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Must Know Antimicrobial Regimens – Adults

Authors: Marina N. Boushra, MD (EM Resident Physician, Vidant Medical Center) and Cassandra Bradby, MD (EM Attending Physician, Vidant Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

A 75-year-old man with a history of diabetes, hypertension, and dementia presents to the emergency department with a complaint of altered mental status. His nursing home caretaker endorses a dry cough for one week that has recently become productive and fevers with a Tmax of 38.9 ºC. She notes that he is not “acting like himself,” and elaborates that he is sleeping more, talking less, and has had multiple episodes of urinary incontinence, which is unusual for him. His vitals on arrival are T 38.5º C, HR 110, RR 30, BP 100/70. His exam is notable for somnolence, increased work of breathing with accessory muscle use, coarse rales at the base of the right lung, tachycardia, and dry mucus membranes.

Bacterial infections are a common diagnosis in the emergency department, and emergency physicians are often tasked with providing antibiotics for outpatient management or beginning antibiotics prior to admission. Antibiotic treatment is not without side effects, and treatment started in the emergency department is frequently empiric. Therefore, an understanding of the most likely causative organisms as well as local patterns of susceptibility and resistance is paramount to adequate treatment, appropriate antibiotic selection, and responsible antibiotic stewardship. Important historical details to elicit include allergies, recent antibiotic use, prior antibiotic failure, dialysis use, use of immunosuppressants or history of immunocompromise, culture results of prior infections, and contact with healthcare facilities, including recent hospitalization, living in a care facility, or recent invasive procedures such as ureteral catheterizations or intubation. These details offer vital information regarding possible bacterial resistance or the presence of opportunistic infection. Because multiple empiric regimens exist for infectious disease in the emergency department, contacting the hospital pharmacy about the local antibiogram may help tailor the empiric regimen to local microbial susceptibilities. Please keep this in mind with the recommendations discussed in each table. The following is a discussion of the most common or most emergent ED-diagnosed bacterial infections, their most likely causative organisms, and current recommendations for empiric treatment.

Pneumonia

Pneumonia is infection of the pleural parenchyma and can be broadly divided into community-acquired (CAP) and hospital-acquired pneumonia (HAP). A third category of pneumonia, healthcare-associated pneumonia, is discussed in more detail later in this paper. The majority of pneumonia is community-acquired but historical details such as recent hospitalization, intubation, or ventilator dependence should raise concern for HAP and multi-drug resistant organisms (MDROs). Travel history may be important for more rare causes of pneumonia. In patients with known or suspected HIV or AIDS, pneumocystis pneumonia should be strongly considered.

Community-Acquired Pneumonia (CAP)

CAP can be caused by a variety of pathogens, with the most common bacterial cause being Streptococcus pneumonia1–3. Other common organisms include respiratory viruses, Haemophilus influenza, and Mycoplasma pneumoniae1–3. In patients requiring ICU admission, S. pneumoniae is still common, but there is increased prevalence of Legionella pneumophila, Staphylococcus aureus, gram-negative bacilli, and influenza4. It is important to remember these differences in etiology and to cover adequately for these serious organisms in patients requiring ICU admission. Patients with risk factors for aspiration pneumonia should receive additional anaerobic coverage. Treatment for CAP has become increasingly more complicated due to rising resistance to antibiotics. Risk factors for drug resistance include age >65, alcoholism, medical comorbidities, immunosuppressive illness or medication use, and use of beta-lactam, macrolide, or fluoroquinolone antibiotics in the last 3-6 months5,6.

Treatment should be initiated as soon as a diagnosis of CAP is made to prevent decompensation. CAP can often be treated on an outpatient basis. Studies have shown that physicians often use inconsistent criteria when making the decision to admit patients for the treatment of CAP and overestimate short-term patient mortality, leading to an increased rate of unnecessary hospitalizations7. The 2007 guidelines for the Infectious Disease Society of America (IDSA) and the American Thoracic Society (ATS) recommend using the CURB-65 score or Pneumonia Severity Index (PSI), both well validated prediction rules and decision aids, to aid in the risk stratification of patients and making the decision to admit for inpatient treatment7–9. Interestingly, a recent article investigating oral vs. intravenous fluoroquinolones for non-critically ill patients with CAP showed no difference in mortality, ICU transfers, or need for vasopressors or intubation10. Studies have shown shorter time to treatment and shorter hospital stays for patients started on oral rather than intravenous antibiotics11. As such, it is important to consider oral therapy in non-critically ill patients with CAP who are being admitted for treatment but are able to tolerate oral medication.

Studies have shown similar efficacy in CAP for fluoroquinolones and macrolides plus a penicillin or cephalosporin12. Importantly, there is a high rate of macrolide resistance in S. pneumoniae in the United States; as such, macrolides should not be used as empiric monotherapy in areas where resistance to macrolides is >25%5,13–15. Recommended regimens are outlined in the Table 1 below. The IDSA is expected to publish new guidelines for the treatment of CAP that better reflect current trends in resistance in the summer of 2017.

Hospital-Acquired (nosocomial) Pneumonia (HAP)

Pneumonia patients with recent hospitalizations present a challenge in antibiotic selection. While the pneumonia may be caused by an MDRO picked up in the healthcare environment, it is also possible that the patient has a simple community-acquired organism. The multi-drug resistant (MDR) score assesses a particular patient’s risk for infection with an MDRO16,17. Patients with a high MDR score should be presumed to have a pneumonia due to a resistant organism and treated accordingly with broad-spectrum coverage as outlined in Table 1 below. Patients with low MDR scores can be treated with the more narrow-spectrum coverage used for CAP, with the possibility of widening the spectrum in the event of treatment failure. The Shorr score is a similar scoring tool to assess the risk of infection by an MDR and tailor empiric coverage appropriately18.  Antibiotic treatment for presumed HAP should cover for Staphylococcus aureus and Pseudomonas aeruginosa19. Local antimicrobial prevalence and susceptibility, especially within the hospital, is helpful to determining a regimen, but can often be deferred to the judgement of the admitting team. Empiric regimens as recommended in the 2016 IDSA/ATS guidelines for empiric management of HAP are outlined in Table 1 below.

Healthcare-Associated Pneumonia (HCAP)

Healthcare-associated pneumonia (HCAP) refers to pneumonia that may have been acquired in healthcare facilities such as nursing homes and dialysis centers. It was formerly grouped with HAP due to presumed increased susceptibility to MDROs. Several studies, however, have shown no increased susceptibility to MDROs in patient with HCAP, and it is conspicuously missing from the IDSA/ATS guidelines on the management of HAP19–24. As such, in the absences of other historical susceptibilities to MDROs such as comorbidities or severe illness, patients with HCAP may be treated as CAP19–24.

Table 1: Empiric Treatment of Pneumonia based on type, setting, and patient-specific factors8,19

Type Setting Patient Factors Regimen
CAP Outpatient No recent antibiotics, co-morbidities, high-rate of resistance -Doxycycline 100mg bid for five days

-Azithromycin 500mg on day 1 followed by 250mg for four days.*

-Clarithromycin 500mg bid for seven days*

Recent antibiotics, co-morbidities, high-rate of resistance -Levofloxacin 750mg daily for five days

-Moxifloxacin 400mg daily for five days

-Gemifloxacin 320mg daily for five days

-Combination therapy with a beta-lactam (amoxicillin 1g tid, amoxicillin-clavulanate 2g bid, cefpodoxime 200mg bid, or cefuroxime 500mg bid) PLUS either a macrolide (azithromycin 500mg on day 1, followed by 250mg for four days, or clarithromycin 500mg bid for five days) or doxycycline 100mg bid for five days.

Inpatient Mild-Moderate disease, managed on general floor -Levofloxacin 750mg IV or po

-Moxifloxacin 400mg IV or po

-Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a macrolide (azithromycin 500mg IV, or clarithromycin 500mg orally)

Severe disease requiring ICU admission -Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a respiratory fluoroquinolone (levofloxacin 750mg IV, or moxifloxacin 400mg IV) OR azithromycin 500mg IV.

-If penicillin allergic, a respiratory fluoroquinolone PLUS aztreonam 1g

-If MRSA suspected, add vancomycin 15-20mg/kg IV

HAP Inpatient Combination therapy is warranted, with one from each of the following 3 categories:

1) Piperacillin-tazobactam 4.5 g IV, Cefepime 2 g IV, Ceftazidime 2g IV, Imipenem/cilastatin 500mg IV

2) Azithromycin 500mg IV, Ciprofloxacin 400mg IV, Levofloxacin 750mg IV, or Gentamicin 5-7mg/kg IV

3) Vancomycin 15-20mg/kg IV, Linezolid 600mg IV

*Macrolide antibiotics should not be used as empiric monotherapy in areas of known S. pneumoniae resistance >25% to macrolides. If such resistance exists, pair with a beta-lactam as shown in the table above.

Urinary Tract Infection

Urinary tract infections can involve the lower urinary tract (cystitis) or the upper tract (pyelonephritis). Urinary tract infections are very common in women, with sexually active women being at higher risk. Risk factors for urinary tract infections include recent sexual intercourse, prior urinary tract infections, and recent spermicide use25. When present in men, urinary tract infections are typically associated with underlying anatomical anomalies, recent catheterization, or other risk factors. While not all urinary tract infections in males are necessarily complicated, a search for these risk factors should be conducted when a male is diagnosed with a urinary tract infection.

Uncomplicated Cystitis

Urinary tract infections in women begin by bacterial colonization of the vagina by fecal bacteria, which may ascend via the urethra to infect the bladder and kidneys. Uncomplicated cystitis and pyelonephritis in women is typically caused by Escherichia coli, though Proteus mirabilis, Klebsiella pneumoniae, and Streptococcus saprophyticus are occasionally found26,27. Empiric treatment for uncomplicated urinary tract infections is best tailored to the regional E. coli sensitivities and is outlined in Table 328. Of note, this table may be modified based on local resistance patterns. Sterile pyuria should raise concern for a possible sexually-transmitted infection (STI) and patients who fail to improve despite appropriate antibiotic treatment should be tested for STI.

Complicated Urinary Tract Infection

A complicated urinary tract infection is one which is associated with a condition that increases the risk for therapeutic failure, as outlined in Table 2. The microbial spectrum of complicated UTI is more broad, including not only the typical organisms associated with uncomplicated UTI but also more varied and resistant pseudomonal, staphylococcal, and Serratia species as well as fungi29,30. Complicated lower urinary tract infections may be managed as an outpatient, but indications for hospitalization include inability to tolerate oral therapy or suspected/ documented infection with a resistant organism such as extended-spectrum beta-lactamase producing organisms (ESBLs). Complicated pyelonephritis is the progression of infection resulting in emphysematous pyelonephritis, corticomedullary or perinephric abscess, or papillary necrosis. Complicated pyelonephritis is an indication for admission and intravenous antibiotic treatment.

Table 2: Conditions that increase the risk of treatment failure in UTI (complicated UTI)

Diabetes
Pregnancy
Renal failure
Hospital-acquired infection
Immunosuppression
Renal transplantation
Anatomic abnormality of the urinary tract
Symptoms >7 days prior to presentation
Presence of an indwelling foreign body (ureteral catheter, nephrostomy tube, ureteral stent)
Ureteral calculus

UTI and Asymptomatic Bacteriuria in the Pregnant Patient

Urinary tract infection and colonization in pregnant patients are worth special mention. While asymptomatic bacteriuria in a non-pregnant female does not warrant treatment, studies have shown a high rate of progression to symptomatic cystitis and pyelonephritis in pregnant patients31. As such, current recommendations suggest that any bacteriuria in a pregnant patient should be treated with antibiotics32. Additionally, although urinary tract infection in a pregnant woman is, by definition, complicated, fluoroquinolones, the first-line treatment for complicated cystitis, are a pregnancy class C medication and should be avoided33. Mild urinary tract infections in pregnant females are treated similarly to uncomplicated UTIs, as shown in Table 3 below. Follow-up cultures for resolution are important in this patient population34.

Table 3: Empiric treatment of uncomplicated and complicated urinary tract infections28,31,35.

Urinary Tract Infection Recommended regimen
Uncomplicated cystitis -Nitrofurantoin 100mg bid for five days*

-Trimethoprim-sulfamethoxazole 160/800mg bid for three days

-Cephalexin 500mg BID for 3-7 days

-Fosfomycin 3g in a single dose*

-Ciprofloxacin 250mg bid or Levofloxacin 250mg once per day for three days**

Complicated cystitis Outpatient:

-Ciprofloxacin 500mg bid or 1000mg daily for five to ten days

-Levofloxacin 750mg daily for five to ten days

Inpatient:

-Levofloxacin 500mg IV

-Ceftriaxone 1g IV

-Ertapenem 1g IV

-Gentamicin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***

-Tobramycin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***

Uncomplicated Pyelonephritis

 

 

Outpatient:

-Ciprofloxacin 500mg po bid for seven days or 1000mg daily for seven days

-Levofloxacin 750mg po daily for five to seven days

Inpatient:

-Levofloxacin 500mg IV

-Ceftriaxone 1g IV

-Ertapenem 1g IV

-Gentamicin 3-5mg/kg IV

-Tobramycin 3-5mg/kg IV

Complicated Pyelonephritis – Inpatient, mild-moderate disease:

-Ceftriaxone 1g IV

-Ciprofloxacin 400mg IV

-Levofloxacin 750 mg IV

-Aztreonam 1g IV

Inpatient, severe disease:

-Cefepime 2g IV

-Ampicillin 1g IV four times per day plus Gentamicin 5mg/kg IV daily

-Piperacillin-tazobactam 3.375g IV

-Meropenem 500mg IV

-Imipenem 500mg IV

-Doripenem 500mg IV

Asymptomatic bacteriuria and acute cystitis in the pregnant patient -Nitrofurantoin 100mg po bid for five to seven days (in second or third trimester)*

-Trimethoprim-sulfamethoxazole 160/800 mg po bid for three days****

-Fosfomycin 3g po in a single dose*

-Amoxicillin-clavulanate 500mg po tid for three to seven days

-Cephalexin 500mg po bid for three to seven days

-Cefpodoxime 100mg po bid for three to seven days

*Fosfomycin and nitrofurantoin should be avoided if there is concern for early pyelonephritis.

**Fluoroquinolones, if possible, should be reserved for other important uses to avoid resistance against this class of antibiotics.

***Adding ampicillin provides Enterococcus coverage

****Should be avoided in first trimester and at term

Cellulitis and Soft-Tissue Infection

Cellulitis and Erysipelas

Cellulitis and erysipelas are bacterial skin infections that differ in that erysipelas involves the upper dermis and superficial lymphatics while cellulitis involves the deeper dermis and subcutaneous fat tissue. Both manifest with localized skin erythema, edema, warmth, and pain. Because of the more superficial nature of erysipelas, these lesions are typically more raised and better demarcated than cellulitis. Erysipelas also presents more acutely and with more systemic symptoms such as fevers and chills. The most common pathogens in cellulitis are beta-hemolytic streptococci and S. aureus, including methicillin-resistant S. aureus (MRSA)36–38. Beta-hemolytic streptococci are the most common cause of erysipelas36,39.

