Core EM - Emergency Medicine Podcast

Dive into the world of septic arthritis with insights on how bacteria invade joints and the alarming consequences of delayed treatment. Discover the critical myths surrounding its presentation and the importance of accurate diagnosis through techniques like arthrocentesis. Learn about the diverse risk factors and pathogens involved, including the challenges posed by prosthetic joints. The conversation highlights diagnostic complexities and emphasizes the urgent need for effective management in emergency medicine to prevent irreversible joint damage.

A look at the most common type of seizures in the young pediatric population. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Febrile_Seizures.mp3 Download Leave a Comment Tags: Pediatrics Show Notes Background The most common type of seizure in children under 5 years of age Occur in 2-5% of children In children with a fever, aged 6 months to 5 years of age, and without a CNS infection Risk Factors 4 times more likely to have a febrile seizure if parent had one Also increase in risk if siblings or nieces / nephews had one Common associated infections Human Herpesvirus 6 Human Herpesvirus 7 Influenza A & B Simple Febrile Seizure Generalized tonic-clonic activity lasting less than 15 minutes in a child 6 months to 5 years of age Complex Febrile Seizure Lasts longer than 15 minutes, occurs in a child outside of this age range, are focal, or that recur within a 24-hour period. Diagnostics / Workup Gather thorough history and perform thorough physical exam Most cases will not require labs, imaging or EEG If e/o meningitis, perform LP AAP suggests considering LP in: Children 6-12 months who are not immunized for H flu type B or strep pneumo Children who had been on antibiotics For complex seizures, clinician may have a lower threshold for obtaining labs Hyponatremia is more common in this group than in the general population. LPs are more commonly done by providers, but these are low yield with one study showing bacterial meningitis being diagnosed in just 0.9% (Kimia 2010), all of whom did not have a normal exam or negative cultures. Neuroimaging is also exceedingly low yield if the patient returns to baseline (Teng 2006) One study that showed that the duration of complex febrile seizure, being greater than 30 minutes, was associated with a higher incidence of bacterial meningitis. (Chin 2005) Of they have history and exam concerning for meningitis, they should get an LP If they look dehydrated or edematous, you would have more of a reason to get a chemistry Treatment Benzodiazepine if seizure lasted for >5 minutes, either IV or IN Supportive care Tylenol or motrin if febrile Fluids if signs of dehydration Antipyretics “around the clock” A majority of data show no benefit in preventing recurrence of seizure One study (Murata 2018) found that giving tylenol q6h at 10 mg/kg for the first 24 hours following the initial seizure decreased the rate of recurrence when compared to children who did not receive antipyretics. NNT here was 7 Questionable whether we can generalize these findings from a single ED in Japan. No role for antiepileptics Prognosis High rate of recurrence (~1/3) within 1 year of initial seizure Risk increases for Younger age at which they had initial seizure Lower temperature at which they had seizure If initial febrile seizure was prolonged, more likely that the next will be prolonged 1-2% develop epilepsy for simple febrile seizure, slightly above risk of general population 5-10% develop epilepsy for complex febrile seizure Follow up with PMD Generally, peds neuro follow up is not necessary References Chin RF, Neville BG, Scott RC. Meningitis is a common cause of convulsive status epilepticus with fever. Arch Dis Child. 2005;90(1):66-9. Kimia A, Ben-Joseph EP, Rudloe T, Capraro A, Sarco D, Hummel D, et al. Yield of lumbar puncture among children who present with their first complex febrile seizure. Pediatrics. 2010;126(1):62-9. Murata S, Okasora K, Tanabe T, Ogino M, Yamazaki S, Oba C, et al. Acetaminophen and Febrile Seizure Recurrences During the Same Fever Episode. Pediatrics. 