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This is going to be a diagnosis that is mainly made through a thorough history, and pay particular attention to those with recent travel to West-Africa
The incubation period for falciparum is 12 days, but there is a range of weeks and we should consider Malaria when consistent symptoms develop within 1 month of travel to an endemic area
Typical signs and symptoms for uncomplicated malaria are periodic fevers, jaundice, pallor
Be mindful of end organ involvement, such as cerebral edema, ATN, and pulmonary edema; these cases are considered to be severe and treated differently than uncomplicated malaria
Uncomplicated cases should get Malarone or Coartem
Severe cases require IV Artesunate
Be judicious with your fluid resuscitation as this can harm our patients
Centers for Disease Control and Prevention. CDC Parasites – Malaria. 2019 https://www.cdc.gov/parasites/malaria/index.html (7 July 2019, date last accessed)
Ashley EA, Pyae Phyo A, Woodrow CJ. Malaria. Lancet. 2018;391(10130):1608-21.
Hanson JP, Lam SW, Mohanty S, Alam S, Pattnaik R, Mahanta KC, et al. Fluid resuscitation of adults with severe falciparum malaria: effects on Acid-base status, renal function, and extravascular lung water. Crit Care Med. 2013;41(4):972-81.
Lampah DA, Yeo TW, Malloy M, Kenangalem E, Douglas NM, Ronaldo D, et al. Severe malarial thrombocytopenia: a risk factor for mortality in Papua, Indonesia. J Infect Dis. 2015;211(4):623-34.
Lokken KL, Stull-Lane AR, Poels K, Tsolis RM. Malaria Parasite-Mediated Alteration of Macrophage Function and Increased Iron Availability Predispose to Disseminated Nontyphoidal Salmonella Infection. Infect Immun. 2018;86(9).
Maitland K, Kiguli S, Opoka RO, Engoru C, Olupot-Olupot P, Akech SO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011;364(26):2483-95.
Park SE, Pak GD, Aaby P, Adu-Sarkodie Y, Ali M, Aseffa A, et al. The Relationship Between Invasive Nontyphoidal Salmonella Disease, Other Bacterial Bloodstream Infections, and Malaria in Sub-Saharan Africa. Clin Infect Dis. 2016;62 Suppl 1:S23-31.
Tintanelli, Judith E., et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Eighth edition. New York: McGraw-Hill Education, 2016: p.1070-1077
World Health Organization. Guidelines for the treatment of malaria. Third edition
Digoxin is the most common formulation of digitalis, a cardiac glycoside used in the management of systolic heart failure and atrial arrhythmias.
The use of medicinal plants containing cardiac glycosides dates back to the ancient Egyptians. Modern digitalis is derived from the foxglove plant and has been used for the last 200 years
Although the use of digoxin has declined over the past 2 decades, digoxin toxicity exposure rates have risen, possibly because of increased use in the elderly.
There are an estimated ~3,500 emergency hospitalizations for digoxin toxicity in the US each year.
Digoxin toxicity can present acutely or chronically.
Acute presentations can occur with accidental or intentional ingestions.
Chronic presentations are seen with renal failure, supratherapeutic dosing, or drug-drug interactions, especially inhibitors of p-glycoprotein(e.g. amiodarone, erythromycin, sertraline).
Digoxin undergoes hepatic metabolism independent of CYP-450 system and is renally excreted.
Half-life is 1.5-2 days in healthy adults, but can be 4-6 days in patients in renal failure.
Digoxin has a narrow therapeutic window, typically 0.5-1.0 ng/mL, with toxicity range beginning at concentrations greater than 2.0 ng/mL.
Serum digoxin concentrations do not necessarily correlate with toxicity, or degree of toxicity. There are many reports of asymptomatic patients with elevated digoxin concentrations, as well as clinical toxicity with concentrations in the therapeutic range.
Mechanism of Action and Pathophysiology
Digoxin reversibly inhibits Na+-K+ ATPase pump in the myocardium, inhibiting Na+-Ca2+ exchange and increasing intracellular calcium concentration.
In toxic doses, intracellular calcium elevates further and triggers afterdepolarizations. This increases the risk of arrhythmias while shortening the refractory period and increasing automaticity.
Digoxin also has neurohormonal effects, which increases parasympathetic tone. Increased vagal tone leads to stronger atrioventricular nodal blockade, leading to more uncontrolled arrhythmia.
The manifestations of digoxin toxicity are divided into cardiac and extra-cardiac effects.
The most common extra-cardiac symptoms of digoxin toxicity are anorexia, nausea, fatigue and visual disturbance.
The classically described visual disturbances are enhanced perception of yellow and green and seeing halos of light, but these manifestations are actually less common than blurred vision.
Other neuropsychiatric effects are possible, including headache, confusion, hallucinations and delirium.
The key laboratory abnormality in acute digoxin toxicity is hyperkalemia, which results from inhibition of the Na+-K+
In acute toxicity, hyperkalemia strongly correlates with mortality. In a 1973 landmark study performed before the development of digoxin-specific antibody fragments, there was 0% mortality with K+ <5 mEq/L and 100% mortality with K+ >5.5 mEq/L.
In chronic toxicity, hypokalemia can exacerbate toxic effects of digoxin on the myocyte and increase risks of arrhythmias.