Lesions consistent with cellulitis should be examined closely for the presence of a drainable abscess. History is particularly important in the patient with possible cellulitis as cellulitis associated with human or animal bites or with water exposure needs different coverage than uncomplicated cellulitis. The presence of an indwelling device near the region of cellulitis is also important, as it is an indication of device infection.

The treatment of uncomplicated cellulitis is based on whether or not there is associated purulence. Current guidelines group erysipelas with non-purulent cellulitis in terms of treatment, as the lesions are often difficult to distinguish from each other and are caused by a similar spectrum of organisms. Patients with purulent cellulitis should receive empiric coverage for MRSA pending culture results40. Patients with non-purulent cellulitis or erysipelas should receive empiric coverage for beta-hemolytic streptococcus and MSSA, although patients with systemic symptoms, recurrent infection, or prior infection with MRSA should receive additional MRSA coverage36. Cellulitis can typically be managed as an outpatient; patients with signs of systemic toxicity, rapid progression, indwelling devices, or failure of outpatient management should be admitted for parenteral antibiotics. In addition to antibiotics, elevation of the affected area is an important aspect of treatment as it helps promotes drainage of edema and inflammatory substances, speeding symptomatic improvement36.

Table 4: Empiric treatment of cellulitis and erysipelas36

Infection Recommended regimen
Uncomplicated nonpurulent cellulitis without MRSA risk factors or erysipelas Outpatient -Dicloxacillin 500mg po qid for 5-10 days

-Cephalexin 500mg po qid for 5-10 days

-Clindamycin 450mg po tid for 5-10 days

Inpatient -Cefazolin 1-2g IV tid

-Ceftriaxone 1g IV every 24 hours

-Oxacillin or nafcillin IV every 4 hours

-Clindamycin 600-900mg IV tid

Uncomplicated purulent cellulitis or nonpurulent cellulitis with MRSA risk factors

 

Outpatient -Clindamycin 300-450mg po 3-4 times per day for 5-7 days

-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days

-Doxycycline 100mg bid for 5-7 days

Inpatient -Vancomycin 15-20mg/kg/dose IV bid

-Clindamycin 600mg IV tid 

-Linezolid 600mg IV two times per day

-Daptomycin 4mg/kg/dose IV once daily

Skin abscesses

Skin abscesses are most commonly due to S. aureus (MRSA or MSSA), although polymicrobial infection with flora from the skin or adjacent mucosal tissues is also common36,40–42. Risk factors for MRSA infection include recent hospitalization or antibiotic use, contact with healthcare environments, institutionalization, HIV infection, intravenous drug use, and diabetes. Source control, in the form of warm compresses to promote drainage or incision and drainage, is important. The role of antibiotics following source control is debated. Studies have shown a slightly increased cure rate with the use of antibiotics following incision and drainage of uncomplicated abscesses, but also a higher rate of diarrhea and adverse effects43,44. Antibiotics should be started for large (>2cm) or multiple abscesses, extensive surrounding cellulitis, systemic symptoms, immunocompromise or co-morbidities, the presence of an indwelling device, or in cases where incision and drainage alone fails to achieve adequate clinical response36. Hospitalization and parenteral antibiotics should be considered for patients with extensive skin involvement or signs of systemic toxicity.

Table 5: Empiric antibiotic treatment of abscesses following source control36

Outpatient If suspicion for MRSA:

-Clindamycin 300-450mg po 3-4 times per day for 5-7 days

-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days

-Doxycycline 100mg po bid for 5-7 days

If no suspicion for MRSA:

-Dicloxacillin 500mg po bid for 5-7 days

-Cephalexin 500mg po bid for 5-7 days

Inpatient -Vancomycin 15-20mg/kg/dose IV bid

-Clindamycin 600mg IV tid 

-Linezolid 600mg IV two times per day

-Daptomycin 4mg/kg/dose IV once daily

Sexually-Transmitted and Vulvovaginal Infections

Sexually transmitted infections (STI) are a diagnosis of immense public health importance. While the results of lab testing are often not available in the emergency department, physicians should have a low threshold for the initiation of treatment in patients with presentations consistent with STI. Treatment for common STIs is outlined in Table 6 below45. Counseling patients about safe sex practices and urging them to inform their partners is paramount to infection control.

Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is infection of the upper genital tract (uterus, endometrium, fallopian tubes, ovaries) in women. PID may extend to involve adjacent structures, causing periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh-Curtis syndrome). The majority of PID is caused by ascending sexually-transmitted infections (STI), with Neisseria gonorrhea and Chlamydia trachomatis being the most commonly implicated pathogens in PID45. The diagnosis of PID is often a presumptive one based on presentation. Due to the risk for tubal scarring leading to infertility or risk of ectopic pregnancy, even minimal symptoms without an alternative diagnosis warrant the start of antibiotic therapy to reduce the risk of serious complications due to delay of therapy. Mild to moderate disease can be treated as an outpatient. Indications for hospitalization and intravenous antibiotics include pregnancy, clinically severe disease, complicated PID (pelvic abscess), and intolerance to, noncompliance with, or failure of oral antibiotics. Empiric coverage for inpatient and outpatient management of pelvic inflammatory disease are outlined in Table 646,47.

Table 6: Recommended treatment regimens for select genitourinary infections45–47

Chlamydia -Azithromycin (1g po in one dose)

-Doxycycline (100mg bid for 7 day)

Gonorrhea* -Ceftriaxone (250mg IM or IV in one dose) plus azithromycin (1g po in one dose) or doxycycline (100mg bid for 7 days)
Trichomonas -Metronidazole (2g po in a single dose or 500mg bid for seven days)

-Tinidazole (2g po in a single dose)

Bacterial Vaginosis -Metronidazole (500mg  po bid for seven days)

-Metronidazole vaginal gel 0.75% (5g intravaginally for five days)

-Clindamycin vaginal gel 2% (5g intravaginally for seven days)

Candida Vulvovaginitis Fluconazole (150mg po in one dose)
Pelvic Inflammatory

Disease

Outpatient management -Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)

-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)

Inpatient management -Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)

-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)

*Patients with gonorrhea should also be treated for chlamydia due to high rates of concomitant infection.

Bacterial meningitis

While meningitis is not as common an emergency department diagnosis as the bacterial infections discussed above, patients with meningitis are often quite ill, and knowledge of appropriate antibiotic coverage can speed time to therapy. The most common causes of community-acquired meningitis in adults in developed countries are Streptococcus pneumoniae, Neisseria meningitidis, and, in older adults, Listeria monocytogenes48,49. Empiric treatment should be initiated as soon as meningitis is suspected. Empiric regimens should include ceftriaxone (2g every 12 hours) or cefotaxime (2g every 4-6 hours) for coverage of N. meningitidis and S. pneumoniae as well as vancomycin due to increasing rates of S. pneumoniae resistance to third-generation cephalosporins50,51. In patients >50 years of age or with immunocompromise, ampicillin (2g every 4 hours) should be added to provide coverage for L. monocytogenes49.

Adverse Effects of Antibiotic Use

A discussion of antibiotic use in the emergency department would be remiss without mention of the adverse effects of antibiotics commonly used in the ED. While the use of certain antibiotics may be unavoidable due to patient allergies or susceptibility patters, knowledge of the adverse effects of antibiotics may help guide therapeutic choices and inform or temper patient expectations.

Clostridium difficile infection should always be a consideration when starting antibiotics. Clindamycin is the most common culprit in antibiotic-associated C. difficile infection, but cephalosporins, penicillins, and fluoroquinolones are also common causes52–56. Aminoglycosides, tetracyclines, metronidazole, and vancomycin are rarely associated with C. difficile infection, though any antibiotic use increases the risk for C. difficile infection57. Other important adverse effects include QT prolongation with arrhythmia associated with macrolide and fluoroquinolone use and the risk of peripheral neuropathy and (the uncommon, but oft-cited) tendon rupture with fluoroquinolone use. Common or serious side effects of antibiotics used in the emergency department are summarized in Table 7 below.

Table 7: Common and serious adverse effects of commonly used antibiotics

Antibiotic Common Adverse Effects Serious Adverse Effects Comments
Beta-lactams C. diff infection, diarrhea Hypersensitivity reactions High risk of C. diff, especially with broader coverage and with ampicillin
Macrolides Diarrhea, nausea, vomiting, abdominal pain QT prolongation (especially with erythromycin)
Clindamycin C. diff infection, diarrhea Serious hypersensitivity reactions Most common cause of C. diff
Fluoroquinolones Anorexia, nausea, vomiting, abdominal pain Tendon rupture, peripheral neuropathy, QT prolongation High C. diff risk
Tetracyclines Nausea, diarrhea, photosensitivity Inhibition of bone growth and tooth discoloration (a concern in children) Low C. diff risk
Vancomycin Abdominal pain, nausea Nephrotoxicity, ototoxicity, Red man syndrome, hypotension Red man syndrome can be prevented with pretreatment with antihistamines
Aminoglycosides Nephrotoxicity, ototoxicity Need frequent monitoring of drug levels
Metronidazole Headache, dizziness, metallic taste Disulfiram-like reaction Low C. diff risk
  • Summary

Table 8: Common and serious bacterial infections and recommended empiric treatment

Infection Important organisms to cover Recommended Regimens
Community-acquired pneumonia S. pneumoniae CAP outpatient: doxycycline, macrolide +/- penicillin or cephalosporin

CAP inpatient, mild: respiratory fluoroquinolone, macrolide + penicillin or cephalosporin

S. pneumoniae, L. pneumophila, S. aureus CAP inpatient, severe: penicillin or cephalosporin+ fluoroquinolone OR azithromycin
Hospital-acquired pneumonia S. pneumoniae, MRSA, P. aeruginosa HAP inpatient: anti-pseudomonal penicillin or cephalosporin, or fluoroquinolone, or carbapenem + vancomycin/linezolid
Uncomplicated cystitis E. coli Nitrofurantoin or fosfomycin or TMP/SMX or ciprofloxacin

 

Complicated cystitis or uncomplicated pyelonephritis E. coli, Pseudomonas sp., Staphylococcus sp. Outpatient: Fluoroquinolone

Inpatient: Fluoroquinolone or aminoglycoside or third-generation cephalosporin or carbapenem

Complicated pyelonephritis E. coli, Pseudomonas sp., Staphylococcus sp. Inpatient, mild-moderate: third-generation cephalosporin or monobactam

Inpatient, severe: anti-pseudomonal penicillin or cephalosporin, carbapenem

Asymptomatic bacteriuria or simple cystitis in the pregnant patient E. coli Nitrofurantoin or TMP/SMX or fosfomycin, or penicillin or cephalosporin with gram-negative coverage
Nonpurulent cellulitis or abscess without MRSA risk factors, erysipelas Beta-hemolytic streptococcal species, MSSA Outpatient and inpatient: staphylococcal penicillin or cephalosporin
Purulent cellulitis, nonpurulent cellulitis or abscess with MRSA risk factors Beta-hemolytic streptococcal species, MSSA, MRSA Outpatient: Clindamycin or TMP/SMX or doxycycline

Inpatient: Vancomycin or clindamycin

Chlamydia C. trachomatis Azithromycin or doxycycline
Gonorrhea N. gonorrhea AND C. trachomatis Ceftriaxone plus azithromycin or doxycycline
Trichomonas Trichomonas vaginalis Metronidazole or tinidazole
Bacterial vaginosis Polymicrobial, anaerobic gram-negative rods Metronidazole oral or intravaginal gel or clindamycin
Candida Vulvovaginitis C. albicans, C. glabrata Fluconazole
Pelvic Inflammatory Disease N. gonorrhea, C. trachomatis Inpatient and outpatient: third generation cephalosporin plus doxycycline
Bacterial meningitis S. pneumoniae, N. meningitidis, L. monocytogenes (if >50 years or immunocompromised) Vancomycin plus third generation cephalosporin +/- ampicillin if age >50 or immunocompromised

 