2018;142(5). Patel N, Ram D, Swiderska N, Mewasingh LD, Newton RW, Offringa M. Febrile seizures. BMJ. 2015;351:h4240. Pavlidou E, Panteliadis C. Prognostic factors for subsequent epilepsy in children with febrile seizures. Epilepsia. 2013;54(12):2101-7. Stapczynski, J. S., & Tintinalli, J. E. (2016). Tintinalli’s emergency medicine: A comprehensive study guide, 8th Edition. New York: McGraw-Hill Education. Subcommittee on Febrile S, American Academy of P. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011;127(2):389-94. Teng D, Dayan P, Tyler S, Hauser WA, Chan S, Leary L, et al. Risk of intracranial pathologic conditions requiring emergency intervention after a first complex febrile seizure episode among children. Pediatrics. 2006;117(2):304-8. Warden CR, Zibulewsky J, Mace S, Gold C, Gausche-Hill M. Evaluation and management of febrile seizures in the out-of-hospital and emergency department settings. Ann Emerg Med. 2003;41(2):215-22. A special thanks to our editors: Michael A. Mojica, MD Director, Pediatric Emergency 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   Read More

A review for the emergency physician of this common tick-borne illness. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Lyme_Disease.mp3 Download Leave a Comment Tags: Infectious Diseases Show Notes Episode Produced by Audrey Bree Tse, MD Background Most common tick-born illness in North America Endemic in Northeast, Upper Midwest, northwest California 80% to 90% in summer months Pathophysiology Ixodes tick (deer tick) has a 3-stage life cycle (larvae, nymph, adult) & takes 1 blood meal per stage Deer tick feeds on an infected wild animal (infected with spirochete Borrelia burgodrferi) then bites humans On humans, they typically move until they encounter resistance (e.g. hairline, waistband, elastic, skin fold).  It takes 24-48 hrs for B. Burgdorferi to move from the tick to the host Pathogenesis: organism induced local inflammation, cytokine release, autoimmunity No person to person transmission Clinical Presentation Stage 1: Early Symptom onset few days to a month after tick bite Erythema migrans rash: bulls eye rash seen in more than 90% of patients with Lyme disease (Irregular expanding annular lesion(s)) Regional adenopathy, intermittent fevers, headache, myalgias, arthralgia, fatigue, malaise Stage 2: disseminated/ secondary Days to weeks after tick bite Intermittent fluctuating sx that eventually resolve Triad of aseptic meningitis, cranial neuritis, and radiculoneuritis: bell palsy most common Cardiac symptoms: tachycardia, bradycardia, AV block, myopericarditis Stage 3: tertiary/ late Symptoms occur >1 year after tick bite Acrodermatitis chronic atrophicans: Atrophic lesions on extensor surfaces of extremities (resembles scleroderma) Monoarthritis, oligoarthritis (knee > shoulder > elbow) GI: Hepatitis, RUQ pain Ocular: keratitis, uveitis, iritis, optic neuritis Neurological: Chronic axonal polyneuropathy or encephalopathy Chronic Lyme disease (versus well-accepted Lyme disease sequelae): Continuation of symptoms after antibiotics Current recommendation for management is supportive care only Pediatric considerations: More likely to be febrile than adults Facial palsy accompanied by aseptic meningitis in 1/3 Untreated kids can develop keratitis Excellent prognosis if appropriately treated History Travel, camping, woods, playing under leaves or in wood piles Living in endemic area (Northeastern area: Maine to Virginia; upper Midwestern: Wisconsin, Minnesota; Northwest California) Endemic in Northern Europe and Eastern Asia as well History of tick bite (- 30-50% of patients recall tick bite) Flu like illness in summer Rash: https://www.cdc.gov/lyme/signs_symptoms/rashes.html Joint complaints Cardiac complaints Neurologic complaints Careful search for tick Diagnosis Labs CBC (leukocytosis, anemia, thrombocytopenia) ESR: most common lab abnormality (>30 mm/hr) Chem 7 LFTs: commonly elevated especially GGT Cultures not typically indicated LP when meningeal signs (CSF: pleocytosis, elevated protein, CSF spirochete ABs).  