The cardiac manifestations of digoxin toxicity are an immediately life-threatening complication. They result from increased automaticity, shortened refractory period and AV nodal blockade.
Digoxin can cause mild PR prolongation and a characteristic scooping of the ST segment. These changes do not necessarily indicate toxicity and can be seen with therapeutic levels of digoxin.
The scooped ST segments characteristic of digoxin
Digoxin can precipitate all degrees of AV heart block and almost any arrhythmia (except for a rapidly conducted supraventricular tachycardia).
The most characteristic arrhythmias associated with digoxin toxicity are bidirectional ventricular tachycardia with alternating wide QRS complexes and atrial tachycardia with AV block. Still, these arrhythmias are not specific for digoxin toxicity.
Other common cardiac manifestations of digoxin toxicity include new-onset AV block, frequent PVCs, sinus bradycardia, and junctional rhythms.
In atrial fibrillation, digoxin toxicity can cause significant slowing of the ventricular rate with increased PVCs.
The key treatment for life-threatening digoxin toxicity is the use of digoxin-specific antibody fragments (Fab), which bind digoxin and rapidly reverse toxicity.
Treatment with antidigoxin-Fab has been shown to be effective in 80-90% of cases, with improvement within 1 hour and complete reversal of symptoms. usually within 4 hours.
The early use of digoxin-specific Fab in patients with life-threatening digoxin poisoning decreases mortality.
Antidigoxin-Fab is indicated in any patient with severe cardiac manifestations of toxicity, including ventricular arrhythmias, high-degree AV block, and hyperkalemia.
Antidigoxin-Fab may also be used in patients with significantly elevated serum digoxin levels >10 ng/mL in acute ingestion.
Use of antidigoxin-Fab may also be cost-effective in patients with evidence of chronic digoxin toxicity and levels as low as 3 ng/mL, especially in patients with renal dysfunction.
Dosing of digoxin-specific Fab can be calculated based on the amount ingested or the serum digoxin level.
Empiric therapy should be used in life-threatening cases instead of waiting for a serum level.
Empiric therapy for acute poisoning: 10-20 vials
Empiric therapy for chronic poisoning: 3-6 vials
One potential side effect of antidigoxin-Fab is hypokalemia, as it will rapidly restore Na+-K+ ATPase activity.
Potassium should be repleted in hypokalemia
GI decontamination with charcoal may be helpful in acute ingestions, as charcoal not only helps with GI elimination but may also increase systemic clearance by acting as a “dialysis membrane”.
For high-degree symptomatic AV block, IV atropine or temporary pacing may be judiciously used. A 2004 retrospective study showed that in accidental digoxin overdose, transvenous temporary pacing was safe for patients with symptomatic bradycardia.
For ventricular arrhythmias, IV lidocaine may be helpful.
Electrical cardioversion patients with digoxin toxicity may precipitate VT or VF and is contraindicated.
In patients with symptoms of digoxin toxicity but no signs concerning for severe poisoning, patients can be observed with cardiac monitoring until symptoms resolve and digoxin concentrations are therapeutic.
Take Home Points
Digoxin toxicity can be a life-threatening condition.
Serum levels do not always correlate with the degree of clinical toxicity – i.e. therapeutic levels may be toxic OR supratherapeutic levels may be benign.
Digoxin toxicity causes a wide variety of dysrhythmias, including ventricular tachycardias and high-degree AV blocks.
Prompt treatment of any severe digoxin poisoning with digoxin-specific antibody fragments (Fab) is essential.
Hyperkalemia is a poor prognostic indicator and should be a concerning sign in digoxin toxicity.
Antman EM, Wenger TL, Butler Jr VP, et al. Treatment of 150 cases of life- threatening digitalis intoxication with digoxin-specific Fab antibody fragments: final report of a multicenter study. Circulation 1990; 81: 1744-52. PMID: 2188752
Bauman JL, Didomenico RJ, Galanter WL. Mechanisms, manifestations, and management of digoxin toxicity in the modern era. Am J Cardiovasc Drugs. 2006;6(2):77-86. PMID: 16555861
Bayer MJ. Recognition and management of digitalis intoxication: implications for emergency medicine. Am J Emerg Med. 1991;9(2):29-34. PMID: 1997019
Bismuth C, et al. Hyperkalemia in acute digitalis poisoning: prognostic significance and therapeutic implications. Clin Toxicol. 1973;6(2):153-162. PMID: 4715199
Budnitz D, et al. Emergency hospitalizations for adverse drug events in older Americans. N Engl J Med. 2011;365(21):2002-2012. PMID: 22111719
Hussain Z, Swindle J, Hauptman PJ. Digoxin use and digoxin toxicity in the post-DIG trial era. J Card Fail. 2006;12(5):343-346. PMID: 16762795
Lapostelle F, et al. Digoxin-specific Fab fragments as single first-line therapy in digitalis poisoning. Crit Care Med. 2008;36(11):3014-3018. PMID: 18824911
Sonnenblick M, et al. Correlation between manifestations of digoxin toxicity and serum digoxin, calcium, potassium, and magnesium concentrations and arterial pH. Br Med J (Clin Res Ed). 1983;286(6371):1089-1091. PMID: 6404339
Smith TW, et al. Digitalis glycosides: mechanisms and manifestations of toxicity. Prog Cardiovasc Dis. 1984;26(5):413-458. PMID: 6371896
Oxygenation is particularly important in children undergoing endotracheal intubation. They have higher oxygen consumption than adults and become hypoxemic more quickly with rapid sequence intubation. Apneic oxygenation (AO) is the process of providing a high flow rate of oxygen through a standard nasal cannula prior to endotracheal intubation (ETI) without bag-valve mask ventilation. It is thought that the high flow rate results in nitrogen washout (replacing nitrogen with oxygen) which provides an oxygen reservoir as well as provides some degree of positive end expiratory pressure keeping airways open. Apneic oxygenation with a standard nasal cannula has the advantage of using readily available airway equipment, does not require removal prior to intubation and avoids the complications that can be associated with bag-valve-mask ventilation. Apneic oxygenation was been shown to be beneficial in adults but pediatric data is limited.