 References / Further Reading

  1. Johansson, N., Kalin, M., Tiveljung-Lindell, A., Giske, C. G. & Hedlund, J. Etiology of community-acquired pneumonia: increased microbiological yield with new diagnostic methods. Clin. Infect. Dis. 50, 202–9 (2010).
  2. Jain, S. et al. Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults. N. Engl. J. Med. 373, 415–27 (2015).
  3. Gadsby, N. J. et al. Comprehensive Molecular Testing for Respiratory Pathogens in Community-Acquired Pneumonia. Clin. Infect. Dis. 62, 817–23 (2016).
  4. Cillóniz, C. et al. Microbial aetiology of community-acquired pneumonia and its relation to severity. Thorax 66, 340–6 (2011).
  5. Vanderkooi, O. G. et al. Predicting antimicrobial resistance in invasive pneumococcal infections. Clin. Infect. Dis. 40, 1288–97 (2005).
  6. Ramsdell, J., Narsavage, G. L. & Fink, J. B. Management of Community-Acquired Pneumonia in the Home: An American College of Chest Physicians Clinical Position Statement. Chest 127, 1752–1763 (2005).
  7. Fine, M. J. et al. The hospital admission decision for patients with community-acquired pneumonia. Results from the pneumonia Patient Outcomes Research Team cohort study. Arch. Intern. Med. 157, 36–44 (1997).
  8. Mandell, L. A. et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin. Infect. Dis. 44 Suppl 2, S27-72 (2007).
  9. Lim, W. S. et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 58, 377–82 (2003).
  10. Belforti, R. K. et al. Association Between Initial Route of Fluoroquinolone Administration and Outcomes in Patients Hospitalized for Community-acquired Pneumonia. Clin. Infect. Dis. 63, 1–9 (2016).
  11. Cyriac, J. M. & James, E. Switch over from intravenous to oral therapy: A concise overview. J. Pharmacol. Pharmacother. 5, 83–7 (2014).
  12. Ruhe, J. & Mildvan, D. Does Empirical Therapy with a Fluoroquinolone or the Combination of a β-Lactam Plus a Macrolide Result in Better Outcomes for Patients Admitted to the General Ward? Infect. Dis. Clin. North Am. 27, 115–132 (2013).
  13. Low, D. E. What Is the Relevance of Antimicrobial Resistance on the Outcome of Community-Acquired Pneumonia Caused by Streptococcus pneumoniae? (Should Macrolide Monotherapy Be Used for Mild Pneumonia?). Infect. Dis. Clin. North Am. 27, 87–97 (2013).
  14. Daneman, N., McGeer, A., Green, K., Low, D. E. & Toronto Invasive Bacterial Diseases Network. Macrolide resistance in bacteremic pneumococcal disease: implications for patient management. Clin. Infect. Dis. 43, 432–8 (2006).
  15. Jones, R. N., Sader, H. S., Moet, G. J. & Farrell, D. J. Declining antimicrobial susceptibility of Streptococcus pneumoniae in the United States: report from the SENTRY Antimicrobial Surveillance Program (1998-2009). Diagn. Microbiol. Infect. Dis. 68, 334–6 (2010).
  16. Park, S. C. et al. Validation of a scoring tool to predict drug-resistant pathogens in hospitalised pneumonia patients. Int. J. Tuberc. Lung Dis. 17, 704–709 (2013).
  17. Maruyama, T. et al. A new strategy for healthcare-associated pneumonia: a 2-year prospective multicenter cohort study using risk factors for multidrug-resistant pathogens to select initial empiric therapy. Clin. Infect. Dis. 57, 1373–83 (2013).
  18. Shorr, A. F. et al. A risk score for identifying methicillin-resistant Staphylococcus aureus in patients presenting to the hospital with pneumonia. BMC Infect. Dis. 13, 268 (2013).
  19. Kalil, A. C. et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin. Infect. Dis. 63, e61–e111 (2016).
  20. Chalmers, J. D., Rother, C., Salih, W. & Ewig, S. Healthcare-associated pneumonia does not accurately identify potentially resistant pathogens: a systematic review and meta-analysis. Clin. Infect. Dis. 58, 330–9 (2014).
  21. Ma, H. M., Wah, J. L. S. & Woo, J. Should nursing home-acquired pneumonia be treated as nosocomial pneumonia? J. Am. Med. Dir. Assoc. 13, 727–31 (2012).
  22. Yap, V., Datta, D. & Metersky, M. L. Is the present definition of health care-associated pneumonia the best way to define risk of infection with antibiotic-resistant pathogens? Infect. Dis. Clin. North Am. 27, 1–18 (2013).
  23. Ewig, S., Welte, T. & Torres, A. Is healthcare-associated pneumonia a distinct entity needing specific therapy? Curr. Opin. Infect. Dis. 25, 166–75 (2012).
  24. Kollef, M. H. Health care-associated pneumonia: perception versus reality. Clin. Infect. Dis. 49, 1875–7 (2009).
  25. Hooton, T. M. et al. A prospective study of risk factors for symptomatic urinary tract infection in young women. N. Engl. J. Med. 335, 468–74 (1996).
  26. Czaja, C. A., Scholes, D., Hooton, T. M. & Stamm, W. E. Population-based epidemiologic analysis of acute pyelonephritis. Clin. Infect. Dis. 45, 273–80 (2007).
  27. Echols, R. M., Tosiello, R. L., Haverstock, D. C. & Tice, A. D. Demographic, clinical, and treatment parameters influencing the outcome of acute cystitis. Clin. Infect. Dis. 29, 113–9 (1999).
  28. Gupta, K. et al. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: A 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases. Clin. Infect. Dis. 52, e103-20 (2011).
  29. Nicolle, L. E. Catheter-related urinary tract infection. Drugs Aging 22, 627–39 (2005).
  30. Nicolle, L. E. A practical guide to the management of complicated urinary tract infection. Drugs 53, 583–92 (1997).
  31. Smaill, F. M. & Vazquez, J. C. Antibiotics for asymptomatic bacteriuria in pregnancy. Cochrane database Syst. Rev. CD000490 (2015). doi:10.1002/14651858.CD000490.pub3
  32. Rouse, D. J., Andrews, W. W., Goldenberg, R. L. & Owen, J. Screening and treatment of asymptomatic bacteriuria of pregnancy to prevent pyelonephritis: a cost-effectiveness and cost-benefit analysis. Obstet. Gynecol. 86, 119–23 (1995).
  33. Hooper, D. C., Wolfson, J. S., Hooper, D. C. & Wolfson, J. S. Fluoroquinolone antimicrobial agents. N. Engl. J. Med. 324, 384–94 (1991).
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  36. Stevens, D. L. et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin. Infect. Dis. 59, (2014).
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  39. Eriksson, B., Jorup-Rönström, C., Karkkonen, K., Sjöblom, A. C. & Holm, S. E. Erysipelas: clinical and bacteriologic spectrum and serological aspects. Clin. Infect. Dis. 23, 1091–8 (1996).
  40. Moran, G. J. et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N. Engl. J. Med. 355, 666–74 (2006).
  41. Singer, A. J. & Talan, D. A. Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus. N. Engl. J. Med. 370, 1039–47 (2014).
  42. Summanen, P. H. et al. Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use. Clin. Infect. Dis. 20 Suppl 2, S279-82 (1995).
  43. Talan, D. A. et al. Trimethoprim–Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess. N. Engl. J. Med. 374, 823–832 (2016).
  44. Schmitz, G. R. et al. Randomized Controlled Trial of Trimethoprim-Sulfamethoxazole for Uncomplicated Skin Abscesses in Patients at Risk for Community-Associated Methicillin-Resistant Staphylococcus aureus Infection. Ann. Emerg. Med. 56, 283–287 (2010).
  45. Workowski, K. A., Bolan, G. A. & Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR. Recomm. reports Morb. Mortal. Wkly. report. Recomm. reports 64, 1–137 (2015).
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  47. Walker, C. K. & Wiesenfeld, H. C. Antibiotic Therapy for Acute Pelvic Inflammatory Disease: The 2006 Centers for Disease Control and Prevention Sexually Transmitted Diseases Treatment Guidelines. Clin. Infect. Dis. 44, S111–S122 (2007).
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  53. Deshpande, A. et al. Community-associated Clostridium difficile infection and antibiotics: a meta-analysis. J. Antimicrob. Chemother. 68, 1951–61 (2013).
  54. Johnson, S. et al. Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals. N. Engl. J. Med. 341, 1645–51 (1999).
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  56. Gurwith, M. J., Rabin, H. R. & Love, K. Diarrhea associated with clindamycin and ampicillin therapy: preliminary results of a cooperative study. J. Infect. Dis. 135 Suppl, S104-10 (1977).
  57. Kelly, C. P., Pothoulakis, C. & LaMont, J. T. Clostridium difficile colitis. N. Engl. J. Med. 330, 257–62 (1994).

 

Seizure Mimics: Pearls & Pitfalls

Authors: James L Webb, MD (Internal Medicine, SAUSHEC, USAF) and Brit Long, MD (@long_brit) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) & Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 20 year-old female presents to the ED after a witnessed fall. According to bystanders, the young woman was walking towards a gym treadmill when she collapsed to the floor below, convulsing for approximately1-2 minutes. Upon EMS arrival VS were within normal limits, GCS was noted as 14 (confusion, orientation only to self), EKG revealed NSR, and accucheck demonstrated a blood glucose of 134. Intravenous access was obtained en route to your facility.

As you interview and examine the patient, you note ABCs intact, a GCS of 15, an ample history remarkable only for report of a “rising feeling in the abdomen” prior to the event, and a secondary survey without obvious signs of trauma. ED evaluation, to include a CBC, CMP, EKG, and non-contrasted head CT are all within normal limits. Urine Hcg is negative.

Was this a seizure? What’s the appropriate patient disposition? If you’ve got questions, we’ve got important details on seizures and their mimics.

 

Background

Current data indicate that nearly 2 million U.S. residents are affected by Epilepsy.1-2 In addition to this population, approximately 150,000 Americans (age >18 years) present to healthcare providers annually following an apparent first seizure.1-2 As assigning a diagnosis a seizure or seizure disorder is not without significant health and quality of life implications (employment repercussions, driving restrictions, etc.1-5), emergency physicians must be aware of conditions that may mimic seizure activity: syncope, psychogenic non-epileptic seizures, metabolic derangements, stroke or TIA, sleep disorders, and migraines.

 

Seizures – A Review

Seizures result from abnormal neurologic electrical activity. This abnormal activity can occur in both hemispheres (generalized seizure) or within one hemisphere (focal seizure), which may spread to the entire brain. Generalized seizures are more common than focal seizures, and often have a genetic association.6 Generalized tonic-clonic seizures most frequently occur in adults – the motions of which consist of a tonic phase with muscle stiffening, followed by a clonic phase with rhythmic muscle contractions.6-7 Focal seizures often occur in the setting of cerebral insult.7 Unlike generalized seizures, symptoms of focal seizures vary according to the anatomic location of the abnormal electrical activity.6,8

Seizures can be classified as provoked or unprovoked. Provoked seizures are those with identifiable causes, which can be isolated to the brain, or are thought to occur secondary to a systemic disorder or illness. Such causes include: brain trauma, CNS infection (i.e. meningitis, encephalitis, brain abscess), anoxic brain injury, intracranial hemorrhage or surgery, metabolic disorders, illicit drug abuse or intoxication (most commonly tricyclic antidepressants and isoniazid), or alcohol withdrawal.9,10  Seizures may also occur in the setting of metabolic derangements (hypoglycemia or hyponatremia).9-12

 Unprovoked seizures are those with no discernible cause, or those occurring greater than seven days following precipitating factors or events. What factors or events might the emergency physician identify through the H&P?

  • Pregnant patient with a seizure –>evaluate for eclampsia
  • Child with an recent illness –>evaluate for personal and familial history of febrile seizures
  • In all patients –>inquire regarding a history of recent head trauma (occurring within 1 week prior to presentation)

It is particularly important to perform a thorough H&P in this patient population, as 50% of individuals experiencing an unprovoked seizure will experience a recurrence.11

 

Approach

Patients presenting with altered mental status (AMS)/seizure concern should be quickly assessed10,13-15,17:

  • ABCs
  • Consider obtaining a POC glucose level
  • First line treatment for seizure activity: benzodiazepines (lorazepam 0.1 mg/kg IV)
    • Second line agents: phenytoin, fosphenytoin, levetiracetam, or valproic acid
      • Intubation with propofol or ketamine with contiguous EEG (in consultation with neurology) may be required.14-17
    • After addressing ABCs, perform an H&P, complete a physical examination (PE), and obtain IV access. Consider: CBC, CMP, EKG, serum Hcg, anticonvulsant level if applicable, imaging as appropriate (CT recommended in the setting of new focal deficits, head trauma, continued AMS, immunocompromised state, history of cancer, persistent fever, focal seizures, history of stroke, or anticoagulation), +/- an LP.13,15-19
      • Note: neuroimaging should be performed in patients with suspected new-onset seizures, but may occur in the outpatient setting for those with a first time generalized tonic-clonic seizure with a normal neurologic exam. MRI is preferable with a higher yield of identifying abnormalities in the non-emergent setting.13,15-19
    • Disposition is often determined in conjunction with specialty consultation. Admission may be required in the setting of persistent neurologic deficit, persistent AMS, or poor social situation.13,15-19 Patients who return to mental status baseline, possess a normal neurologic exam, and whose labs and imaging are without pathology, may be discharged with outpatient follow-up.13,19

 For an in-depth discussion of seizure evaluation and management, see:  http://www.emdocs.net/treatment-of-seizures-in-the-emergency-department-pearls-and-pitfalls/

 

Evaluating Seizure Activity in Patients with Return to Mental Status Baseline

 A definitive diagnosis of seizure is made by EEG interpretation during seizure activity. As this is often times impossible in the ED setting, the emergency physician must seek out signs and symptoms commonly associated with seizure activity9,13,20:

  • HPI significant for aura: déjà vu, a rising sensation in the abdomen, abnormal taste or smell, or autonomic changes.
    • Activity commonly associated with a true seizure: witnessed tonic/clonic movements or observed head turning in the setting of a generalized seizure, or the abrupt onset of limb movements, abnormal sensations, or hallucinations in the setting of a focal seizure. 6,7,20
    • A postictal period occurring for minutes to hours with confusion, disorientation, and drowsiness.
  • Physical exam remarkable for tongue biting.

See Table 1 for signs and symptoms related to seizure activity in studies comparing seizures versus syncope. *Urinary incontinence was demonstrated to lack clinical significance.

screen-shot-2017-01-01-at-3-57-34-pm

What about laboratory studies?

 A lactate level may be useful in differentiating seizures from psychogenic non-epileptic seizures and syncope (sensitivity of 88%, specificity 87% for true seizure activity), 24 while an elevated CK is suggestive of epileptic seizures (specificity 85-100%), but demonstrates variable sensitivity (15-88%).25

 

Seizure Mimics

Studies indicate that approximately 20% of patients presenting for evaluation of seizure are misdiagnosed as having epilepsy.26  Conditions most commonly mistaken for epitileptiform seizure activity include syncope and psychogenic non-epileptic seizures.5 Detailed below is a review of seizure mimics with tips and tricks for ED evaluation and disposition.

Syncope

Syncope is a sudden loss of consciousness (LOC) due to decreased cerebral perfusion, resulting in loss of postural tone, with rapid return to mental status baseline. Syncope may be cardiac, orthostatic, or neurocardiogenic (vasovagal) in origin.

Historical evidence favoring a syncopal episode versus a seizure27-34:

  • Presentation –>LOC with rapid return to mental status baseline.
  • History –>Remarkable for precipitating factors: recent illness (emesis/diarrhea – hypovolemia), recent medication changes (i.e. B-blockers and bradycardia, diuretics causing hypovolemia, etc.), LOC following increased vagal tone (coughing, defecation, shaving).  LOC during physical exertion. In obtaining the HPI, it is important to note that myoclonic jerking occurs in up to 90% of patients experiencing syncope.27

Management and Disposition Pearls:

  • Evaluation –> EKG for dysrhythmias, consider a CBC and CMP to assess for anemia and electrolyte derangement, consider cardiac markers as indicated.
  • Disposition–>As appropriate. Referral for tilt-table testing in the setting of neurocardiogenic syncope may be considered after ruling out life-threatening conditions.

Notes on Syncope of Cardiac Origin

Syncope secondary to cardiac dysrhythmias or structural heart disease may present similarly to a seizure, however, the following suggest cardiac origin27-29, 33,34:

  • Presentation –>Most commonly an elderly patient.
  • History –>The absence of a prodrome; ROS positive for palpitations prior to LOC; CP or LOC during exertion.

Management and Disposition Pearls:

  • Evaluation –>PE for murmurs, rubs, gallops and s/s of heart failure (JVD, peripheral edema, hepatojugular reflex, etc.); EKG for dysrhythmias: SVT, VT, Mobitz type II second-degree, or third-degree AV block, bundle branch blocks, Long QT Syndrome, Brugada Syndrome, WPW Syndrome, Right Ventricular Dysplasia, and pacemaker malfunction have all been associated with syncopal episodes.33 Consider bedside POCUS or formal echocardiogram to evaluate for cardiac structural anomalies.
  • Disposition –>As appropriate. In the large majority of cases admission is required for adjunct testing.

 

Psychogenic Non-Epileptic Seizure (PNES) Disorder

PNES, a condition characterized by the presence of seizure-like activity occurring in the absence of EEG changes, is difficult to differentiate from a true seizure in the emergency setting; even more so as nearly 40% of patients with epilepsy suffer from the disorder.35 Characteristics that make PNES more likely include35-39:

  • Presentation –>Patient in their 20s-30s,35 experiencing an event characterized by asynchronous extremity movements, rapid head turning, pelvic thrusting, eye closing, or geotropic eye movements. Clinical clues useful for the provider: the absence of tongue biting, a prolonged duration (>2 mins), a patient who can recall the event, or a patient who was witnessed to have been crying during the seizure-like activity.
  • History –>Approximately 70% have a PMHx of a psychiatric disorder (depression, PTSD, personality disorder).36,37

Management and Disposition Pearls:

  • Evaluation –>When in doubt: treatment as appropriate (ABCs +/- benzodiazepines). Video EEG is the gold standard for diagnosis, therefore specialty consultation is required.
  • Disposition –>In consultation with neurology/neuropsychiatry. Treatment is often targeted to the underlying psychiatric disorder.39

 

Metabolic Derangements

Metabolic disorders are identified in 2.4-8% of patients presenting with first generalized seizure.9,10,13 Hypoglycemia and hyponatremia are the most common, but other disorders may include hypernatremia, hyperglycemia, hypercalcemia, and uremia.9,10,13

 Management and Disposition Pearls:

  • Evaluation –>Accucheck for all patients with AMS/seizure activity. CMP as appropriate.
  • Disposition –>Treatment and admission requirements based upon laboratory findings.

