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).
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.
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)
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.
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.
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!
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]
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
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
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
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?
A. Administer adenosine 6 mg IV
B. Administer diltiazem 10 mg IV
C. Administer lopressor 10 mg IV
D. Administer procainamide 100mg IV
References
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.
Answers
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.
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!
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]
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
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
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
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?
A. Administer adenosine 6 mg IV
B. Administer diltiazem 10 mg IV
C. Administer lopressor 10 mg IV
D. Administer procainamide 100mg IV
References
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.
Answers
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.
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
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.
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.
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
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.
Answers.
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.
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%)
[4]
Treatment
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
Disposition:
Asymptomatic patients six hours after ingestion (no sinus tachycardia) can be medically cleared.
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?
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%.
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!
Anaphylaxis
Diagnosis –
Two or more systems involved after likely allergen exposure (within hours):
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 al, Benklefat ].
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.
Adjuncts:
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 –
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?
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.
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
Answers.
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 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%.
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!
Anaphylaxis
Diagnosis –
Two or more systems involved after likely allergen exposure (within hours):
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 al, Benklefat ].
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.
Adjuncts:
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 –
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?
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.
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
Answers.
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).
Answers
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.
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).
Answers
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.
Ask for color descriptors or look at the emesis yourself rather rely on typical descriptors of emesis.
Bilious vomiting, medical speaking, means emesis that appears like cooked, green spinach – not the yellow color that parents often mean. While sometimes normal in older children with gastroenteritis, in neonates or anyone sick appearing, this represents a surgical emergency such as volvulus, malrotation, necrotizing enterocolitis etc.
Projectile vomiting – Most vomit is projected at least a short distance, so parents may say even reflux is projectile. Observe a test feed to gauge whether a baby is vomiting or has true projectile vomiting which may represent idiopathic hypertrophic pyloric stenosis.
Coffee ground emesis – this is a blackish-brown gritty emesis but parents may mean any brown-ish vomit. This is typically indicative of upper GI bleed, which is pretty rare in pediatric patients.
The Bread and Butter
We summarize some key topics from the following readings, Tintinalli (7e) Chapters 111,124; Rosen’s 8(e) Chapter 172 but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself!
Neonatal Jaundice
Physiologic Jaundice – Jaundice in healthy, full-term newborns typically develops during the 2nd – 3rd day of life and resolves by the 5th or 6th day. This occurs a little later in Asian and premature infants.
Mean peak total serum bilirubin is 6 mg/dL
Use the nomogram in infants >35 weeks gestational age to determine need for phototherapy
Non-physiologic Jaundice – bad.
Jaundice in the first 24 hours
Bilirubin rising faster than 5 mg/dL in 24 hours •Clinical jaundice >1 week
Direct bilirubin >2 mg/dL
In healthy term infants total serum bilirubin concentration >15 mg/dL (so remember: average of 6 but more than 15 is bad. But check out the nomogram in non-preemies).
Indirect Neonatal Jaundice – 3 main causes, listed below. Treatment is with phototherapy and mitigation of underlying causes.
Increased lysis – this can be due to lysis of red blood cells or sequestration of blood – ABO incompatibility, splenic sequestration, spherocytosis.
Decreased hepatic uptake/decreased conjugation – Immature transfer enzymes (babies grow out of this), breastmilk jaundice (lack certain enzymes, idiopathic hypertrophic pyloric stenosis (unclear why), as well as Gilberts, Crigler Najjar Syndrome
Increased enterohepatic uptake (i.e. too much reclaimed from the gut) – obstruction or breastfeeding jaundice (dehydrated babies who are breast feeding).
Direct Bilirubinemia
Etiology – biliary tree obstruction or biliary atresia, enzyme deficiencies (cystic fibrosis, alpha-1 antitrypsin deficiency, glycogen storage diseases)
Conjugated bilirubin is non-toxic so treat the underlying cause
Emergency Department Diagnostics:
Total and Fractionated Bilirubin, Blood Type with Rh factor, Coomb’s test, blood count, Reticulocyte count, consider sepsis work-up .
