosh Review Questions
Question 1. [polldaddy poll=8241932]
Question 2. A 3-year-old boy presents to the ED with 3 days of fever, cough, and runny nose. On exam, you note conjunctival injection and an erythematous, nonblanching, nonvesicular, maculopapular rash behind his ears and on his hairline, with a few spots on his chest. [polldaddy poll=8241939]
Cline DM. “Chapter 157. Occupational Exposures, Infection Control, and Standard Precautions” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (2011).
1. Chickenpox is a highly contagious but generally benign and self-limited viral disease caused by the varicella-zoster virus (also known as human herpesvirus 3). The disease is characterized by the sudden onset of fever, malaise, and a pustular maculopapular rash that can occur anywhere on the skin or mucus membranes. The lesions then become vesiculated followed by scabbing over the course of 3-4 days before resolving. Skin lesions appear in crops with multiple lesions of various stages appearing on the skin at the same time. Uncomplicated infection is generally treated with supportive measures, including antipyretic, antipruritic, and pain control medications. Antivirals such as acyclovir, valacyclovir, and foscarnet may also be initiated in severe disease or immunosuppressed individuals. Parents should be cautioned to avoid giving their children aspirin or aspirin containing medications due to the risk of developing Reye’s syndrome.
The lesions of chickenpox appear suddenly rather than gradually (A). Smallpox lesions may appear similar to chickenpox lesions, however they are found in the same stage (B) of development. Rubella (German measles) is associated with the sudden onset of a maculopapular rash that first appears on the face then rapidly spreads inferiorly to the neck, trunk, and extremities and fades by the 3rd day (C).
2. Rubeola, or measles, is associated with fever and rash with cough, conjunctivitis, coryza, and Koplik spots. The characteristic rash is erythematous, nonblanching, and maculopapular. It begins on the head, usually behind the ears and around the hairline, with subsequent spread down the face, to the trunk, and extremities (centrifugal spread). The rash may coalesce into salmon-colored patches and typically disappears within 1 week. Koplik spots or pinpoint-sized white lesions on a red background that appear on the buccal mucosa opposite the molars are pathognomonic.
Roseola (A) is a viral infection with the onset of a rash that occurs upon resolution of a high fever. It is common in ages 6–18 months. Rubella (B) is often referred to as “three-day measles.” It is a mild illness, except for congenital infection, which can cause major birth defects. It is associated with fever, rash, and prominent lymphadenopathy, with tender posterior auricular, cervical, and occipital nodes. Varicella (D) (chicken pox) is associated with a flu-like illness and the formation of macules that progress to fluid-filled vesicles in an erythematous base (“dew drops on a rose petal”). Crops of lesions typically appear at the same time with vesicles in various stages of healing.