 

Stroke and TIA 

Stroke/TIA can be confused with a seizure when there is resolution of the neurologic deficit previously caused by cerebral ischemia. Characteristics of Stroke/TIA18,40,41:

  • Presentation –>Most commonly a middle-aged or elderly patient. HPI remarkable for negative symptoms: numbness, weakness, or blindness.
  • History –>PMHx significant for HTN, HLD, cardiac arrhythmia, family history of CVA

Management and Disposition Pearls:

  • Evaluation –>PE: focused neurological examination, accucheck, EKG for dysrhythmias, performance of risk stratification to determine the requirement for cerebral vasculature imaging.
  • Disposition –>As appropriate. Inpatient admission may be required for MRI, carotid ultrasonography, echocardiography, and medication optimization.

 

Sleep Disorders

Narcolepsy with cataplexy may present similarly to seizures. Narcolepsy is defined by excessive daytime sleepiness, lapses into sleep, or multiple naps during the same day at least 3 times per week for a duration of 3 months time. Cataplexy is the sudden loss of tone in response to emotion. 42-45

  • Presentation –>Patient suddenly collapses, but rapidly recovers to mental status baseline with complete recollection of the  event. 42-45

Management and Disposition Pearls:

  • Evaluation –>Thorough history-taking often allows differentiation from seizure activity.
  • Disposition –>Specialty referral for overnight polysomnography and sleep latency testing. Driving restriction is often state-mandated if the condition is suspected. 42-45

 

Migraines

 Migraines are recurrent headaches with or without aura (visual or sensory symptoms). Symptoms include throbbing headache, nausea, vomiting, and sensitivity to light and sound. Auras are often positive visual symptoms. Migraines with aura are similar to certain focal seizures with visual symptoms (hallucinations) or generalized seizure prodrome (aura). Signs and symptoms making a diagnosis of migraine more likely19, 50-52:

  • Presentation –>headache characterized by unilateral pain, throbbing pain, moderate-severe pain, and aggravated by physical activity, +/- nausea/vomiting or photo-/phonophobia
  • History –>PMHx significant for migraines.

Keep in mind, complex migraines may present with neurologic symptoms causing weakness, alteration in consciousness, or LOC.

Management and Disposition Pearls:

  • Evaluation –>PE: focused neurological examination. Rule out intracranial pathology as appropriate (CVA/SAH/meningitis/encephalitis – CT, LP, etc.)
  • Disposition –>As appropriate. In the setting of negative imaging (+/- negative LP), neurology consultation is appropriate as prophylactic medications (TCAs, B-blockers, anti-epileptics) may be considered for outpatient therapy.

 

Summary

– Seizures are caused by abnormal neurologic electrical activity resulting in motor, sensory, and behavioral symptoms.
In all patients presenting with AMS or actively seizing: ABCs, accucheck, initiate therapy as appropriate (benzodiazepines first line).
– For patients presenting after return to baseline mental status: a thorough history and physical examination are key to differentiating between a true seizure and its mimic.
– If a seizure is not suspected, consider syncope, psychogenic non-epileptic seizures, stroke or TIA, sleep disorders, and migraines.

 

References/Further Reading

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  2. Krumholz A, Wiebe S, Gronseth GS, et al. Evidence-Based Guideline: Management of an Unprovoked First Seizure in Adults: Report of the Guideline Development Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsy Curr. 2015 May-Jun;15(3):144-52.
  3. Lowenstein DH, Alldredge BK. Status epilepticus. N Engl J Med. 1998 Apr 2;338(14):970-6.
  4. England MJ, Livermari CT, Schultz AM, Strawbridge LM Institute of Medicine (US) Committee on the Public Health Dimensions of the Epilepsies; England MJ, Livermari CT, Schultz AM, Strawbridge LM, editors. Epilepsy Across the Spectrum: Promoting Health and Understanding. Washington, DC: The National Academies Press; 2012.
  5. Xu Y, Nguyen D, Mohamed A, et al. Frequency of a false positive diagnosis of epilepsy: A systematic review of observational studies. 2016 Aug 23;41:167-174.
  6. Berg AT, Berkovic SF, Brodie MJ, et al. Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005-2009. Epilepsia. 2010 Apr;51(4):676-85.
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  49. Albanese A, Barnes MP, Bhatia KP, et al. A systematic review on the diagnosis and treatment of primary (idiopathic) dystonia and dystonia plus syndromes: report of an EFNS/MDS-ES Task Force. Eur J Neurol. 2006 May;13(5):433-44.
  50. Sances G, Guaschino E, Perucca P, et al. Migralepsy: a call for a revision of the definition. Epilepsia 2009;50:2487–96.
  51. Goadsby PJ, Lipton RB, Ferrari MD. Migraine–current understanding and treatment. N Engl J Med. 2002 Jan 24;346(4):257-70.
  52. Chawla J. Migraine. Emedicine: Medscape. http://emedicine.medscape.com/article/1142556-overv

 

 

The Road to Academic Emergency Medicine

Authors: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Jennifer Robertson, MD, MSEd (Assistant Professor, Emory University, Atlanta GA)

Emergency physicians train to be highly proficient in the resuscitation and management of acutely ill patients.  In addition, all emergency medicine (EM) training programs focus on preparing physicians to care for these patients in community practice settings. While most EM graduates go on to practice in community settings, academic EM is an option for interested physicians.

In general, academic EM was established to provide the teaching, research, and leadership goals of the specialty. For current residents and community doctors, specific pathways for practicing academic EM are now available, which allow new graduates to directly enter academic EM from residency or transition from community to academic EM.

The decision to practice academic or community practice can be a difficult one to make, as there are perks and drawbacks in both settings. This post will evaluate the road to academic emergency medicine, the positives and negatives, and provide tips for success. However, before we start, we need to understand the difference between academic and community EM.

What is academic emergency medicine?

An academic emergency medicine practice is defined by its providers spending the majority of their time in resident education/supervision, along with scholarly activity (academic writing, teaching, or research).1-5 This focus came into existence in order to meet the teaching, research, administrative, and educational aspects of emergency medicine. The majority of academic providers are associated with a teaching hospital, and many have time protected for academic pursuits. Over 40% of current residents are interested in pursuing an academic career, but the road to determining whether an academic or community practice is right for you can be difficult.1

Unfortunately, many graduating residents feel ill prepared to begin a career in academics, and program directors agree. A survey of EM residency directors found that only 29% feel their program graduates are prepared for an academic career involving original research.2 Obstacles include insufficient research training and resident difficulty in finding knowledgeable collaborators and mentors.

What is community practice?

Community EM refers to practices based mostly on clinical medicine. In community EM, providers spend the majority of their time on clinical duties (usually shifts), rather than supervising and educating residents. Providers may have other obligations such as administrative tasks, but their primary focus is direct patient care. However, the actual amount of patient care duties will vary within individual departments, hospitals, and even parts of the country. Pay is often based on the number of shifts and relative value units (RVUs) per shift. However, overall pay can be also be affected by partnerships, bonuses based on productivity, patient satisfaction, and quality measures.

 Why academic EM?

Academic medicine seeks to pursue scholarship, expand knowledge, and pass on that knowledge. This is most commonly done through resident education and supervision. Education and scholarly activity are ultimately the goals, though these can take several forms. Academics provides career diversity, expertise development, formation of educational philosophy and techniques, specialty advancement, networking and formation of relationships, and research development. It can allow physicians to influence hospital and institution practices, and provide a bit of control in his or her schedule. Best of all, academic EM gives physicians the chance to affect and improve the care of many patients through resident education and scholarly activity.

There are several negative factors associated with academic EM. You will likely work more hours combined, make less money, work fewer clinical hours, and experience more pressure to be scholarly productive (we will cover this later), as compared to community practice.

We know the decision is difficult.

Residency rotations in both settings can provide glimpses of both types of practice. Hybrid programs are also in existence, and it is never too late to switch from one to the other.

In the meantime, how should a resident prepare for academic EM? Residency is the time to obtain several important skills.

1) The first is the most fundamental and important: clinical competency. Excellence in patient care is fine-tuned during residency. Every patient encounter, lecture, and time spent studying should focus on learning and enhancing clinical evaluation and management.

2) The next skill is teaching and knowledge dissemination. This is primarily learned via supervising junior residents or medical students at the bedside or by mentorship. In addition, lecture-based learning and teaching are also paramount.

3) Research skills are essential, no matter what environment you will practice in. Experience in reviewing the literature, establishing research questions and study designs, data collection/analysis, and presentation of data is important.  This can be difficult to obtain through journal clubs only, and some form of higher education is often beneficial for developing key research skills.

4) Expressing ideas and disseminating your knowledge are important, not only for abstracts, papers, and grants, but for hospital protocols and committees.

5) Administrative skills are helpful for both community and academic settings.

6) As most physicians (especially in EM) know, “people” skills are essential, not only to your clinical practice but also in forming long-lasting relationships and collaborations. Whether you go into academic or community EM, these skills are critical.

7) Finally, developing a personal learning strategy is important for continued clinical development.

Ok, so academic EM sounds like your thing… Now what?

There are several aspects of career planning that will help you find the best fit and succeed in academic EM. Each of the following components summarize key information for not only academic survival, but also for long term success.

Preparing for Academics

  1. The importance of a mentor – Mentorship is a key component of a healthy career. Forming a healthy mentoring relationship leads to academic success and career satisfaction, especially when formal postgraduate training is not completed.15-19 Look for mentors within the department, your institution, other institutions, prior training places, and from regional/national meetings. Mentors assist in setting and achieving goals, providing feedback on performance, building confidence and moral support, helping you get involved in committee work, introducing mentees to leaders in your field, protecting you and your interests, and keeping you on track. Your mentor is your advocate.   When choosing a mentor, there are several considerations. These include ensuring the mentor has a track record in the area of your interest, has available time and interest, possesses a personality that fits, and does not possess conflicts of interest. More than one mentor can be helpful, and mentors outside of EM can provide a different viewpoint for you.
  1. Setting time goals: 1, 3, 5, 10 years – Short and long term goals are necessary for a successful career, as a resident and faculty member. You have probably been setting goals all of your life, and just like before, it is important to possess concrete and obtainable goals. A career plan should be established, with each year broken down into separate goals that work toward achieving the long term goal. Keep in mind these may need to be revised, and these goals should be used as a guide for feedback/evaluation sessions. These goals should be discussed with your mentor, with regular meetings and feedback sessions to keep you on track.
  1. Finding your niche – Even though EM is a broad specialty, the majority of academic leaders are known for expertise in one or several areas of knowledge. This is essential for those forming a career: determine what interests or excites you and what opportunities are available to focus on these interests. Ask yourself what your passion is and what excites you. Another key is to consider what you do not enjoy. When you recognize what you like and dislike, then seek to get involved in your area of interest, with a goal of academic productivity (through research, lectures, or publishing). Research projects should also focus on this. Because of EM’s broad spectrum, some may want to target what’s currently available at their institution. Others may take too much on, spreading themselves too thin. It can be difficult to focus on one or two areas, but do your best to choose what interests you the most.
  1. Keep an academic portfolio and curriculum vitae – As most know, a curriculum vitae (CV) is a necessity. Even though different formats may be used, all contain the same information. Your mentor and senior department leadership can provide valuable assistance in forming and fine-tuning your CV. A personal academic profile or portfolio should also be maintained, as this summarizes your teaching, compiles your awards and evaluations, and should also contain examples of lectures and other academic achievements. Both are vital for academic success and promotion.
  1. Join an EM organization – Several emergency medicine societies are available, and each can provide significant benefits. Organizations include AAEM, ACEP, SAEM, CORD, NAEMSP, and several others. These organizations provide valuable networking and socializing opportunities for residents and faculty of all levels. Many of these organizations also have committees, which provide opportunities to improve nonclinical educational skills, form relationships with physicians with similar interests, and contribute to EM. If you can, attend meetings that allow open attendance. You will gain valuable skills in learning how to manage meetings and conferences by watching those in charge.
  1. Networking – There are several aspects to networking. Joining a committee or task force can be helpful and provide links to other departments and senior leaders. Speaking with everyone in the department, from interns to department chair, can form relationships that last. Everyone in EM has lessons learned or advice they can offer. Ask senior department members for connections or to introduce you to other leaders.
  1. Remember your colleagues and provide assistance to others – An academic physician with goals will develop and advance. As you begin to grow in your career, seek to help and mentor others. You obtained your success with the assistance of others, including your mentor and family, and you need to extend this same courtesy to others around you. Involve others in your projects and educational goals. By seeking the advancement of other EM colleagues, you form friendships and long-lasting relationships. If you switched programs, remember those back home and acknowledge them in your success.

What about postgraduate training?

Postgraduate training can help through providing focus on future work, as well as training in teaching, writing, research, and funding. Unfortunately, medical school and residency often do not prepare physicians for an academic career. Though not mandatory for an academic position, postgraduate training can facilitate academic training, enhance career satisfaction, and increase chances of academic success. This training also assists mentoring relationships and collaborative relationships. Dedicated postgraduate training may be the only means of obtaining truly protected time to develop academic skills. Interestingly, fellowship or postgraduate-trained physicians are more likely to obtain success and career satisfaction if involved in an academic program. This training provides increased job mastery, leading to less stress, greater certainty, and improved vision of career goals. Fellowships include pediatric EM, toxicology, undersea and hyperbaric medicine, sports medicine, ultrasound, palliative care, EMS, critical care, and several others. However, further training does delay maximum salary potential.

If you are considering a fellowship, look at each program’s expected clinical time, training value, access to mentors, research opportunities, and total experience. The vast majority of EM fellowship programs offer complete, valuable experiences. If interested in education, fellowship training necessity is less defined. This fellowship is growing, but many departments offer formal, structured, multiyear educational training opportunities. For more information on fellowships, please see EMRA’s complete guide at: https://www.emra.org/uploadedfiles/emra/emra_publications/emra_fellowshipguide_v1_0816.pdf

The nuts and bolts for success in academic EM

What roles are there? Academic EM is comprised of many positions, and each institution and program will vary. Research roles include director, clinical trial director, research advisor, and research assistants’ program director. Educational roles can be residency director, associate residency director, medical student director, medical school leadership (dean), rotating resident director, fellowship director, CME director, hospital committee director, and others. There are also specialty roles such as ultrasound, hyperbaric chamber, chest pain, etc. Administrative roles include chief/chair, EMS director, operations director, pediatric ED director, CQI/Risk management director, and others.

Finding the right program – A program that will provide the environment and tools to help you flourish is important. First, characterize the institution, and evaluate what the program rewards (publications, lectures, clinical throughput). Are you just another cog in a vast machine? What would happen if you leave the program? You should ensure true opportunities to advance clinically and professionally exist in the program. Ultimately, look at what the institution and the program can do for you, rather than what you can do for the institution/program.  