LP function is more to rule out other etiologies of meningitis rather than diagnose Lyme meningitis given that lyme PCR and lyme Ab index are not very accurate. Serological Testing Serological testing is not always warranted because of the very high incidence of false positive results Serologies are not useful in acute phase (<30 days of infection) because they are negative; it takes several weeks to develop enough antibodies for either test below (ELISA or Western Blot) Acute Lyme is a clinical diagnosis and does not need laboratory testing, especially in endemic areas such as NY If pretest probability is high (symptoms consistent with Lyme + epidemiological background), say patients with CN palsy, meningitis, carditis, or migratory large joint arthritis, then serologies can be very helpful Do not test if patients in endemic areas with potential tick exposure present with EM — just treat with antibiotics Do not test if patients in endemic areas present with no history of tick exposure or only nonspecific symptoms Test if you have high suspicion of lyme without EM PCR is highly specific and sensitive but not available for routine use.  There are two tests you need to use together: 1) ELISA: this detects antibodies to lyme bacteria (borrelia burgdorferi)  in your blood, BUT it can’t distinguish between borrelia and similar bacteria (even sometimes normal flora that lives in you).  In addition, IgM response takes 1-2 weeks while IgG response takes 2-4 weeks. If ELISA is positive or equivocal, then you move onto the: 2) Western blot test: this looks for antibodies not to the whole organism, but to the basic building blocks of the lyme bacteria — the individual proteins, BUT many types of bacteria use the same building blocks. So the CDC says that the Western Blot test must detect IgG antibodies to 5 out of the 10 proteins. See figure 2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918152/ Two-tiered testing has sensitivity between 70-100% and specificity ~95% in late stages Interpretation of Lyme serologies should be done by an ID specialist because they can be confusing and can lead to wrong conclusions if unfamiliar with them NYC is an endemic region where 5% of the population can have a positive without symptoms! If somebody who HAD Lyme disease but successfully treated it with doxycycline tested themselves years later, they could still have the antibodies and therefore it would look like they still had Lyme disease (despite being cured) Positive serology or previous Lyme disease not ensure protective immunity Other tests: Arthrocentesis for acute arthritis: elevated cryoglobulin XRs: may show soft tissue, cartilaginous, osseous changes ECG Differential Diagnosis Tick-borne diseases: Rocky Mountain Spotted fever, tularemia, relapsing fever, Colorado tick fever, tick-bite paralysis, babesiosis, anaplasmosis, powassan virus Remember that doxycycline covers anaplasmosis and lyme but not babesiosis, which requires Atovaquone Rheumatic fever (usually presents with erythema marginatum rash, valvular involvement rather than heart block, TM joint arthritis) Viral meningitis Septic arthritis Syphilis Parvovirus B19 Infectious endocarditis Juvenile rheumatoid arthritis Reiter syndrome Brown recluse spider bite Fibromyalgia Chronic fatigue syndrome Treatment Remove tick: disinfect site then with blunt instrument, grasp tick proximal to skin and pull upward with gentle constant traction.  Mouthparts will release after about a minute. If residual mouthparts are left in skin, leave them alone to avoid infection (they will extrude from skin naturally over time).  Since ticks that have not attached or are moving on the skin cannot transmit Lyme, they can just be brushed off. NS IVF bolus, supportive care Cardiac monitoring, temporary pacemaker for heart block Beware Jarisch Herxheimer reaction: worsening of sx a few hours after treatment initiated Aspirin for cardiac involvement, NSAIDs for arthralgias/ arthritis Prophylaxis: Per the IDSA, give a single dose of 200 mg PO doxycycline to patients who meet all of the following criteria: Deer tick has been attached for 36 hours or more  (the rationale for time of attachment relates to the fact that the spirochetes live in the tick’s gut so they need a long time to multiply and travel to the salivary glands (event that’s triggered by a blood meal) and later overcome the salivary gland  (which only a few do) and finally reach the patient’ skin Prophylaxis can be provided within 72 hours of tick removal Local rate of B. Burgdorferi infection in ticks exceeds 20% (in the northeast USA, the prevalence of infected ticks is between 15-20%) Doxycycline can be used (children >8 years old, non-pregnant females) A 2001 study examined doxycycline vs placebo prophylaxis.  