In pediatric patients undergoing endotracheal intubation in the emergency department, is apneic oxygenation (high flow oxygen through a standard nasal cannula without ventilation), when compared to intubation without apneic oxygenation, associated with a decrease in hypoxemia during the procedure?
Inclusion: <22 years, presenting to the ED, requiring endotracheal intubation (ETI) with/without rapid sequence medications
Before AO: n = 59 (includes 14 who did not receive AO in the after AO time period)
Hypoxemia during endotracheal intubation was less common in the After AO cohort in both the univariable (unadjusted) analysis and the regression (adjusted) analysis.
Adjusted odds ratio (AO/no AO): 3, 95% CI (0.1, 0.8)
The difference in the proportion with hypoxia was greater than the 13% difference indicated by the authors as clinically significant.
Additional independent predictors of hypoxia during ETI included
Age (Every 1-year ): aOR: 8, 95% CI (0.7, 1.0)
SpO2 before endotracheal intubation (Every 1% ): aOR: 8, 95% CI (0.7, 1.0)
Each additional attempts at endotracheal intubation: aOR: 0, 95% CI (2.2, 7.2)
Not independent predictors: Proceduralist level of training, direct versus video laryngoscopy
PRIMARY OUTCOME: HYPOXIA DURING ENDOTRACHEAL INTUBATION
Before Apneic Oxygenation
After Apneic Oxygenation
Lowest SpO2 (Median (IQR))
93% (69, 99%)
100% (95, 100%)
25th% of Lowest SpO2*
*The authors considered a difference a 13% to be clinically significant
Regression analysis to accounts for potential confounders and differences in the two study cohorts
Outcomes of sensitivity analysis excluding patients in the after AO cohort who did not receive AO and included in the before AO were similar to outcomes with all patients included
Relatively small sample size (n= 149)
Single children’s hospital possibly limiting generalizability to other settings
Observational Before/After design. Concern that something other than the intervention of interest changed between the study periods (3-year interval between)
Pediatric resident intubation and video laryngoscopy more common in the After AO cohort though neither was an independent predictor of hypoxia in the regression analysis
Data not presented to calculate risk differences, confidence intervals and number needed to treat for the unadjusted analyses.
Preoxygenation method (NRB Face mask or BVM ventilation) at discretion of treating physicians and data not presented about the distribution of this variable in the two cohorts
“In summary, in this observational analysis, utilizing apneic oxygenation was associated with reduced odds of hypoxemia during endotracheal intubation. Further, although a subset of patients in the apneic oxygenation group did experience hypoxemia, a larger proportion of patients not receiving the intervention experienced marked hypoxemia, with one quarter of patients having SpO2 69% during endotracheal intubation. Providers should recognize the potential importance of this easily-applied intervention at reducing the incidence of hypoxemia during endotracheal intubation. Future studies should aim at optimizing endotracheal intubation attempts and reducing hypoxemia using randomized, controlled methodologies, as well as identifying other potentially modifiable interventions associated with this outcome.”
Apneic oxygenation is simple to perform and readily available in the Emergency Department. Its use in this study was associated with a statistical and clinical improvement in the proportion of patients with hypoxia during ETI.
This question would benefit from a larger, multicenter clinical trial in the pediatric population. The potential for the nasal cannula to prevent an adequate seal during bag-valve mask ventilation merits further study.
It is important to acknowledge that approximately one quarter of the patients in the after apneic oxygenation cohort experienced hypoxia. This indicates room for improvement and further evaluation of targeting the other variables in the regression analysis that were found to be independent predictors of hypoxia during ETI.
Potential Impact To Current Practice
Since there are few if any adverse effects associated with its use it would seem prudent to recommend routine use apneic oxygenation the pediatric population.
The most common infection seen in pediatrics and the most common reason these kids receive antibiotics
The release of the PCV (pneumococcal conjugate vaccine), or Prevnar vaccine, has made a big difference since its release in 2000 (Marom 2014)
This, along with more stringent criteria for what we are calling AOM, has led to a significant decrease in the number of cases seen since then
29% reduction in AOM caused by all pneumococcal serotypes among children who received PCV7 before 24 months of age
The peak incidence is between 6 and 18 months of age
Risk factors: winter season, genetic predisposition, day care, low socioeconomic status, males, reduced duration of or no breast feeding, and exposure to tobacco smoke.
The predominant organisms: Streptococcus pneumoniae, non-typable Haemophilus influenzae (NTHi), and Moraxella catarrhalis.