Several program types or models possess different attributes. The egalitarian model treats everyone the same, regardless of specific talents or interests. Faculty work similar numbers of shifts, teach a similar number of lectures, carry similar administrate duties, and are expected to have similar productivity. The specialization model demonstrates a more team-based approach. All faculty work clinically, but the department can modify career development to better match faculty member strengths, weaknesses, interests, and dislikes. Shift numbers can vary based on faculty member roles and productivity.

Promotion and tenure – There are progressive ranks with timelines for academic physicians including assistant professor, associate professor, and full professor. Many are based on specific criteria such as publications, grants, regional/national recognition, teaching portfolios, and clinical productivity. An area of focus or niche can be helpful. This should be discussed with your department/program leadership and mentor. A mark of a strong program is a definitive track for career advancement, so you must inquire about this component of the academic program. Many offer workshops or provide further faculty development, which can significantly improve your advancement.

Research – Research is one of the fundamental means of growth for EM. The research environment physicians experience during residency often shapes future interest in research.1,4  At its core, research involves formulating a question, addressing the question with appropriate study design, collection and interpretation of data, and presenting the results in a peer-reviewed journal. This is often a long process, requiring time, effort, and mentorship for residents. Faculty have several goals when it comes to research: conducting research themselves, educating residents on scientific study, and/or how to conduct a study.

A large number of relevant areas of study are in existence. The majority of academic centers will desire their physicians to be “academically productive,” or obtain clinically relevant publications or grants. Research topics can be clinical, basic science, education, policy, or clinical operations. Mentorship and senior physician assistance to residents and new faculty seeking a research track are essential. Properly forming a research question and designing a protocol can be challenging, and thus, the more experience you can obtain, the better.

Teaching – Education is one of the key factors in an academic position. All physicians teach, whether the audience is nurses, technicians, or other physicians. One major component of an academic program is working with residents. Most programs expect academic clinicians to teach on shift as well as present lectures at conferences several times per year. This aspect is often one of the most fulfilling aspects of academic medicine, as you have the opportunity to affect the growth of future EM physicians. You may also work with students and off-service residents, and your relationship with these learners can have significant impact on their education, patient care, and relationships with the emergency department in their future careers.

Residency provides valuable time for honing educational skills. Some programs have dedicated programs for teaching, while others expect those interested in teaching to pick up the skills on their own. Focusing on shift teaching, presentation skills, and creation of lectures are great places to start for residents and new faculty. In emergency medicine, it can be difficult to work on your teaching skills, as there are so many options for teaching and so many different learners. Many adult learners seek information that will directly and positively impact their future careers. Thus, it is important to focus on how individuals learn and how you can make a difference in their learning experiences.

Teaching involves the ability to observe, question, and review trainee performance in actual patient care settings. When developing your own education techniques, look at the educators around you. New faculty and senior residents should pay close attention to those teachers who demonstrate master education skills. At the same time, strongly consider providers who are working on their own deficiencies. You should seek to recognize and understand these deficiencies so you can avoid them. Recognizing these skills and one’s own shortcomings will allow you to grow as an educator.

Scholarly Activity – One major aspect of an academic career is scholarly activity. In the past this included writing, either book chapters, original research, or review articles. The majority of academic programs still rely on clinical research and formal publication in medical journals. The academic environment is evolving, with several other opportunities. Free Open Access Medical Education (FOAMed) is one of these, with a growth of blogs and podcasts. Many academic physicians have now based their career on this avenue. Other options include ACEP’s Critical Decisions in Emergency Medicine, case reports, images, and specialty organization newsletters. Most programs will ask for at least one lecture per academic year, often grand rounds. However, speaking at regional, national, or international meetings is another means of scholarly productivity.

Once you have a project, seek to present the results in multiple settings and formats. Start with presenting an abstract at a conference, then seek publishing in a peer-reviewed journal. A FOAMed blog publication is also an option. Presenting this further at other functions, such as a grand rounds lecture, offers another avenue.  Publication in this format develops writing skills, develops an area of expertise, and advances your career. Remember, most programs still focus productivity on peer-reviewed publications.

The Literature – Residency programs usually promote some form of literature understanding through several formats: journal clubs, evidence-based medicine projects, and education on clinical shifts. Faculty may lead discussions or projects for literature awareness, aimed at promoting a deeper understanding of EM studies. For faculty, a key component of academics is staying abreast of the current literature, as well as “classic” studies. This can be difficult with all of your other duties and clinical shifts, but this is vital to your own education. There are multiple means of remaining current, from subscriptions to journals (Annals of EM, American Journal of EM, Journal of EM, etc.), podcasts (EM:RAP, EMA, EMCrit), and blogs (ALiEM, emDocs, Core EM, EM Updates, REBEL EM). FOAMed has revolutionized medical learning, and residents and faculty can use FOAMed to remain abreast of new, exciting medical updates.

Goals and Persistence – Specific goals with a timeline are a necessity for success in academic medicine, and they must be written down to solidify their importance. The act of setting the goal with timeline, verbalizing it, and writing it creates a commitment. Remember, academic medicine can be and will be difficult. There will be setbacks, but do not be discouraged. You will have papers and grants rejected. Make changes and keep going.

Collaboration – Finding others interested in your niche or topic can benefit. With our schedules, it can be difficult to frequently meet with your mentor to discuss areas of interest. This is where collaboration can help. Team members can provide skills and perspectives that will improve the quality of projects. Just make sure you set specific goals for the project, with a timeline.

Other Specifics – Determine what percentage of your work week should be clinical and what should be given to the rest of your academic pursuits. You should consider what you want to be doing in 5-10 years. Where do you see yourself? Saying “no” is ok if you have too much on your plate.

I think I know how to succeed, but what can I mess up?

There are many pitfalls in academics. These include not enough protection from other duties (working too many clinical shifts with the expectation for academic productivity), not enough training for an academic career (research focus without training on research question and protocol formation), failure to have a mentor (one of the cornerstones of academic success), failure to form a plan/timeline of goals, lack of balance (which leads to burnout), biting off too much, and not listening to feedback.

Importance of Balance – Maintain balance and block off time for your family and hobbies. Success takes time, and it will not occur overnight. Recent years have seen an emphasis on physician health. This really comes down to balancing many aspects of life including your shifts, academics, community activities, exercise, hobbies, family, religious/spiritual concerns, friends, and future plans. Pushing too hard and too fast with too much will lead to burnout.

The Decision – Residency is a great time to explore academics and community practice. Rotations in both settings can help you determine which practice is the best fit for you. You can always switch settings, or in other words, it is never too late to go from community to academic practice. Work on perfecting your clinical skills and management early, as this is essential to both academic and community medicine.

Thanks for reading. Please comment below with other tips or questions!

References/Further Reading

  1. Stern SA, Kim HM, Neacy K, Dronen SC, Mertz M. The impact of environmental factors on emergency medicine resident career choice. Acad Emerg Med. 1999 Apr;6(4):262-70.
  2. Neacy K, Stern SA, Kim HM, Dronen SC. Resident perception of academic skills training and impact on academic career choice. Acad Emerg Med. 2000; 7:1408–15.
  3. Aycock RD, Weizberg M, Hahn B, Weiserbs KF, Ardolic B. A survey of academic emergency medicine department chairs on hiring new attending physicians. J Emerg Med. 2014 Jul;47(1):92-8.
  4. Sanders AB, Fulginiti JV, Witzke DB, Bangs KA. Characteristics influencing career decisions of academic and nonacademic emergency physicians. Ann Emerg Med. 1994;23:81–7
  5. Clinton JE. Educating academic emergency physicians. Acad Emerg Med. 1999;6:260–1.
  6. Stead LG, Sadosty AT, Decker WW. Academic career development for emergency medicine residents: a road map. Acad Emerg Med 2005 May;12(5):412-16.
  7. Hobgood C, Zink B (eds). Emergency Medicine: An Academic Career Guide, ed 2. Lansing, MI: Society for Academic Emergency Medicine; 2000.
  8. Faculty Development Web site. Available at: www.saem.org/ facdev/fac_dev_handbook/. Accessed Nov 10, 2016.
  9. Cydulka C. Preparing for a career in academics. Emergency Medicine: An Academic Career Guide. Available at: http:// www.saem.org. Accessed Sep 18, 2001.
  10. Hall KN, Wakeman MA. Residency-trained emergency physicians: their demographics, practice evolution and attrition from emergency medicine. J Emerg Med. 1999;17(1):7-15.
  11. Reinhart MA, Munger BS, Rund DA. American Board of Emergency Medicine Longitudinal Study of Emergency Physicians. Ann Emerg Med 1999;33(1):22-32.
  12. Kellerman AL. Are you considering an academic career? EMRA. Available at https://www.emra.org/resources/career-planning/practice-spaces/are-you-considering-an-academic-career-/. Accessed 04 November 2016.
  13. Pines JM. The young physician in academic emergency medicine: tips for success. AAEM. Available at http://www.ypsaaem.org/yps-articles/past-yps-articles/2006/the-young-physician-in-academic-emergency-medicine-tips-for-success. Accessed 04 November 2016.
  14. Sokolove P, Stern S, Baren J. An academic career: is it right for you? 2008 SAEM Annual Meeting, May 2008. Available at http://www.slideshare.net/changezkn/life-after-residency-academic-emergency-medicine. Accessed 04 November 2016.
  15. Taylor JS. Academic Medicine 2001;76:366-372.
  16. Stack SJ, Watson MJ. Enriching the resident-faculty relationship. Ann Emerg Med. 2001; 38:336–8.
  17. Osborn TM, Waeckerle JF, Perina D, Keyes LE. Mentorship: through the looking glass into our future. Ann Emerg Med. 1999; 34:285–9.
  18. Hazzard WR. Mentoring across the professional lifespan in academic geriatrics. J Am Geriatr Soc. 1999; 47:1466–70.
  19. Peluchette JV, Jeanquart S. Professionals’ use of different mentor sources at various career stages: implications for career success. J Soc Psychol. 2000; 140:549–64.
  20. Holmboe ES, Ward DS, Reznick RK, Katsufrakis PJ, Leslie KM, Patel VL, Ray DD, Nelson EA. Faculty development in assessment: the missing link in competency-based medical education. Acad Med. 2011; 86(4):460-7.

The Thromboelastogram (TEG®): A Five-Minute Primer for the Emergency Physician

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC)

It’s three o’clock in the morning on your fourth night shift in a row.  While mustering the courage to rescue your energy drink from the dank, dark depths of the staff mini-fridge, you hear a familiar page: “trauma team to the trauma room.”  As you walk towards the ambulance bay, the trauma surgeon approaches with information regarding the incoming transfer:

  • 17 year-old male – MVC versus pedestrian
  • Seen at OSH where CTs demonstrated: epidural hematoma, grade III liver laceration, grade II splenic laceration, open book pelvic fracture, and extraperitoneal bladder rupture
  • Patient underwent external pelvic fixation and transfusion of blood products (8U PRBCs, 8U FFP and 4U Plts)
  • Most recent VS: BP 136/89, HR 92, RR (intubated/ventilated):14, SpO2 99% (FiO2 70%)

Drawing your attention to a piece of paper in his hand, detailing what appear to be labs from the outside facility, the surgeon points to a colorful figure: “I’m very concerned about this”:

screen-shot-2016-12-20-at-10-18-26-pm

Scanning your mind for intelligent thought, you realize that it’s been some time since you’ve ordered a thromboelastogram (TEG), let alone interpreted one.

If you’re like this physician, take a few minutes to scan the following review – the quick and dirty on TEGs is coming your way.

Thromboelastography – What is it?

Developed in 1948 by Dr. Hellmut Harter, thromboelastography is a mechanism of assessing coagulation based upon the viscoelastic properties of whole blood.2-8  In contrast to traditional, static measurements of hemostasis (PT, aPTT, INR, fibrinogen level, and fibrin degradation products), thromboelastography allows for an assessment of near real-time, in-vivo clotting capacity, providing the interpreter information regarding the dynamics of clot development, stabilization, and dissolution.7  When utilized as a point-of-care assay, graphic interpretation of thromboelastography (the TEG), offers the opportunity for an expedited assessment of coagulopathies (thrombocytopenia, factor deficiency, heparin effect, hypofibrinogenemia, and hyperfibrinolysis).7,9,12,13

How is a TEG performed?

In order to perform a TEG, a citrated-sample of whole blood is placed into a heated sample cup with calcium chloride (to overcome the effects of the citrate), kaolin (a negatively charged molecule known to initiate the intrinsic pathway10), and phospholipids (required for optimal functioning of the extrinsic pathway11) (Figure 2).  As the sample cup oscillates in a limited arc, formation of clot results in the generation of rotational forces on a pin suspended from a torsion wire.  Forces translated to the torsion wire are then, in turn, transmitted to an electrical transducer, creating a characteristic waveform (Figure 3).

screen-shot-2016-12-20-at-10-20-43-pm

screen-shot-2016-12-20-at-10-20-31-pm

I’ve heard of the Rapid TEG (r-TEG), is there a Difference?

When performed by a trained laboratory specialist, an r-TEG may be completed within 15 minutes as compared to the average 30-45 minutes processing time for a standard TEG.4,5,14  In contrast to a TEG, whole blood samples for an r-TEG may be performed with citrated or non-citrated samples.4 Samples utilized for an r-TEG are combined with tissue factor (activating the extrinsic pathway), and kaolin (activating the intrinsic pathway as above) +/- calcium chloride as applicable.4

I’ve also heard of ROTEM, what is it?

Although utilizing the technique developed by Dr. Harter, rotational thromboelastometry (ROTEM) differs from traditional thromboelastography in its mechanical application.  Unlike traditional thromboelastography, which utilizes a sample cup rotating in a limited arc, ROTEM employs a static sample cup with an oscillating pin/wire transduction system.  By comparison, ROTEM is also a more complex diagnostic test as it requires a number of differing reagents.  A complete discussion of ROTEM is outside the scope of this review.  If interested in further reading, see:

Tanaka K, Bolliger D. Practical aspects of rotational thromboelastometry (ROTEM). Available from: https://www.scahq.org/sca3/events/2009/annual/syllabus/workshops/subs/wkshp6pdfs/ROTEM%20-%20Tanaka.doc.pdf

Haemoview Diagnostics. ROTEM analysis: thromboelastometry. Available from http://www.haemoview.com.au/rotem-analysis.html

Haemoview. The 5 ROTEM tests. Available from http://www.haemoview.com.au/uploads/2/5/4/9/25498232/the_5_rotem_tests.pdf

How Do I Interpret TEG and r-TEG Results?

Drs. Semon and Cheatham of the Orlando Regional Medical Center Department of Surgical Education generated an excellent quick reference chart:

screen-shot-2016-12-20-at-10-23-21-pm

*Note: TEG-ACT (rapid) – reported for r-TEG only.