A single dose of 200 mg of oral doxycycline or placebo was given to persons presenting within 72 hours of removal of an I scapularis tick. One of 235 persons in the doxycycline group developed erythema migrans (EM) versus 8 of 247 in the placebo group, for treatment efficacy of 87% (95% CI, 25%–98%; P<0.04) (9). Reasonable alternative strategy: monitor for EM or other signs of infection then initiate treatment if they develop Lyme disease (excellent outcomes in patients treated during early EM stage of disease) Antibiotics: Antibiotics can speed resolution of arthritis and cardiac conduction delays, but not necessarily facial palsy Doxycycline has the best bioavailability and CNS penetration Always check with your ID colleagues to determine appropriate duration of treatment in more serious cases of Lyme disease Stage 1: Amoxicillin (500 mg PO TID) or cefuroxime (500 mg PO BID) or doxycycline (100 mg PO BID; > 8 years old & not pregnant) x 21 days; azithromycin (500 mg PO qday x 14-21 days) IV therapy in pregnant patients Stage 2: PO antibiotics for isolated Bell palsy and mild involvement Amoxicillin with probenecid (500 mg PO TID) x 30 days or doxycycline (100 mg PO BID; > 8 years old & not pregnant) x 10-21 days IV ceftriaxone (2 g IV qday) x 14-21 days, or penicillin G (20-24 million units IV q4-6h x 14-28 days) for meningitis, carditis, severe arthritis Stage 3: Penicillin G (20-24 million units IV q4-6h) x 14-21 days or ceftriaxone (2 g IV qday x 14-28 days) Dispotition Admit unstable or sick patients, those with meningoencephalitis, & carditis (telemetry/ ICU admission) DC patients treated with PO therapy Future prevention strategies: wear long pants & shirts, light-colored clothing (easier to spot crawling ticks), tuck pants into socks, DEET spray, clothing impregnated with permethrin References Baker C et al, Lyme Disease Review Panel of the Infectious Diseases Society of America (IDSA).  Final report of the lyme disease review panel of the infectious diseases society of America (IDSA). 2006.  https://www.idsociety.org/globalassets/idsa/topics-of-interest/lyme/idsalymediseasefinalreport.pdf (22 July 2019, date last accessed) Centers for Disease Control and Prevention.  CDC — Lyme. 2019. https://www.cdc.gov/lyme/index.html (22 July 2019, date last accessed) Hilton E, DeVoti J,, Benach JL, Halluska ML, White DJ, Paxton H, Dumler JS.  Seroprevalence and seroconversion for tick-borne diseases in a high-risk population in the northeast United States.  Am J Med. 1999 Apr;106(4):404-9. Hu LT.  Lyme Disease.  Ann Intern Med.  2016;164:ITC65-ITC80.  Doi: 10.7326/AITC201605030 Lee, M.  Lyme Disease.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  2015; 664-665. Nadelman RB, Nowakowski J, Fish D et al., Tick Bite Study Group.  Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite.  N Engl J Med.  2001;345:79-84. Sanders, L.  (2009). Every patient tells a story: Medical mysteries and the art of diagnosis. A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine Read More

An in depth review of this notorious parasite. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Malaria.mp3 Download Leave a Comment Tags: Infectious Diseases Show Notes Background In 2017, there were 219 million cases and 435,000 people deaths from malaria Five species: Falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi. Falciparum, Vivax and Knowlesi can be fatal History of recent travel to Africa (69% of cases in US), particularly to west-Africa should raise suspicion for malaria Clinical Manifestations Average incubation period for Falciparum is 12 days 95% will develop symptoms within 1 month Clinical findings with high likelihood ratios include periodic