Prevalence rates of infections due to Streptococcus pneumoniae are declining due to widespread use of the Prevnar vaccine while the proportion of Moraxella and NTHi infection increases with NTHi now the most common causative bacterium
Strep pneumo is associated worse illness, like worse fevers, otalgia and also increased incidence of complications like mastoiditis.
The diagnosis of acute otitis media is a clinical one without a gold standard in the ED (tympanocentesis)
Ear pain (+LR 3.0-7.3), or in the preverbal child, ear-tugging or rubbing is going to be the most common symptom but far from universally present in children. Parents may also report fevers, excessive crying, decreased activity, and difficulty sleeping.
Challenging especially in the younger patient, whose symptoms may be non-specific and exam is difficult
Important to keep in mind that otitis media with effusion, which does not require antibiotics, can masquerade as AOM
AAP: Diagnosis of Acute Otitis Media (2013)*
In 2013, the AAP came out with a paper to help guide the diagnosis of AOM
Moderate-Severe bulging of the tympanic membrane or new-onset otorrhea not due to acute otitis externa (grade B)
The presence of bulging is a specific sign and will help us distinguish between AOM and OME, the latter has opacification of the tympanic membrane or air-fluid level without bulging (Shaikh 2012, with algorithm)
Bulging of the TM is the most important feature and one systematic review found that its presence had an adjusted LR of 51 (Rothman 2003)
Classic triad is bulging along with impaired mobility and redness or cloudiness of TM
Mild bulging of the tympanic membrane AND (grade C)
Recent onset (48hrs)
Ear pain (verbal child)
Holding, tugging, rubbing of the ear (non-verbal child)
Intense erythema of the tympanic membrane
* The diagnosis should not be made in the absence of a middle ear effusion (grade B)
A strategy of “watchful waiting” in which children with acute otitis media are not immediately treated with antibiotic therapy, has been endorsed by the American Academy of Pediatrics.
Who gets antibiotics?
Depends on age, temperature, duration of otalgia, laterality / otorrhea, and access to follow up
<6 months: Treat
6 months to 2 years: Treat
Exception, AAP permits initial observation: unilateral AOM with mild symptoms (mild ear pain, <48h, T <102.2)
But know that there is a high rate of treatment failure (Hoberman 2013)
Unless they have mild symptoms and it’s unilateral, you can observe for 48-72 hours
Why do we give antibiotics?
Demonstrated reduction in pain, TM perforations, contralateral episodes of AOM
They are no walk in the park, with increased adverse events (vomiting, diarrhea, rash)
Two well-designed clinical trials (2011) randomized approximately 600 children meeting strict diagnostic criteria for acute otitis media to receive Augmentin or placebo. These studies demonstrated a significant reduction in symptom burden and clinical failures in those who received antibiotics.
The authors conclude that those patients with a clear diagnosis of acute otitis media would benefit from antibiotic therapy
AAP AOM Treatment Algorithm
High-dose amoxicillin in most (for now)
Amoxicillin should not be used if the patient has received Amoxicillin in the past 30 days, has concomitant purulent conjunctivitis (likely H flu) or is allergic to penicillin.
beta lactamase resistant antibiotic should be used.
Amoxicillin clavulanate or 2nd or 3rd generation cephalosporins (including intramuscular ceftriaxone).
Patients with a history of type 1 hypersensitivity reactions to penicillin should be treated macrolides.
Studies on duration of therapy have shown better results with 10-day duration in children younger than 2 years and suggest improved efficacy in those 2-5 years.
For patients older than 5 years, shorter course therapy (5-7 days) can be utilized.
Motrin and APAP may have benefit with otalgia reduction
Decongestants and antihistamines have been shown to not benefit patients in terms of duration of symptoms or complication rate. Not surprisingly, these agents increase the side-effects experienced by patients.
If you chose to observe, let the parents know to return to ED or f/u with their provider in 48-72 hours if they symptoms do not improve. Providing a prescription to parents with clear instructions on when to fill it is also an acceptable option. Strict return precautions should be given if patient develops meningismus or facial nerve palsy.
If antibiotics were initiated, and there isn’t improvement in 2-3 days, the diagnosis of AOM should be revisited and, if still suspected, we have to consider that the causative bug is resistant to the prescribed antibiotic.
These patients should RTED or f/u with their pediatrician for escalation of care
Amoxicillin → Augmentin
Augmentin → Ceftriaxone IM
Macrolide → no clear antimicrobial agent, consult pediatric ENT
If antibiotics are initiated with resolution of symptoms, the patient should f/u in 2-3 months to ensure resolution of the middle ear effusion and ensure that there is no associated conductive hearing loss
Coker TR, Chan LS, Newberry SJ, Limbos MA, Suttorp MJ, Shekelle PG, et al. Diagnosis, microbial epidemiology, and antibiotic treatment of acute otitis media in children: a systematic review. JAMA. 2010;304(19):2161-9.
Hoberman A, Ruohola A, Shaikh N, Tahtinen PA, Paradise JL. Acute otitis media in children younger than 2 years. JAMA Pediatr. 2013;167(12):1171-2.
Lieberthal AS, Carroll AE, Chonmaitree T, Ganiats TG, Hoberman A, Jackson MA, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013;131(3):e964-99.