A TEG-Guided Transfusion Strategy

In addressing TEG and r-TEG abnormalities, experts recommend the following3:

screen-shot-2016-12-20-at-10-23-39-pm

The Quick and Dirty: Pattern Recognition

Perhaps most useful for the ED physician is knowledge of qualitative TEG representations:

screen-shot-2016-12-20-at-10-23-52-pm

Some clarification on DIC Stage 1 and 2:

  • Stage 1: Fibrinolysis results in the degradation of fibrin, increasing fibrin degradation products (FDPs). Excess FDPs result in clot de-stabilization.1
  • Stage 2: The cycle of clot formation and breakdown results in platelet and clotting factor consumption.1

Why Might an Emergency Medicine Physician Want to Know about this Test?

Coagulation abnormalities in trauma patients have demonstrated a significant association with infection, multi-organ failure, and death.15-18 Given its ability to quickly detect hematologic pathology, the TEG is becoming a tool for the evaluation of transfusion requirements/coagulopathy post transfusion in this patient population.3,12,13

What does the literature say?

Cotton, et al., 20114:

  • Pilot study to evaluate the timeliness of r-TEG results, their correlation to conventional coagulation testing (CCT – PT, aPTT, INR, platelet count, fibrinogen), and the ability of r-TEG to predict early blood transfusion.
    • 272 patients meeting requirements for major trauma activation
    • Outcomes:
      • All r-TEG values available within 15 minutes vs. 48 minutes for CCTs
      • ACT, r-value, k-time correlated with PT, INR, PTT (r >0.70; p<0.001)
      • MA and a-angle correlated with platelet count (p<0.001, p<0.001)
      • Controlling for demographics and ED vitals: ACT>128 predicted massive transfusion (>10 U) in the first 6 hours of presentation and treatment

Bottom line – r-TEG results were available within minutes, results correlated with conventional coagulation test results, and were predictive of the requirement for early massive transfusion.

Holocomb, et al., 201219:

  • Study to evaluate the reliability of r-TEGs versus CCTs in predicting blood product transfusion
    • 1974 major trauma patients, median ISS 17 (25% meeting criteria for shock; 28% transfused, 6% died within 24 hours)
    • Outcomes
      • When controlling for age, injury mechanism, weighted-Revised Trauma Score, base excess and hemoglobin, ACT predicted RBC transfusion and a-angle predicted massive transfusion better than PT/aPTT or INR (p<0.001).
      • a-angle was superior to fibrinogen for predicting plasma transfusion, and MA was superior to platelet count for predicting platelet transfusion (p<0.001)

Bottom line – r-TEG was more accurate in the prediction of requirements for RBC, plasma, and platelet transfusions as compared to traditional CCTs.

Wikkelso A, et al., 201612:

  • Cochrane Review including 17 current RCTs (n=1493 participants)
    • Per the authors:
      • Low quality studies: numerous biases
      • Limited generalizability: majority of studies center on cardiac patients undergoing surgical intervention

Bottom line – There is growing evidence to suggest that the utilization of TEG and ROTEM reduce transfusion requirements and improve morbidity in patients with bleeding, but additional studies are required.

Back to Our Case

Why was the trauma surgeon concerned? If we interpret our TEG values:

  • R time 20.0 => well above the upper limit of normal (10.0 minutes) = significantly prolonged time for clot formation
  • K time 13.2 => normal: up to 10.0 = prolonged fibrin cross-linking
  • a-angle 16.5 => normal >53.0 = limited clot formation
  • MA 38 => normal platelet function >50 = limited platelet function

More importantly, one quick glance at our TEG and through pattern recognition, we known that aside from his significant traumatic injuries, the patient is in trouble. This waveform is characteristic of DIC Stage 2.

Key Pearls

  • A TEG can be used as a rapid assessment of thrombosis and fibrinolysis.
  • Although additional RCTs are needed, TEGs utilized in trauma patients have been demonstrated to reduce transfusion requirements (important when we consider TACO/TRALI, risk of DIC, and blood-borne pathogens).
  • If nothing else, take a few minutes to review the characteristic TEG waveforms – depending on your laboratory processing time, knowledge of above tracings could allow early identification of coagulopathy and immediate treatment.

 

References / Further Reading

  1. Williams. Haemscope Basic Clinician Training: Fibrinolysis and Hyperfibrinolysis TEG Analysis. Available from: www.medicine.wisc.edu/~williams/TEG5_analysis.ppt
  2. Walsh M, Thomas S, Howard J, Evans E, Guyer K, et al. Blood component therapy in trauma guided with the utilization of the perfusionist and thromboelastography. J Extra Corpor Technol. 2001; 43(4):162-167.
  3. Semon G, Cheatham M. Thromboelastography in Trauma. Surgical Critical Care Evidence-Based Guidelines Committee. 2014. Available from: www.surgicalcriticalcare.net/Guidelines/TEG%202014.pdf
  4. Cotton B, Faz G, Hatch Q, Radwan Z, Podbielski J, et al. Rapid thromboelastography delivers real-time results that predict transfusion within 1 hour of admission. J Trauma. 2011; 71:407-417.
  5. Teodoro da Luz L, Nascimento B, Rizoli S. Thromboelastography (TEG): practical considerations on its clinical use in trauma resuscitation. Scand J Trauma Resusc Emerg Med. 2013; 21:29.
  6. Bollinger D, Seeberg M, Tanaka K. Principles and practice of thromboelastography in clinical coagulation management and transfusion practice. Transfus Med Rev. 2012: 26(1): 1-13.
  7. Thakur M, Ahmed A. A review of thromboelastography. Int J periop Ultrasound Apply Technol. 2012; 1(1):25-29.
  8. Nickson C. Critical Care Compendium: Thromboelastogram (TEG). 2014. Available from http://lifeinthefastlane.com/ccc/thromboelastogram-teg/
  9. Kashuk J, Moore E, Sawyer M, Wolhauer M, Pezold M, et al. Primary fibrinolysis is integral in the pathogenesis of acute coagulopathy of trauma. Ann Surg. 2010; 252: 434-444.
  10. Zhu S, Diamond S. Contact activation of blood coagulation on a defined kaolin/collagen surface in microfluidic assay. Thromb Res. 2014; 134(6): 1335-1343.
  11. Heemskerk J, Bevers E, Lindhout T. Platelet activation and blood coagulation. Throm Haemost. 2002; 88(2):186-193.
  12. Wikkelso A, Wetterslev J, Moller A, Afshari A. Thromboelastography (TEG) or thromboelastometry (ROTEM) to monitor haemostatic treatment versus usual care in adults or children with bleeding (Review). Cochrane Database of Systematic Reviews. 2016; 8:1-149.
  13. Luddington R. Thromboelastography/thromboelastometry. Clin Lab Haematol. 2005; 27(2):81-90.
  14. Jeger V, Zimmerman H, Exadaktylos A. Can rapid TEG accelerate the search for coagulopathies in the patient with multiple injuries? J Trauma. 2009; 66:1253-1257.
  15. Niles S, McLaughlin D, Perkins J et al. Increased mortality associated with the early coagulopathy of trauma in combat casualties. J Trauma. 2008; 64:1459-1463.
  16. Brohi K, Sing J, Heron M. Coats T. Acute traumatic coagulopathy. J Trauma. 2003; 54:1127-1130.
  17. Cotton B, Gunter O, Isbell J, et al. Damage control hematology: the impact of a trauma exsanguination protocol on survival and blood product utilization. J Trauma. 2008; 64;1177-1182.
  18. Cohen J, Call M, Nelson M, et al. Clinical and mechanistic drivers of cute traumatic coagulopathy. J Trauma Acute Care Surg. 2013; 75:S40-47.
  19. Holocomb J, Minei K, Scerbo M, Radwan Z, Wade C, et al. Admission rapid thromboelastography can replace conventional coagulation tests in the emergency department: experience with 1974 consecutive trauma patients. Ann Surg. 2012

Healthy Patients with Potential to Crash

Authors: Daniel Ritter (Medical Student, The Ohio State University College of Medicine) and Mark J Conroy, MD (Assistant Professor of EM, The Ohio State University Wexner Medical Center, @mjconroy_md) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

 Introduction

A 30-year-old healthy female presents to the emergency department (ED) complaining of nausea, vomiting, and diarrhea that have worsened over the last 24 hours. She admits to some lightheadedness and states that she feels “just out of it”.  She denies any abdominal pain or blood in her emesis and stool. Some coworkers have been out sick with similar symptoms following a company party over the weekend.  She takes “some pill” for a “gland problem”, but she lost the bottle a few days prior.

The patient’s initial vital signs include a heart rate of 105 beats per minute (bpm) and a blood pressure of 90/50 mmHg. The patient is physically fit and reports that her blood pressure always runs on the “low side”. Her examination reveals dry mucous membranes and tachycardia but it is otherwise normal.  The patient has no neck stiffness, cardiac murmurs, abdominal pain, or rashes. You order routine laboratory tests and and treat her symptoms with an antiemetic and intravenous (IV) fluids.

After about 30 minutes, the patient’s chemistry returns and demonstrates a marked hyperkalemia and hyponatremia. When you reassess the patient, you note that she has an altered mental status and her blood pressure is 72/40 mmHg.

Unhealthy healthy patients

One of the first steps in any ED evaluation is differentiating between those patients who are sick and those who are not sick. While a lifetime of patient care can make this a subconscious decision for most emergency providers, the process is still subjective. Criteria, algorithms, and/or clinical decision tools exist for many scenarios, but not all. It is especially difficult for clinicians to determine the severity of an illness in an otherwise young healthy patient with non-specific symptoms.

Among every group of nonspecific presentations is a new (or overlooked) diagnosis that, if missed, can seriously harm or even kill a patient. The goal of training and lifetime learning is for emergency physicians to become experts at teasing out those who are covertly sick. Several of the conditions discussed below can easily be overlooked because they may present, at least initially, with non-concerning symptoms. However, they have the ability to cause serious harm.

Acute Adrenal Insufficiency (Adrenal Crisis)

Background

Adrenal insufficiency is divided into three categories: primary, secondary, and tertiary.1  Primary disease is due to intrinsic problem(s) with the adrenal cortex, while secondary adrenal insufficiency is due to pituitary failure or a lack of responsiveness of the adrenal glands to adrenocorticotropic hormone (ACTH). Tertiary adrenal insufficiency is due to the impaired hypothalamic production or action of ACTH, vasopressin or both.1

Adrenal crisis can occur as an exacerbation of any chronic cause of adrenal insufficiency, or as an abrupt injury to any component of a healthy adrenal axis.  Common causes include abrupt cessation of exogenous glucocorticoid use, bilateral adrenal infarction/hemorrhage, or acute stress in the setting of previously undiagnosed chronic adrenal insufficiency.2

How it presents

Acute adrenal insufficiency can present with hypotension, abdominal pain and/or rigidity, nausea, vomiting, and fever due to coexisting infection.  Hyperpigmentation may be a feature of those with chronic adrenal insufficiency.  A history of chronic fatigue or abrupt cessation of chronic glucocorticoid use could be present depending on the etiology.2

Why the diagnosis can be challenging

Acute adrenal insufficiency is rare. The risk of developing acute adrenal insufficiency in a patient with chronic adrenal insufficiency is about 6-10 per 100 patient-years.3  It can also be easily overlooked as a diagnosis early on in a patient’s presentation.  Furthermore, endocrine causes of hemodynamic instability are not generally considered to be one of the four main categories of shock (obstructive, cardiogenic, distributive, and hypovolemic).  These factors can delay diagnosis and lead to worsening crisis before appropriate treatment is initiated.

How to catch it

A more thorough history can be key in identifying the right track for the emergency physician. Routine laboratory analysis often reveals hyperkalemia and hyponatremia.2 Patients in adrenal crisis face significant morbidity and mortality. Immediate treatment with fluid resuscitation and steroid replacement (dexamethasone 4-10 mg IV when no prior diagnosis exists4, otherwise hydrocortisone 100 mg IV or IM, with 100-300 mg every day thereafter for the duration of treatment2) is necessary before receiving confirmatory diagnostic tests in patients who are at risk.2

Other pearls

Cessation of inhaled glucocorticoids can precipitate acute adrenal insufficiency.5

Acute Pancreatitis

Background

A condition involving inflammation, and often hemorrhagic necrosis, of the pancreatic parenchyma. Several causes exist but gallstone obstruction of the pancreatic duct, metabolic/hereditary disorders, and alcohol use most commonly underlie this painful condition6.  In necrotizing pancreatitis, mortality can be as high as 17%.7 Severe cases can lead to marked hypotension and end-organ failure.6

How it presents

About 50% of the time, patients present with severe, persistent epigastric pain radiating to the back.8 Pain is usually associated with severe nausea and vomiting.6

Why the diagnosis can be challenging

The differential diagnosis for patients with abdominal pain is, unfortunately, very broad.  Epigastric pain could be the manifestation of intra-abdominal, cardiac, or intra-thoracic processes. In addition, pancreatitis due to alcohol or metabolic disorders can have a more gradual onset with poor localization of pain.  Degree of pain is also variable, and some patients may not be as uncomfortable as others.  In a patient who is otherwise healthy, and who presents with gradual onset, localized and unimpressive epigastric pain, acute pancreatitis could easily be missed.

How to catch it

Keeping broad differential diagnoses for patients with abdominal pain is key.  Consider abdominal computed tomography (CT) for lipase (+/ amylase) levels that are only mildly elevated, or with atypical presentations not otherwise explainable.

Other pearls

Acute pancreatitis on ultrasound appears enlarged and heterogeneous.  Hypoechoic fluid may be visualized, as well as gallstones in the gallbladder or common bile duct.9

Arrhythmia

Background

Abnormal cardiac rhythms vary in pathophysiology, appearance on electrocardiogram (ECG), and lethality.  They can range from benign ectopic beats (like PVCs) to very dangerous (like atrial fibrillation in patients with Wolff-Parkinson-White).

How it presents

Presenting symptoms are variable and can include palpitations, anxiety, syncope, dizziness, chest pain, and shortness of breath.

Why the diagnosis can be challenging

The difficulty is not in obtaining the ECG but instead the interpretation. Outside of the overt arrhythmia, ECG signs of channelopathy or structural abnormality in asymptomatic patients can easily be overlooked.

 How to catch it

Key features on ECG for high-risk syndromes include:

  • Long QT interval: A sign of the aptly named Long QT Syndrome. It can be congenital or can be acquired in the setting of electrolyte abnormalities or certain pharmacologic agents.  A long QT interval puts patients at risk for sudden cardiac death due to Torsades de pointes.10
  • Delta wave: Classic for Wolff-Parkinson-White syndrome. The “slurring” of the R wave is a sign of an accessory pathway, which can lead to an unstable tachycardia (rate often greater than 200), cardiovascular instability and death.11
  • Q waves, atrial enlargement, left axis deviation, inverted T waves: In a young, healthy patient, any of these could be a sign of hypertrophic cardiomyopathy. Look for signs of structural changes, such as P wave abnormalities suggesting atrial enlargement.  Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in young athletes.12
  • Pseudo-right bundle branch block and ST elevation in V1 and V2: Suggestive of Brugada syndrome, a sodium channelopathy. ST elevation can be divided into two patterns: type 1 features a convex, descending ST segment followed by an inverted T-wave, and type 2 features a “saddle-back” ST-T morphology.  A third type exists involving the criteria of Type 1 & 2 but with < 2 mm of elevation. Brugada syndrome predisposes patients to sudden-onset ventricular tachyarrhythmias.13

Other pearls

Often genetic, but not always, a family history is very helpful for assessing risk for different arrhythmias.