fevers, jaundice, splenomegaly, pallor. Can also have vomiting, headache, chills, abdominal pain, cough, and diarrhea Severe malaria has a mortality of 5% to 30%, even with therapy Diagnostic criteria for severe malaria: Ashley 2018 Most common manifestations of severe malaria affect the brain, lungs, and kidneys Patients with cerebral malaria can present encephalopathic or comatose, some severe enough to exhibit extensor posturing, or seizures Can have acute lung injury with a quarter of these patients progressing to ARDS Can have AKI from ATN and resultant acidosis Labs may be unremarkable but watch for anemia and thrombocytopenia Hgb <5 has an OR = 4.9 for death Severe thrombocytopenia has an OR = 2.8 Anemia + Thrombocytopenia has an OR = 13.8 (Lampah 2015, PMID 25170106) Watch for hypoglycemia Be mindful of co-infection with salmonella and HIV Obtain BCx, cover with ceftriaxone Diagnosis Blood smear Thick smear to increase sensitivity for detecting parasites Thin smear for quantifying parasitemia and species The first smear is positive in over 90% of cases, but if suspicion is high, it has to be repeated BID for 2-3 days for proper exclusion of malaria (CDC 2019) Management For uncomplicated, non-severe cases, most patients with falciparum should be admitted, especially those with no prior exposure to malaria parasites Malarone is one of the first line options Check out other suggested regimens from the CDC Important to note that when they take this, ensure they take with milk or food containing fat to enhance absorption Severe Malaria Resuscitative efforts directed at affected organ Can deteriorate rapidly Initiate IV Artesunate if high level of suspicion Requires call to CDC: CDC Malaria Hotline: (770) 488-7788 or (855) 856-4713 (toll-free) Monday–Friday 9am–5pm EST – (770) 488-7100 after hours, weekends, and holidays Benzodiazepines for seizures Be judicious with fluids as this can precipitate pulmonary edema and cerebral edema a/w increased mortality in children at 48 hour (Maitland 2011, PMID: 21615299; Hanson 2013, PMID: 23324951) Take Home Points 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 References 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 April 2015. WHO. 2015 https://www.who.int/malaria/publications/atoz/9789241549127/en/ (7 July 2019, date last accessed) A special thanks to our editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine   Read More

A look at this common and controversial topic. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Otitis_Media.mp3 Download Leave a Comment Tags: Pediatrics Show Notes Background: 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 with more severe illness, like worse fevers, otalgia and also increased incidence of complications like mastoiditis. Diagnosis 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) OR Intense erythema of the tympanic membrane * The diagnosis should not be made in the absence of a middle ear effusion (grade B) Treatment Options 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 Get’s antibiotics: <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) >2: Treat 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 Antibiotic Selection 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. Pain Control Motrin and APAP may have benefit with otalgia reduction Other 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. Follow up 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 References: 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 editors: Michael A. Mojica, MD Director, Pediatric Emergency 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 Read More

Discover the complexities of foot fractures, particularly the notorious Jones fracture and its healing challenges. Delve into the mechanics and symptoms of various fractures, including fifth metatarsal injuries and the Liz Frank injuries. Learn about classification systems and the critical need for accurate diagnosis, imaging, and tailored treatment options. The discussion also touches on non-operative approaches and rehabilitation strategies for athletes, making this a must-listen for anyone interested in emergency medicine and orthopedic insights.