Marom T, Tan A, Wilkinson GS, Pierson KS, Freeman JL, Chonmaitree T. Trends in otitis media-related health care use in the United States, 2001-2011. JAMA Pediatr. 2014;168(1):68-75.
Rothman R, Owens T, Simel DL. Does this child have acute otitis media? JAMA. 2003;290(12):1633-40.
Shaikh N, Hoberman A, Rockette HE, Kurs-Lasky M. Development of an algorithm for the diagnosis of otitis media. Acad Pediatr. 2012;12(3):214-8.
Venekamp RP, Sanders S, Glasziou PP, Del Mar CB, Rovers MM. Antibiotics for acute otitis media in children. Cochrane Database Syst Rev. 2013(1):CD000219.
See our core article on the topic by Dr. Deborah Levine and Dr. Michael Mojica here
A special thanks to our specialist editors:
Michael A. Mojica, MD
Director, Pediatric Emergrency Medicine Fellowship
Bellevue Hospital Center
Christie M. Gutierrez, MD
Pediatric Emergency Medicine Fellow
Columbia University Medical Center
Morgan Stanley Children’s Hospital
New York Presbyterian
Provides parasympathetic innervation to the submandibular salivary glands, sublingual salivary glands, and lacrimal glands
Conveys taste sensations from the anterior two-thirds of the tongue via sensory fibers
Controls the muscles of facial expression
The right facial nerve controls the right face, and the left facial nerve controls the left face
The upper muscles of facial expression are innervated by fibers from both the ipsilateral as well as contralateral cortex; in other words, innervation to each side of the forehead is from both motor cortices
Therefore, a peripheral lesion should completely affect one side of the face, while a central lesion should spare the motor function of the forehead, since the contralateral cortex supplies fibers to the affected side
Idiopathic by definition
See differential for possible etiologies
Mechanism: edema, inflammation, and nerve degeneration at the geniculate ganglion within stylomastoid foramen which can lead to compression and possible ischemia and demyelination
Incidence of 15-40 / 100,000
Affects men and women equally
All ages are affected, with peak incidence in the 30s to 50s
Risk factors include pregnancy, diabetes, and previous episode(s) of Bell’s palsy
Sudden onset unilateral facial droop, incomplete eyelid closure, and loss of forehead muscle tone
Onset over the course of hours and peaks within three to seven days
Facial asymmetry with disappearance of nasolabial fold and facial creases
Eye irritation from decreased tearing and inability to close the affected eye
Abnormal taste and drooling from the affected side
Subjective “numbness” of the affected side due to paralysis but preserved facial sensation
Unilateral eyebrow sagging and inability to close the eye
Disappearance of unilateral facial creases, especially nasolabial fold and forehead furrows
Drooping at the corner of the mouth
Although absolute tear production may be decreased, the inability to blink may allow tears to spill from the eye
Preservation of the upper muscles of facial expression suggests a central cause
Assess bilateral ear canals with otoscopy
Assess parotid gland for masses
Perform a full neurological exam: should expect an otherwise normal neurological exam including all other cranial nerves and extremity motor function
Herpes Zoster (Ramsay Hunt syndrome): evaluate for vesicles, tinnitus, or vertigo
Infectious mononucleosis: evaluate for pharyngitis, posterior cervical adenopathy, or viral prodrome
Guillain-Barré Syndrome: usually presents with ascending motor weakness
Lyme Disease: history of rash or tick bite in endemic area
Parotid gland masses
Multiple Sclerosis: usually bilateral peripheral CN VII palsy
Sarcoidosis: usually bilateral peripheral CN VII palsy
Brainstem events (mass, bleed, infarct): will usually present with other cranial nerve palsies
Basilar artery aneurysm
Tumors: consider parotid, bone, metastatic masses, or acoustic neuroma
Trauma: skull fracture or penetrating facial injury
For high pre-test probability of Bell’s Palsy, there is no indication for labs or imaging: diagnosis is based on history and physical
If you suspect another cause of facial nerve palsy, order targeted labs and/or imaging (e.g. Lyme titers or monospot if high suspicion for viral etiology)
Consider blood glucose in Bell’s Palsy patients with other diabetic risk factors as 10% of Bell’s Palsy patients have diabetes
Glucocorticoids may hasten recovery if started within 72 hours of symptom onset: 1mg/kg prednisone (or 60 to 80 mg) PO daily for 7 days (pediatric dose: 2mg/ kg/ day PO [max 60mg])
NNT to prevent one incomplete recovery = 10
No clear regimen, most studies use 7-10 days of PO prednisone
Anti-viral therapy with steroids may improve functional nerve recovery if started within 72 hours of symptom onset: valacyclovir 1000 mg PO daily for 7 days (pediatric dose: 20mg/ kg TID PO)
Low quality evidence that antivirals with glucocorticoids is superior to glucocorticoids alone
American Academy of Neurology recommends offering antivirals while explaining limited evidence but also limited harm
Corneal damage may occur due to incomplete eye closure
prescribe lubricating and hydrating ophthalmic ointment and/ or drops (artificial tears qhs and prn dryness/ irritation in affected eye)
instruct patient on wearing eye patch at night on affected eye
In the Copenhagen Facial Nerve Study (2002), 2,570 cases of untreated peripheral facial nerve palsy were studied during a period of 25 years (1,701 cases of Bell’s palsy)
71% of Bell’s palsy patients returned to baseline function in three weeks without treatment
Almost all patients noticed some improvement in three to four months
Prognosis is related to initial severity: with incomplete lesions, 94% returned to baseline whereas of those with complete lesions, 60% returned to baseline
Patient Education and Discharge Instructions:
While not life threatening, Bell’s palsy can cause significant distress
Symptoms peak within three to seven days, and almost always improve somewhat by 3 months
With incomplete lesions, ~95% return to baseline; with complete lesions, ~60% return to baseline
Prescribe artificial tears during the day and ointments with eye patch at night
1 week follow-up with outpatient neurologist for management of symptoms and to monitor recovery
Take Home Points:
Bell’s palsy is acute, peripheral, and idiopathic
A non-acute onset of symptoms (gradual onset of more than two weeks duration) should suggest a mass lesion
Perform a very careful thorough exam, including full neurological exam, dermatological exam (evaluate for vesicles or rash), and ENT exam (evaluate for pharyngitis, posterior cervical adenopathy, otitis media, deafness)
No role for labs or imaging, but deviation from the typical history and physical should prompt further workup
Start glucocorticoids and antivirals in the ED if symptoms started within 72 hours and if there are no contraindications
Provide patient education about the prognosis and eye care to prevent corneal abrasions
Arrange for close neurology follow-up
Zhang W, Xu L, Luo T, Wu F, Zhao B, Li X. The etiology of Bell’s palsy: a review. Journal of Neurology. 2019. doi:10.1007/s00415-019-09282-4.