Substance Abuse

Background

Overdoses and withdrawal are an increasingly large burden on emergency medical service (EMS) providers and emergency departments as newly synthesized illicit drugs are abused and opioid addiction across the United States grows.14

How it presents

Signs and symptoms of overdose or withdrawal depends on the substance in question.  Some common examples include:

  • Opioids
    • Intoxication: Respiratory depression, altered mental status, bradycardia, miotic pupils.15,16
    • Withdrawal: Dysphoria, restlessness, myalgias/arthralgias, nausea, vomiting, tachycardia, diarrhea.16
  • Cocaine
    • Intoxication: Hypertension, tachycardia, mydriatic pupils, agitation.16,17
    • Withdrawal: Depression/anxiety, fatigue, anhedonia, increased sleep.18
  • Amphetamines
    • Intoxication: agitation/psychosis, tachycardia, hypertension, mydriatic pupils, diaphoresis.19
    • Withdrawal: dysphoria, fatigue, increased sleep, anxiety.18,19
  • Phencyclidine (PCP)
    • Intoxication: Hypertension, hallucinations, nystagmus, tachycardia, agitation.20
    • Withdrawal: Confusion, anxiety, depression, memory loss.19
  • Alcohol
    • Intoxication: Slurred speech, nystagmus, unsteady gait, nystagmus, disinhibition.21
    • Withdrawal: Insomnia, tremulousness, hallucinations, headache, diaphoresis, seizures, delirium tremens.22,23

 Why the diagnosis can be challenging

Intoxication or overdose from alcohol or drugs can be easy to diagnose with sufficient history.  Otherwise, an acutely altered patient with little available history can be a diagnostic challenge. Additional conditions can also be overlooked in the patients – head trauma following opiate and alcohol abuse, myocardial infarction with cocaine intoxication, or delirium tremens in a patient with no known history of alcohol abuse.

 How to catch it

Whenever possible, accurately identify the substance in question in order to prepare for potentially dangerous sequelae.  Try to keep a wide differential in patients who are altered or agitated.

 Other pearls

Remember to ask about alcohol, tobacco, and drug use in all patients.

Crush Injury

Background

The development of rhabdomyolysis and acute kidney injury in the setting of a crush injury is well-known. A more severe results of crush injury can occur in disaster victims who become trapped in fallen structures. In this case, these victims can often become hypotensive following extrication due to third-spacing of fluids into the freed crushed tissue. Thus, compartment pressures should be monitored closely in these patients.24,25

 How it presents

Providers in the field will most often encounter hypotensive patients following a crush injury.  However, providers in the ED should be aware of this possibility when caring for victims of natural or man-made disasters.

 Why the diagnosis can be challenging

Providers in the field must be aware of the dangers of crush injuries beyond the direct trauma to limbs.  If an IV is not placed and fluids not started before extrication, deterioration should be an ongoing concern. Additionally, it is possible that a provider in the emergency department setting could be unaware of a crush injury in a hypotensive trauma patient, prompting him or her to look for other causes of hypotension.

 How to catch it

When dealing with entrapped victims, an IV line and fluids should be started before extrication whenever possible.  This can prevent post-extrication hypotension as well as ameliorate the potential for acute kidney injury (AKI).25

 Other pearls

Bicarbonate and mannitol (1 amp and 10 g IV, respectively, during extrication) can be used to avoid AKI following crush injury.24

Heat Illness

Background

Heat illness is considered a failure of the body’s thermoregulatory system to handle intrinsic and extrinsic heat. It can be further classified based on signs and symptoms. Syncope, muscle cramps, heat exhaustion are all part of the spectrum of heat related illness, with heat stroke having the highest rates of morbidity and mortality.26

How it presents

Heat illness can affect populations of all ages, from very young to very old. Typically, younger patients present following a period of exertion.  Any rectal temperature greater than 104° Fahrenheit (F) with mental status changes necessitates active cooling. For patients with a temperature less than 104° but still greater than 98.6°, active cooling (ice water immersion, cooling mattress, etc) should seriously be considered. Passive cooling (removing the patient from the warm environment, getting rid of wet clothing, and hydration) is still a must. Rechecking a rectal temperature to ensure improvement is also necessary as some patients can continue increasing early on before passive methods have taken effect.

Why the diagnosis can be challenging

Older patients often present with heat illness without any preceding exertion. Often left unattended in the heat as well as additional medications complicating the diagnosis, these patients present with little to no history to direct your evaluation and treatment. Additionally, these patients can suffer from secondary electrolyte and cardiovascular complications. 26

How to catch it

Obtaining a rectal temperature is the gold standard when evaluating patients for heat illness. Keep heat illness in your list of differential diagnoses, especially when working on days with high heat indices or an endurance event nearby.

Other pearls

Ice packs in the axillae and groin as well as evaporative cooling with misting and a fan are the most feasible cooling options in the ED. Cold water immersion is the gold-standard when working events. Goal rate for cooling is 1° (F) every 3 minutes.  Antipyretics are not useful for decreasing temperature in these patients.27,28

“Vitals are vital” and “Keep your differential broad”

Providers have heard these phrases repeated since beginning medical school, and nowhere are they more applicable than when dealing with young healthy patients.

Abnormal vital signs need to be explained within the clinical context.  Hydration status can be an easy go-to for tachycardia but anchoring can lead you down the wrong diagnosis and treatment pathways if other alternative causes are not considered. In the case at the start of this post, symptomatic hypotension and an unclear medication history are key red flags that should not be overlooked.

Finally, when a patient does not respond as you expect (improved heart rate with IV fluids, decreased pain with medication, etc.) emergency providers should step back and re-evaluate. Make sure you have considered all life threatening diagnoses and that you have adequately evaluated patients for these diagnoses. Not every potential diagnosis needs to be tested for. However, considering the diagnosis is important because it helps avoid bias and potentially, missed diagnoses.

Pearls

Address abnormal vital signs or have a cohesive explanation as to why you are not addressing them.

Abnormal vital signs without a clear explanation, as well as vital signs that do not resolve with treatment, should prompt expanded consideration of the patient’s complaint, further investigation, and likely both.

-Bad things happen and even healthy people get sick.

References / Further Reading

1Charmandari E, Nicolaides NC, Chrousos GP. Adrenal insufficiency. The Lancet. 2014;383(9935):2152-2167.

2Puar TH, Stikkelbroeck NM, Smans LC, Zelissen PM, Hermus AR. Adrenal Crisis: Still a Deadly Event in the 21st Century. The American Journal of Medicine. 2016;129(3).

3Arlt W, Allolio B. Adrenal insufficiency. The Lancet. 2003;361(9372):1881-1893.

4Asare K. Diagnosis and Treatment of Adrenal Insufficiency in the Critically Ill Patient. Pharmacotherapy. 2007;27(11):1512-1528.

5Piédrola G, Casado JL, López E, Moreno A, Perez-Elías MJ, García-Robles R. Clinical features of adrenal insufficiency in patients with acquired immunodeficiency syndrome. Clinical Endocrinology. 1996;45(1):97-101.

6Lankisch PG, Apte M, Banks PA. Acute pancreatitis. The Lancet. 2015;386(9988):85-96.

7Banks PA, Freeman ML. Practice Guidelines in Acute Pancreatitis. The American Journal of Gastroenterology. 2006;101(10):2379-2400.

8Banks PA. Acute pancreatitis: Diagnosis. In: Pancreatitis, Lankisch PG, Banks PA (Eds), Springer-Verlag, New York 1998. p.75.

9Bollen TL, Santvoort HCV, Besselink MG, Es WHV, Gooszen HG, Leeuwen MSV. Update on Acute Pancreatitis: Ultrasound, Computed Tomography, and Magnetic Resonance Imaging Features. Seminars in Ultrasound, CT and MRI. 2007;28(5):371-383.

10Khan IA. Long QT syndrome: Diagnosis and management. American Heart Journal. 2002;143(1):7-14.

11Bhatia A, Sra J, Akhtar M. Preexcitation Syndromes. Current Problems in Cardiology. 2016;41(3):99-137.

12Elliott P, Mckenna WJ. Hypertrophic cardiomyopathy. The Lancet. 2004;363(9424):1881-1891.

13Littmann L, Monroe MH, Kerns WP 2nd, Svenson RH, Gallagher JJ. Brugada syndrome and “Brugada sign”: clinical spectrum with a guide for the clinician.  Am Heart J. 2003 May; 145(5):768-78.

14Rudd RA, Aleshire N, Zibbell JE, Gladden RM. Increases in Drug and Opioid Overdose Deaths — United States, 2000–2014. MMWR Morbidity and Mortality Weekly Report. 2016;64(50-51):1378-1382.

15Sporer KA. Acute Heroin Overdose. Annals of Internal Medicine. 1999;130(7):584.

16Hughes JR, Higgins ST, Bickel WK. Nicotine withdrawal versus other drug withdrawal syndromes: similarities and dissimilarities. Addiction. 1994;89(11):1461-1470.

17Merigian KS, Roberts JR. Cocaine Intoxication: Hyperpyrexia, Rhabdomyolysis and Acute Renal Failure. Journal of Toxicology: Clinical Toxicology. 1987;25(1-2):135-148.

18Lago JA, Kosten TR. Stimulant withdrawal. Addiction. 1994;89(11):1477-1481.

19Khantzian EJ. Acute Toxic and Withdrawal Reactions Associated with Drug Use and Abuse. Annals of Internal Medicine. 1979;90(3):361.

20Mccarron MM, Schulze BW, Thompson GA, Conder MC, Goetz WA. Acute phencyclidine intoxication: Incidence of clinical findings in 1,000 cases. Annals of Emergency Medicine. 1981;10(5):237-242.

21Camí J, Farré M. Drug Addiction. New England Journal of Medicine. 2003;349(10):975-986.

22Etherington JM. Emergency management of acute alcohol problems Part 1: Uncomplicated withdrawal. Canadian Family Physician. 1996;42:2186-2190.

23Ferguson JA, Suelzer CJ, Eckert GJ, Zhou X-H, Diffus RS. Risk factors for delirium tremens development. Journal of General Internal Medicine. 1996;11(7):410-414.

24Gonzalez D. Crush syndrome. Crit Care Med. 2005 Jan;33(1 Suppl):S34-41.

25Sever MS, Vanholder R, Lameire N. Management of Crush-Related Injuries after Disasters. New England Journal of Medicine. 2006;354(10):1052-1063.

26Leon LR, Bouchama A. Heat Stroke. Comprehensive Physiology. March 2015:611-647.

27Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 2007;11(3):R54

28Smith JE.  Cooling methods used in the treatment of exertional heat illness. Br J Sports Med. 2005;39:503-7.

A Myth Revisited: Epinephrine for Cardiac Arrest

Author: Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

 You receive a radio call from an EMS unit. They are transporting a 61-year-old male who collapsed approximately 5 minutes ago. He is currently in ventricular fibrillation, and the EMS crew is actively doing compressions. They have obtained IV access, defibrillated the patient once, given 1mg epinephrine IV, and are actively bagging the patient. The patient arrives, and you take over the resuscitation. Your partner cleanly intubates the patient while chest compressions are ongoing. The patient receives another defibrillation, and compressions resume. Should the patient receive more epinephrine? What’s the evidence behind its use?

Sudden cardiac arrest accounts for over 450,000 deaths per year in the U.S., with 15% of total deaths due to arrest.1-4 Close to half are out-of-hospital, with poor survival rate (7-9%).1-5

A prior emdocs.net post evaluated epinephrine use in cardiac arrest. Please see this at: http://www.emdocs.net/epinephrine-cardiac-arrest/. Epinephrine is a staple of the AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Updated guidelines were released in 2015, building on a “Chain of Survival”: recognition and activation of emergency response system, immediate high-quality cardiopulmonary resuscitation (CPR), rapid defibrillation, basic and advanced emergency medical services, and advanced life support and post arrest care including advanced cardiac life support (ACLS) for out-of-hospital cardiac arrest (OHCA).7,8 ACLS is considered the standard of care in cardiac arrest, though some argue a lack of evidence.

For more information on the updated guidelines, see http://eccguidelines.heart.org/wp-content/uploads/2015/10/2015-AHA-Guidelines-Highlights-English.pdf, https://emergencymedicinecases.com/acls-guidelines-2015-cardiac-arrest/, https://first10em.com/2015/10/21/acls-2015/, http://rebelem.com/rebel-cast-wee-our-top-5-aha-2015-guideline-updates-for-cpr-and-ecc/.

The Myth: Epinephrine improves patient survival and neurologic outcome in cardiac arrest.

Is this important?

A class IIb recommendation from the AHA states “standard dose epinephrine may be reasonable for patients with cardiac arrest” in the 2015 updates, with doses of 1mg of 1:10,000 epinephrine every 3-5 minutes intravenously.7 Epinephrine has alpha and beta adrenergic effects, which are thought to improve coronary perfusion pressure, though the effect on cerebral perfusion is controversial (and may worsen cerebral perfusion).

The recommendation for epinephrine is based on studies in the 1960s, which found epinephrine given to asphyxiated dogs improved survival.9 The alpha-adrenergic effects improved coronary perfusion in these dogs, with some benefit in survival.

If some is good, is more better? High dose epinephrine was assumed to be better, with several studies finding increased ROSC and survival to hospital admission, but no improvement in survival to hospital discharge or neurologic recovery.10-14 Studies suggest worse survival to hospital discharge and neurologic recovery with higher doses of epinephrine.7,15-20

What about standard dose epinephrine?  Studies suggest improvement in ROSC, but worse neurologic and survival to discharge. Why? The beta agonism provided by epinephrine increases myocardial work, increases tachydysrhythmias, promotes thrombogenesis and platelet activation, and reduces microvascular perfusion (including the brain).7,15

Now down to the nuts and bolts: the evidence on epinephrine…

Table 1 shows the studies on epinephrine. A study in 2011 evaluated over 600 patients with OHCA (one of the few randomized trials).16 Improved likelihood of ROSC, 24% in the epinephrine group versus 8%, with an odds ratio (OR) of 3.4 (95% CI 2.0-5.6) was found. Patients demonstrated no improvement in survival to hospital discharge.16 Ong et al. in 2007 found no difference in survival to discharge, survival to admission, or ROSC with epinephrine versus no epinephrine.17

Nakahara et al. conducted a retrospective study comparing epinephrine versus no epinephrine for patients with ventricular fibrillation, PEA, or asystole.18 Higher overall survival with epinephrine (17.0% vs 13.4%) was found, but not neurologically intact survival.18 Hagihara et al. conducted a prospective non-randomized analysis of over 400,000 patients and found an increase in ROSC with epinephrine (adjusted odds ratio 2.36), but no increase in survival or functional outcome.19 As discussed, ROSC occurred in the epinephrine group at higher rate (18.5% vs. 5.7%), but patients receiving epinephrine had lower survival at one month and worse neurologic outcome.19

One study found those with initially shockable rhythm demonstrated worse outcomes if they receive epinephrine for prehospital ROSC, survival at one month, and neurologic outcome at one month.20 A Swedish study found patients receiving epinephrine experience lower survival, with OR 0.30 (95% CI 0.07-0.82).21

How about BLS compared with ACLS?