A discussion with Drs. McNamara and Leifer on the essentials and beyond of debriefing Hosts: Brian Gilberti, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Debriefing.mp3 Download One Comment Tags: Resuscitation, Simulation Show Notes TAKE HOME POINTS Debriefing after a clinical case in the ED is a way to have an interprofessional, reflective conversation with a focus on improving for the next patient.  We can debrief routine cases, challenging cases, or even cases that go well. Follow a structure when leading a debrief. The prebrief sets ground rules and informs the team that the debrief is optional and will only take 3-5 minutes. Introduce names and roles Then give a one-liner about what happened in the case, followed by a plus/ delta: address  what went well and why, then how to improve Finally, wrap up with take home points Pitfalls to watch out for in clinical debriefing include: Avoid siloing or alienating any learners.  Learn from all your colleagues on your team- it’s less about medicine and more about interprofessional and systems issues Don’t pick on individual performance.  It’s not about shaming- it’s about improving patient care Avoid “guess what I’m thinking” questions; ask real questions Proceed with caution in order to dampen or avoid psychological trauma and second victim syndrome.  The learner may ask “was this my fault?”; we never want a learner to feel this way.  Ask, what systems supported or did not support you today?  Talk about what happened.  Avoid shame and blame. Have the right values and do it for the right reasons. ADDITIONAL TOOLS PEARLS Debriefing Tool INFO Model: GUESTS Dr. Shannon McNamara completed residency in Emergency Medicine at Temple University hospital and fellowship in Medical Simulation at Mount Sinai St. Lukes-Roosevelt. She now is the Director of the Simulation Division in the NYU Department of Emergency Medicine. She’s thrilled to have somehow made a career out of teaching people to talk about their feelings using big computers shaped like people. Dr. Jessica Leifer attended NYU for medical school and completed her residency training in emergency medicine at Mount Sinai St. Luke’s-Roosevelt. She completed a fellowship in medical simulation at the Mount Sinai Hospital. She is now simulation faculty in the NYU department of Emergency Medicine. Her academic interests include using simulation for patient safety, operations, and improving teamwork. Read More

Croup is a common viral infection that strikes children, leading to a barking cough and inspiratory stridor. The hosts unpack its causes, primarily the parainfluenza virus, and discuss the typical presentation of croup, including the alarming 'steeple sign' seen on X-rays. They also emphasize the critical importance of assessing symptom severity through tools like the Westley Croup Score and offer management strategies for mild to severe cases. Learn how to navigate this challenging condition in young patients!

A look at this deadly mucocutaneous reaction and how to best manage these patients in the ED https://media.blubrry.com/coreem/content.blubrry.com/coreem/SJS.mp3 Download Leave a Comment Tags: Critical Care, Dermatology Show Notes Episode Produced by Audrey Bree Tse, MD Rash with dysuria should raise concern for SJS with associated urethritis Dysuria present in a majority of cases SJS is a mucocutaneous reaction caused by Type IV hypersensitivity Cytotoxic t-lymphocytes apoptose keratinocytes → blistering, bullae formation, and sloughing of the detached skin Disease spectrum SJS = <10% TBSA TEN = >30% TBSA SJS/ TEN Overlap = 10-30% TBSA Incidence is estimated at around 9 per 1 million people in the US Mortality is 10% for SJS and 30-50% for TEN Mainly 2/2 sepsis and end organ dysfunction. SJS can occur even without a precipitating medication Infection can set it off especially in patients with risk factors including HIV, lupus, underlying malignancy, and genetic factors SATAN for the most common drugs Sulfa, Allopurinol, Tetracyclines, Anticonvulsants, and NSAIDS Anti-epileptics include carbamazepine, lamictal, phenobarb, and phenytoin Can have a curious course Hypersensitivity reaction can develop while taking medication, or even one to four weeks after exposure In pediatric population, mycoplasma pneumonia and herpes simplex have been identified as precipitating infections Patients often have a prodrome 1-3 days prior to the skin lesions appearing May complain of fever, myalgias, headaches, URI symptoms, and malaise Rash may be the sole complaint Starts as dark purple or erythematous lesions with purpuric centers that progress to bullae Skin surrounding the lesions detaches from the dermis with just light pressure (Nikolsky Sign) Up to 95% of patients will have mucous membrane lesions ~85% will have conjunctival lesions Symptoms: Burning or itching eyes, a cough or sore throat, pain with eating, pain with urinating or defecating Source: JAMA Dermatol. 