Tiemstra JD, Khatkhate N. Bell’s Palsy: Diagnosis and Management. American Family Physician. https://www.aafp.org/afp/2007/1001/p997.html. Published October 1, 2007. Accessed May 22, 2019.
Gronseth GS, Paduga R. Evidence-based guideline update: Steroids and antivirals for Bell palsy: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2012;79(22):2209-2213. doi:10.1212/wnl.0b013e318275978c.
Madhok VB, Gagyor I, Daly F, et al. Corticosteroids for Bells palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews. 2016. doi:10.1002/14651858.cd001942.pub5.
Gagyor I, Madhok VB, Daly F, et al. Antiviral treatment for Bells palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews. 2015. doi:10.1002/14651858.cd001869.pub6.
Loomis C, Mullen MT. Differentiating Facial Weakness Caused by Bell’s Palsy vs. Acute Stroke. Journal of Emergency Medical Services. https://www.jems.com/articles/print/volume-39/issue-5/features/differentiating-facial-weakness-caused-b.html. Published May 7, 2014. Accessed May 22, 2019.
Peitersen E. Bell’s palsy: the spontaneous course of 2,500 peripheral facial nerve palsies of different etiologies. Acta Otolaryngol Suppl. 2002:4-30.
Schaider et al. Rosen & Barkin’s 5-Minute Emergency Medicine Consult, 5th Edition. Wolters Kluwer.
Status epilepticus is associated with significant morbidity and mortality. Benzodiazepines are recommended as first line agents but their efficacy is approximately 50%. The most commonly recommended 2nd line agents are Phenytoin and Fosphenytoin. Their use is associated with an efficacy of approximately 50%. In addition, their use is associated with significant adverse events. Levetiracetam (Keppra) had been proven efficacious in small case series, can be administered more rapidly (5 minutes vs 20 minutes) and has the potential for fewer adverse events.
In pediatric patients in convulsive status epilepticus unresponsive to first line therapy with 2 doses of a benzodiazepine, is Levetiracetam superior to Phenytoin as a second line anticonvulsant in improving the rate of seizure cessation 5 minutes after study drug infusion is completed?
3 month to 6 years
Status epilepticus: International League Against Epilepsy definition
Unresponsive with continued movements (tonic, jerky) > 5 minutes
>2 recurrent seizures without a recovery of consciousness between
>3 seizures in the past hour with current seizure
Unresponsive to 2 doses of a benzodiazepine (94% received Midazolam)
On Levetiracetam or Phenytoin at baseline
2nd line AED in past 24 hrs
History of seizures refractory to Phenytoin
Status Epilepticus due to major trauma or eclampsia
PREDICT Network (Australia, New Zealand), n = 13 (8 Children’s, 5 General Hospitals), 3/2015-11/2017
In the primary intention to treat analysis, there was not a statistically significant difference between the two study medication in the primary outcome of seizure cessation 5 minutes after the completion of the study medication infusion
The authors considered a 20% improvement clinically significant
There was no statistically significant difference between the two study medications in any of the secondary safety outcomes analyzed. The sample size is inadequate to assess the likelihood of rare adverse events such as Steven’s Johnson Syndrome.
See “Read More” Section for tables
Multicenter, randomized trial (PREDICT Network: Australia, New Zealand)
Cross-over design: Received second study medication if first was ineffective
International League Against Epilepsy definition of Status Epilepticus
Relevant emergency department outcomes
Reasonable sample size: N=239
Included an intention-to-treat, modified intention-to-treat and per protocol analyses
Excluded patients on Keppra or Phenytoin at baseline
Superiority rather than non-inferiority hypothesis
Time to first study medication: 73 minutes
Sample size inadequate to assess the likelihood of rare adverse events
“In conclusion, we found that levetiracetam is not superior to phenytoin for treatment of children with convulsive status epilepticus with continued clinical seizure activity after treatment with benzodiazepines. Although both drugs were associated with considerable failure rates when given by themselves, treatment with one drug and then the other reduced the failure rate by more than 50%, at the expense of only an additional 10 minutes (compared with giving phenytoin alone). Clinicians should therefore consider sequential use of phenytoin and levetiracetam, or levetiracetam and phenytoin, for management of paediatric convulsive status epilepticus before moving on to RSI and intubation.”