Presentation: Abdominal pain, vomiting, bloody or guaiac positive stool. The classic triad is not useful and present in 15-20%. While intussusception is most common at approximately 1 year of age and, moreover 2 months -6 years, it can present at any time, including the elderly.
Etiology: The bowel telescopes on itself and
Diagnosis: Clinical, ultrasound (target sign), or diagnostic and therapeutic air contrast enema. It’s also reasonable to get plain films, if desired.
Treatment: Air contrast enema in radiology results in approximately 60% success so most recommend a surgery consult in the event there’s a complication or failure in radiology. Also, give these patients 20cc/kg fluid bolus and treat their pain.
Generously donated Rosh Review questions (scroll for answers)
Question 1. A 10-month-old previously healthy boy presents with 1 day of bilious vomiting and fever. The patient is ill-appearing. Physical examination reveals a distended and diffusely tender abdomen with guarding and rebound. [polldaddy poll=8224476]
Question 2. A 2-year-old ex-33 week premature girl presents with vomiting, diarrhea and poor feeding. The patient has episodes of fussiness and inconsolable crying followed by periods of lethargy and sleeping. During periods of fussiness, the patient draws her legs up to her chest. [polldaddy poll=8225869]
Also, check out “Ketamine, The Album” – A musical written by and for emergency physicians as a tribute to ketamine
Answers.
1.Correct Answer ( A ) This patient presents with signs and symptoms concerning for an obstruction secondary to a volvulus and requires emergent surgical evaluation. Malrotation is a relatively common occurrence (1 in 500 live births) and about 75% of patients with malrotation will develop volvulus. During embryonic development, rotation of the gut arrests. This allows for the small bowel to twist around the superior mesenteric artery causing an acute obstruction. Patients will present with sudden onset of abdominal distension and bilious emesis. These infants will be ill-appearing and possibly toxic on presentation. Although a number of diagnostic modalities can be employed for definitive diagnosis, the priority in an ill-appearing infant with bilious emesis is emergent surgical consultation. All other interventions risk delaying definitive management. While waiting for the surgical consultation, the patient should have an IV placed, fluid resuscitation begun and a nasogastric tube placed for decompression of the stomach. Additionally, broad spectrum antibiotics should be administered. After consultation, an upper GI series may be obtained for definitive diagnosis.
Stool cultures (B) are useful when there is a suspicion for infectious process such as a parasitic or bacterial infection. Laboratory studies (C) will provide limited data and should not delay definitive management by a surgeon. The patient should receive intravenous hydration, not oral rehydration (D) as there is a high likelihood that this patient will be taken to the operating room. As such, the patient should be kept NPO.
2. D. This patient presents with symptoms concerning for intussusception and should have an emergent ultrasound performed to make the diagnosis. Intussusception is defined as the telescoping of one segment of the intestine into another. It is the most common cause of obstruction in children younger than 2 years of age. The classic triadof intussusception is abdominal pain, vomiting and bloody stools but all three features are only present in about 33% of patients. Bowel movements may be loose with mucous and blood and appear like “currant jelly.” Often patients will have cycles of severe abdominal pain lasting 10 to 15 minutes during which they are inconsolable. These episodes are followed by periods of painlessness during which the child may be lethargic. Palpation of the abdomen may reveal a sausage-like mass in the right upper quadrant representing the actual intussusception. The lead point for the telescoping may be due to Henoch-Schonlein purpura vasculitis, Meckel’s divericulum, lymphoma or polyps in children over 5 years of age. In younger children, enlarge Peyer’s patches may be the culprit. These occur after viral infections. Ultrasound of the abdomen is the best initial modality for identifying the intussusception. It may reveal the classic findings of a target sign or “pseudokidney” sign. Sensitivity and specificity of ultrasound approach 100%. Abdominal X-ray (A) may show intussusception but may be negative in up to 20% of patients. CT(B) and MRI (C) of the abdomen and pelvis are also unreliable in the diagnosis.