2017 Differential Diagnosis: SSSS, autoimmune bullous diseases, bullous fixed drug eruption, erythema multiforme, thermal burns, phototoxic reactions, and TSS SJS is a clinical diagnosis Basic workup: CBC, chemistry panel, LFTs, and a UA Treatment Supportive care IV fluid repletion guided by TBSA affected, as well as electrolyte, protein, and energy supplementation Consider protecting airway if significant oral mucosal involvement Stop the offending agent (if there is one) Advanced wound care and pain control Consults: Derm to do a biopsy, +/- ophthalmology, gyn / urology to prevent strictures or contractures Consider transferring to a burn center Dispo: Low threshold for ICU admission SCORTEN ( max of 7 points) 1 point each for Age over 40 Current cancer >30% body surface area affected HR >120 BUN >28 Glucose >240 Bicarb <20 Score of 2 points or higher should -> ICU Take Home Points SJS may begin like the flu, with lesions appearing 1-3 days after the prodrome starts Have to have a high suspicion for SJS because it is deadly. It’s a clinical diagnosis — derm biopsy is supportive A thorough history and physical exam are key.  Remember the characteristic rash and bullae, and always look in the mouth and eyes.  Ask about dysuria, sore throat, and eye irritation, as well as preceding medications or infections.  Think SATAN! Prompt supportive care focused on ABCs and IVF repletion are critical.  These patients can get sick really fast, so consider an ICU or burn unit. References: Barrett W.  Quick Consult: Symptoms: Rash, Dysuria, and Mouth Sores.  Emergency Medicine News.  41(4): 15-16, April 2019. Bivins H, Comes J.  Stevens-Johnson Syndrome.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  2015; 1076-1077. Ergen EN, Hughey LC. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. JAMA Dermatol.2017;153(12):1344. doi:10.1001/jamadermatol.2017.3957 Gerull R, Nelle M, Schaible T.  Toxic epidermal necrolysis and Stevens-Johnson syndrome: A review.  Crit Care Med.  2011; 39:1521-1532. Lerch M, Mainetti C, Terziroli Beretta-Piccoli B, Harr T. Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. Clin Rev Allergy Immunol. 2018;54(1):147-76. McNeil, D. (2019). Measles Cases Surpass 700 as Outbreak Continues Unabated. [online] Nytimes.com. Available at: https://www.nytimes.com/2019/04/29/health/measles-outbreak-cdc.html [Accessed 6 May 2019]. Mustafa SS, Ostrov D, Yerly D. Severe Cutaneous Adverse Drug Reactions: Presentation, Risk Factors, and Management. Curr Allergy Asthma Rep. 2018;18(4):26. Read More

A look at the opioid epidemic and what ED providers can do to combat this formidable foe. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Opioid_Epidemic.mp3 Download Leave a Comment Tags: Opioid Dependence, Opioid Free ED Show Notes Consider alternatives to opiates for acute pain NSAIDs Subdissociative ketamine Nerve blocks Curb misuse and diversion through prescribing a short supply and perform I-STOP checks Narcan is not just for acute overdose treatment by EMS or within the ED anymore We can equip patients, family members and friends with Narcan kits prior to discharge In New York state, can prescribe Narcan to patients with near fatal overdoses or who screen positive for an opioid use disorder Intranasal formulation is cheaper and more commonly prescribed than IM Buprenorphine induction can be done in the ED for patients in active withdrawal, as calculated by the COWS score. MDcalc calculator: https://www.mdcalc.com/cows-score-opiate-withdrawal Providers do not need an X-waiver to give a dose of Buprenorphine in the ED for 3 days Home induction can be considered for patients not actively withdrawing but would like to enter medication assisted treatment Some considerations: Contraindicated in patients with severe liver dysfunction and with hypersensitivity reaction to drug Oversedation can occur with concurrent use of benzodiazepines and alcohol Will precipitate withdrawal if concurrently using full opioid agonists Longitudinal care has to be established for patients started on Buprenorphine SAMHSA’s Buprenorphine practitioner locator site: https://www.samhsa.gov/medication-assisted-treatment/practitioner-program-data/treatment-practitioner-locator Buprenorphine Induction Pamphlet Read More