While Keppra was not found to be superior the Phenytoin its safety profile and short time of administration makes it an attractive alternative. An additional 22% of patients responded to the alternative drug is the first was not efficacious potentially reducing the rapid sequence intubation rate. Giving both drugs serially should be considered.
Approximately 50% of the patients were still seizing after the first study drug and 25% after the second alternative study drug. This makes it essential to anticipate the need for addition antiepileptic medications and prepare equipment and medications for rapid sequence intubation.
Potential Impact To Current Practice
Consider Keppra as 2nd line antiepileptic
Consider giving Keppra and Phenytoin serially to prevent RSI
Lyttle MD, Rainford NEA, Gamble C, Messahel S, Humphreys A, Hickey H, Woolfall K, Roper L, Noblet J, Lee ED, Potter S, Tate P, Iyer A, Evans V, Appleton RE; Paediatric Emergency Research in the United Kingdom & Ireland (PERUKI) collaborative.
Levetiracetam Versus Phenytoin For Second-Line Treatment Of Paediatric Convulsive Status Epilepticus (EcLiPSE): A Multicentre, Open-Label, Randomised Trial.
Acute stress fractures are typically not detected on the standard 3 views; therefore, repeat XRs 10-14d after onset of sx (may see radiolucent reabsorption gap around fracture)
For more complex mid foot trauma, consider CT to r/o Lisfranc
Consider classification of fracture, patient demographics & activity level when deciding on treatment
Tertiary care centers that have access to Orthopedics/Podiatry services
Consider consultation for “true” Jones fractures, as some cases may be operatively managed acutely and/or for expedited follow-up to be arranged
If working in community/rural locations: other than patients that present with “open” injuries, concerns for compartment syndrome (almost never), and “high-end”/professional athletes, there are generally no other circumstances that would require expedited transfer to a tertiary care center for immediate further evaluation.
Less favorable outcomes associated with certain patient factors: female gender, DM, obesity
Different modalities of surgery:
Closed reduction and fixation with K-wire
ORIF (all +/- need for bone graft)
Surgery likely recommended for displacement >10 degrees of plantar angulation or 3-4 mm of translation in any plane
Indications for OR:
Neck and shaft fractures with >10 degrees plantar angulation or 3mm of displacement in any plane with insufficient closed reduction
Avulsion fractures (zone one) with >3 mm of displacement or comminuted
Zone two fractures: displaced zone two fractures require operative management. For acute non displaced Jones fractures, consider early intramedullary screw fixation in athletes (studies have shown return to sport ~ 8 weeks, weight bearing within 1-2 weeks)
Zone three fractures (diaphyseal stress fractures) in athletes
All non displaced fifth metatarsal fractures can be treated non operatively
Non displaced zone 1 fractures: protected weight bearing/ symptomatic care in short leg walking cast, air-boot, posterior splint, or compression wrap/ rigid shoe until discomfort subsides
Zone 2 and 3 fractures are more complex because they often result in prolonged healing time and potential for delayed/ nonunion
Acute zone 2 fractures: nonweightbearing in short leg cast for 6-8 weeks
Acute zone 3 fractures: nonweightbearing in short leg cast for up to 20 weeks
With respective to athletes: repeat fracture after surgical treatment of Jones fracture can offer after healing and screw removal; thus it is recommended that the screw be left in until the end of the athlete’s career
Bowes J, Buckley R. Fifth metatarsal fractures and current treatment. World J Orthop. 2016;7(12):793–800. Published 2016 Dec 18. doi:10.5312/wjo.v7.i12.793
Petrisor BA, Ekrol I, Court-Brown C. The epidemiology of metatarsal fractures. Foot Ankle Int. 2006 Mar; 27(3): 172-4.
Congratulations on your graduation. This milestone and the commencement of your increased independence are a tribute to your fine work. Your future accomplishments will be substantial.
You as a class will have developed immensely profound bonds. Being a physician is a creative task. Stay undaunted, nurture inspiration in each other. Recognition of the importance of creating a quality healthcare team allows “’us” to succeed in rendering care to patients, ensuring our success as physician advocates and social activists. Each patient needs more analysis, attention and devotion than any of us can accomplish as individuals, no matter how hard we strive.
Fast vs. Slow medicine
You must always try to improve your understanding of your patients’ needs and the complexity of their problems. Your commitment to your patients can only achieve an improvement in health when you understand your patients. There are phases of your work when procrastination might be lethal for your patients, when fast medicine is essential. There are also phases of your work when rushing will limit your understanding, your creativity, and your devotion to your patients. Technology offers to speed our efforts and although it can be efficient for emergency physicians, it may not be effective and may even be counterproductive.
Attempting to accomplish a task is often done too quickly—which deprives you of wholly understanding the patient’s needs and limits your potential to achieve excellent care. It is under those circumstances that slow medicine is essential.
Remember: All the essential questions should be asked and all of the patient’s queries, addressed. As well, remind yourself each day that there are no inconsequential questions. When thought about in depth, questions or problems that seem inconsequential at first, often actually represent matters of great consequence.
Humanism and science
Your equal devotion to humanism and scientific rigor will be essential. Your skills, expertise and commitment should lead to research, innovation, and team development. To maintain your creativity and integrity you must recognize the unique importance of your role, while never distancing yourself from those aspects of your tasks that are often considered routine. Your patients’ lives will be in your hands each day. Your students’ careers will be in your hands each day. Your acts will heal, innovate and educate. Experiences with those patients whose lives you impact will stay with you not silent and still as photographs but as noisy, fraught, poignant videos—shared and replayed by your patients and coworkers.
Indeed, these experiences will create memories for many. Make sure that you have done the best you can do. Be a model of good leadership—independent of hierarchy and continuously demonstrating significant respect for all.
Teaching and mentoring
The simple approach to learning is that the more we learn, indeed the more we know BUT—the less certain we are and therefore the more we need to study. Make opportunities to share your immense knowledge and wisdom, as that will be very useful to others and will continue to expand the breadth and depth of your knowledge. Take your roles as mentors very seriously. You will learn as much from your mentees as I have from you. Some relationships will be transient, and others will continue development over a lifetime. Both types of experiences are immensely valuable and are often remembered as important and even foundational for your entire career.
You now understand the emergency department work environment. Each of you must find a reasonable approach to patients and peers that allows you to retain the humanistic values all must search for in medicine. Pessimism in medicine will become a self-inflicted wound, diminishing your vision, resilience and commitment. There is no place for pessimism or the faint hearted in emergency medicine.
Your skills are too great, your roles too important to allow an error, a criticism, or uncertainty to lessen your enthusiasm, your creativity or your integrity and belief in humanity. A powerful debate continues among the historic optimists, the new optimists and the possibilists. Voltaire, as an optimist, could not have written “Candide” had he not believed that most people in the world were quite good. Bill Gates, as a new optimist, would say you need to be inspired by people and that you must proclaim discontent with the world and demand progress. Hans Rosling, a Swedish Physician/Statistician as a “possibilist,” might say that “he neither hopes without reason nor fears without reason” and acts to achieve that which is possible. Each of these important thinkers chose a divergent pathway to advance societal good through humanism. I believe that your patient care experiences and your patients’ stories will preserve your love of medicine.
Our nation is a theoretical champion of individual rights, which have only been achieved by sacrificing the principle of a common good. That sacrifice is unacceptable. I believe that you have the curiosity and wisdom to meet the great challenges of our society. I believe that you—now with your skills and training—have the obligation to use your knowledge, your positions of power and privilege, your capacity to understand and empathize and your strong voices to protect those abused because of race, religion, gender—or their otherness.
You now must speak up and speak out against the injustices and inequalities inherent in our communities, here and elsewhere. You must speak out against xenophobia, isolationism and the fear of destruction by others. Your task is complicated and enriched by caring for a large number of people with extreme heterogeneity of cultures, social determinants and health needs making the achievement of excellence remarkably valuable, and often seeming just out of reach. Your task is to do what is right, which is often, neither the convenient, nor the profitable. Your roles will be those of big vision physician activists who will be intelligent, courageous physician advocates and leaders. Your task for the foreseeable future will be to achieve healthcare rights for all.
You have been privileged to study at the bedside of many, you have been exposed to innumerable problems and now you must choose to correct the problems and to search for or create the essential solutions. My experience here at New York University and Bellevue Hospital in New York City has shown me that nothing is impossible. One often thinks of these problems as the intractable social determinants, but you have been at work every day with faculty who have successfully devoted their careers to addressing social determinants previously considered insoluble. Certainly, this approach has personal risks—you will recognize, however, that if your patients are suffering injustices, and you timidly do nothing, or not enough, your suffering will be greater.
Setting out/stepping forth now, you surely have many goals, but the energy that allows you to achieve a goal or dream—usually leads to satisfaction—often not elation—because by the time success arrives you will already be preparing for the next dream or project. The destination we physicians have in emergency medicine is uncertain. It is often determined by a series of patients, a family or one memorable individual human being.
The almost infinite variety of human experiences which we have in common with our patients forces us to delve into and analyze all of medicine, anthropology, ethics, public policy, population health and much more. It is these patients and our experiences in the service of their needs, our research and ongoing learning that sustains us and offers us an antidote to burnout.
We are truly doctors without borders. You will have unlimited opportunities to express your immense potentials. Enjoy the experience! Recognize the opportunity! You and I and our profession will be judged by the progress we make in addressing the needs of those who have been neglected, discriminated against, or abused—the uninsured, the undocumented, and many more.
It is unconscionable that healthcare in America is considered a privilege. It must be our goal to achieve equity for all in healthcare. We must meet the health needs of every single person. Universal health care is fundamental, if our values are to be realized. In the future people will ask: Where were you and what did you do when the homeless, the opioid users, the uninsured and the newest immigrants were neglected?
Your first response should be—I was trained and worked at Bellevue Hospital.
We count on you to make remarkable contributions to address these issues as the future leaders of medicine.
Congratulations—your advocacy and activism will be essential.