ACLS measures include epinephrine, as compared with BLS focusing on optimizing compressions. Stiell et al. in 2004 analyzed 1,400 patients before use of ACLS measures, followed by 4,300 patients after ACLS was implemented.22 Admission rate increased by 3.7% (10.9% to 14.6%), but survival to discharge did not change.  Survivor neurologic status worsened after ACLS implementation (78.3% versus 66.8%).22  Olasveengen et al. evaluated ACLS with and without epinephrine, finding a 40% rate of ROSC in the group receiving epinephrine, versus 25% in the group receiving no epinephrine.23 Survival to discharge and neurologic outcomes were similar, though the epinephrine group had higher hospital admission rates.23  Sanghavi et al. compared BLS and ACLS in an observational cohort study.24 BLS patients had higher survival to hospital discharge (13.1% versus 9.2%), improved survival to 90 days, and better neurologic function.24

Table 1 – Studies evaluating epinephrine16-24

Study Outcome Odds Ratio (95% CI)
Holmberg et al. Survival decrease with epinephrine Survival 0.43 (0.27-.066) for shockable, 0.30 (0.07-0.82) for non-shockable rhythms
Stiell et al. Improved ROSC, no difference in survival to discharge Survival to discharge 1.1 (0.8-1.5)
Ong et al. No difference in ROSC or survival to discharge ROSC 0.9 (0.6-4.5), survival to discharge 1.7 (0.6-4.5)
Olasveengen et al. Improved ROSC, No difference in survival to discharge Survival to discharge 1.15 (0.69-1.91)
Jacobs et al. Improved ROSC, No difference in survival to discharge ROSC 3.4 (2.0-5.6), Survival to discharge 2.2 (0.7-6.3)
Hagihara et al. Improved ROSC, Worse survival and functional outcome ROSC 2.35 (2.22-2.5), Survival 0.46 (0.42-0.51), Functional outcome 0.31-0.32 (0.26-0.38)
Nakahara et al. No difference in neurologic outcome or total survival Neurologic outcome 1.01 (0.78-1.30) for shockable and 1.57 (1.04-2.37) for nonshockable rhythms; Total survival 1.34 (1.12-1.60) for shockable and 1.72 (1.45-2.05) for nonshockable rhythms
Sanghavi et al. No epinephrine associated with improved neurologic outcome, survival to discharge, and total survival Improved neurologic outcome 23.0 (18.6-27.4) for no epinephrine, Survival to discharge 4.0 (2.3-5.7) for no epinephrine, Total survival 2.6 (1.2-4.0) for no epinephrine

The Bottom Line: Epinephrine can increase ROSC, but it does not improve survival to hospital discharge or neurological improvement and may worsen these outcomes.

How does this change practice? Epinephrine is a significant component of the AHA guidelines, despite the controversial literature. A role may exist for epinephrine, though further study is required. Studies suggest three phases (electrical, circulatory, and metabolic) are present in cardiac arrest.25 The electrical phase needs rapid defibrillation and compressions.15,25 The circulatory phase (within 10 minutes of arrest) focuses on perfusion, where epinephrine may improve cardiac perfusion. Epinephrine during the final metabolic phase (greater than 10 minutes after arrest) can impair oxygen utilization, increase oxygen demand and ischemia, cause dysrhythmia, increase clotting, and increase lactate.15,25

The timing and total dose of epinephrine can impact patient outcome.7,15,25-27 A study by Dumas et al. suggests timing of first administration and total epinephrine given impacts survival (with less epinephrine given related to improved outcome).25 This study found that 17% of patients in the group receiving epinephrine demonstrated a good outcome defined by “favorable discharge outcome coded by Cerebral Performance Category,” compared to 63% not receiving epinephrine. However, in this study patients with a shockable rhythm, patients receiving 1mg epinephrine, and patients receiving epinephrine less than 9 minutes after arrest demonstrate the best outcomes, not impacted by the total time of resuscitation. Patients receiving late or multiple doses of epinephrine have decreased neurologic survival.25

Table 2 – Epinephrine Dosing Outcomes25

Treatment Adjusted OR (95% CI)
Time to Epinephrine Dose

< 9 min

10-15 min

16-22 min

> 22 min

 

0.54 (0.32-0.91)

0.33 (0.20-0.56)

0.23 (0.12-0.43)

0.17 (0.09-0.34)

Total Epinephrine Dose

1 mg

2-5 mg

> 5 mg

 

0.48 (0.27-0.84)

0.30 (0.20-0.47)

0.23 (0.14-0.37)

Epinephrine within 10 minutes of arrest may provide the most benefit. Koscik et al. found earlier provision of epinephrine improved ROSC, from 21.5% to 48.6% (OR 3.45).26 Nakahara et al. compared early epinephrine in OHCA (within 10 minutes of arrest), finding early epinephrine was associated with survival (OR 1.73, 95% CI 1.46-2.04) and improved neurologic outcome (OR 1.39, 95% CI 1.08-1.78).27 However, there is potential harm with epinephrine within the first two minutes of arrest.27 Anderson et al. compared epinephrine before or after the second defibrillation attempt.28 Patients receiving epinephrine before the second defibrillation demonstrated decreased survival (OR 0.70), decreased functional outcome (OR 0.69), and decreased ROSC (OR 0.71). This study suggests epinephrine within the first two minutes after arrest can be harmful, and they recommend epinephrine should be given after the second defibrillation.27

Some support targeting coronary perfusion pressure (CPP), or the aortic to right atrial pressure gradient during the relaxation phase of CPR. Targeting coronary perfusion pressure is supported by several animal studies.29,30 CPP levels > 15 mm Hg demonstrate greater likelihood of ROSC.31 Epinephrine is most commonly used to maintain CPP levels with compressions. However, this needs further study and requires the use of invasive monitoring.25,31

What improves outcomes?

Components that improve outcomes include witnessed arrest, witnessed by EMS, bystander CPR, shockable rhythm (VF/VT), early defibrillation, minimal interruptions to CPR, automated external AED use, and therapeutic hypothermia in comatose cardiac arrest patients.7,15,32 Optimal chest compressions and early defibrillation if warranted are essential.7 Emergency PCI is recommended for all patients with STEMI and for hemodynamically unstable patients without ST elevation infarction if a cardiovascular lesion is suspected. Targeted temperature management between 32oC and 36oC is acceptable for comatose patients with ROSC.7 The 2015 recommendations for BLS measures are shown below. 7,32

2015 Guideline Recommendations for Compressions
-Perform compressions at rate 100-120 per minute

-Perform compressions at depth of 5-6 cm (at least 2 inches), but not more than 6 cm (2.4 in)

-Rescuers should allow full chest wall recoil and avoid leaning on the chest between compressions

-Rescuers should minimize the frequency and duration of intervals between compressions

-Audiovisual devices and compression depth analyzers can be used to optimize CPR quality

Bottom Line: The most important aspect of care in cardiac arrest is basic life support measures with compressions and early defibrillation.

 

Takeaways:

– 2015 AHA Guidelines state epinephrine is reasonable to give for patients in cardiac arrest.

– Recommendations are based on studies with asphyxiated dogs in the 1960s.

High dose epinephrine is harmful and is not advised.

– Epinephrine can increase ROSC, but it may worsen neurologic outcome and survival upon discharge.

– Epinephrine may provide the greatest benefit if given within 10 minutes of arrest (though it may be harmful if given before 2 minutes).

BLS measures with optimal compressions and early defibrillation are essential!

 

References / Further Reading

  1. Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation 2001; 104:2158.
  2. Rea TD, Pearce RM, Raghunathan TE, et al. Incidence of out-of-hospital cardiac arrest. Am J Cardiol 2004; 93:1455.
  3. Centers for Disease Control and Prevention (CDC). State-specific mortality from sudden cardiac death–United States, 1999. MMWR Morb Mortal Wkly Rep 2002; 51:123.
  4. Chugh SS, Jui J, Gunson K, et al. Current burden of sudden cardiac death: multiple source surveillance versus retrospective death certificate-based review in a large U.S. community. J Am Coll Cardio 2004;44:1268.
  5. Kuller LH. Sudden death–definition and epidemiologic considerations. Prog Cardiovasc Dis 1980; 23:1.
  6. Gillum RF. Sudden coronary death in the United States: 1980-1985. Circulation 1989; 79:756.
  7. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132:S444-S464.
  8. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(Suppl 3):S729-67.
  9. Callaham M. Evidence in support of a back-to-basics approach in out-of-hospital cardiopulmonary resuscitation vs. “advanced treatment.” JAMA Intern Med. 2015;175:205-206.
  10. Stiell IG, Hebert PC, Weitzman BN, et al. High-dose epinephrine in adult cardiac arrest. N Engl J Med. 1992;327:1045-1050.
  11. Brown CG, Martin DR, Pepe PE, et al. A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group. N Engl J Med. 1992;327:1051-1055.
  12. Rivers EP, Wortsman J, Rady MY, et al. The effect of total cumulative epinephrine dose administered during human CPR on hemodynamic, oxygen transport, and utilization variables in the postresuscitation period. Chest. 1994;106:1499-1507.
  13. Behringer W, Kittler H, Sterz F, et al. Cumulative epinephrine dose during cardiopulmonary resuscitation and neurologic outcome. Ann Intern Med. 1998;129:450-456.
  14. Guegniaud PY, Mols P, Goldstein P, et al. A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. N Engl J Med. 1998;339:1595-1601.
  15. Callaway CW. Questioning the use of epinephrine to treat cardiac arrest. JAMA. 2012;307:1198-1199.
  16. Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011 Sep;82(9):1138-43.
  17. Ong ME, Tan EH, Ng FS, Panchalingham A, Lim SH, Manning PG, et al. Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest. Ann Emerg Med. 2007 Dec;50(6):635-42.
  18. Nakahara S, Tomio J, Takahashi H, et al. Evaluation of pre-hospital administration of adrenaline (epinephrine) by emergency medical services for patients with out of hospital cardiac arrest in Japan: controlled propensity matched retrospective cohort study. The BMJ. 2013;347:f6829. doi:10.1136/bmj.f6829.
  19. Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA. 2012 Mar 21;307(11):1161-8. doi: 10.1001/jama.2012.294.
  20. Goto Y, Maeda T, Goto YN. Effects of prehospital epinephrine during out-of-hospital cardiac arrest with initial non-shockable rhythm: an observational cohort study. Critical Care. 2013;17(5):R188. doi:10.1186/cc12872.
  21. Holmberg M, Holmberg S, Herlitz J. Low chance of survival among patients requiring adrenaline (epinephrine) or intubation after out-of-hospital cardiac arrest in Sweden. Resuscitation. 2002 Jul;54(1):37-45.
  22. Stiell IG, Wells GA, Field B, Spaite DW, Nesbitt LP, De Maio VJ, Nichol G, Cousineau D, Blackburn J, Munkley D, Luinstra-Toohey L, Campeau T, Dagnone E, Lyver M; Ontario Prehospital Advanced Life Support Study Group. Advanced cardiac life support in out-of-hospital cardiac arrest. N Engl J Med. 2004 Aug 12;351(7):647-56.
  23. Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L. Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. JAMA. 2009 Nov 25;302(20):2222-9.
  24. Sanghavi P, Jena AB, Newhouse JP, Zaslavsky AM. Outcomes After Out-of-Hospital Cardiac Arrest Treated by Basic vs Advanced Life Support. JAMA Intern Med 2015;175(2):196-204.
  25. Dumas F, Bougouin W, Geri G, Lamhaut L, Bougle A, Daviaud F, et al. Is epinephrine during cardiac arrest associated with worse outcomes in resuscitated patients? J Am Coll Cardiol. 2014; 64(22):2360–7.
  26. Koscik C, Pinawin A, McGovern H, Allen D, Media DE, Ferguson T, Hopkins W, Sawyer KN, Boura J, Swor R. Rapid epinephrine administration improves early outcomes in out-of-hospital cardiac arrest. Resuscitation. 2013 Jul;84(7):915-20.
  27. Nakahara S, Tomio J, Nishida M, Morimura N, Ichikawa M, Sakamoto T. Association between timing of epinephrine administration and intact neurologic survival following out-of-hospital cardiac arrest in Japan: a population-based prospective observational study. Acad Emerg Med. 2012 Jul;19(7):782-92.
  28. Andersen LW, Kurth T, Chase M, et al. Early administration of epinephrine (adrenaline) in patients with cardiac arrest with initial shockable rhythm in hospital: propensity score matched analysis. BMJ 2016; 353:i1577.
  29. Friess SH, Sutton RM, French B, et al. Hemodynamic Directed CPR Improves Cerebral Perfusion Pressure and Brain Tissue Oxygenation. Resuscitation. 2014;85(9):1298-1303.
  30. Sutton RM, Friess SH, Naim MY, et al. Patient-centric Blood Pressure–targeted Cardiopulmonary Resuscitation Improves Survival from Cardiac Arrest. American Journal of Respiratory and Critical Care Medicine. 2014;190(11):1255-1262.
  31. Paradis NA, Martin GB, Rivers EP, et al. Coronary Perfusion Pressure and the Return of Spontaneous Circulation in Human Cardiopulmonary Resuscitation. JAMA. 1990;263(8):1106-1113.
  32. Sasson C, Rogers MA, Dahl J, Kellermann AL. Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2010 Jan;3(1):63-81.

GI Bleeds: Who Needs ICU Level Care?

Authors: Christina Thorngren, MD, MPH and Janna Welch, MD (University of Texas Dell School of Medicine Emergency Medicine Residency Program) // Edited by: Erica Simon, DO, MHA (@E_M_Simon), Brit Long, MD (@long_brit ), and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

It’s a busy Saturday night in the ED. Scanning the patient tracking board, you come across an ESI 2: A 55 year-old woman with a chief complaint of generalized weakness. The nursing note details a review of systems positive for epigastric abdominal pain and black stools of one week duration. VS: HR 110, BP 105/64. As the patient rolls by in a wheelchair, you note her impressive pallor. After offering a quick greeting, placing her on the monitor, and dropping orders, you make your way to the clerk’s desk to notify him of an anticipated admission. As the clerk makes inquires regarding the required bed, your focus shifts to the patient: is she stable enough for the ward or does she require ICU level care?

If you’ve had a similar inner monologue while treating a GI bleed, the discussion below offers a number of tools to aid in your clinical decision-making.

Introduction

Developing a clinical gestalt regarding a patient with a gastrointestinal bleed (GIB) can be challenging even for the seasoned emergency medicine physician. Anecdotally, we’ve all heard of the hemodynamically stable patient with one bloody bowel movement prior to arrival that acutely decompensates in the ED. While the decision to admit these patients to the ward versus the ICU may be clear in the setting of unstable VS or post endotracheal intubation, there are often times when we encounter shades of gray. The following discussion will hopefully shed some light on topic, and offer a quick discussion of risk stratification methods for EM physicians to utilize when addressing upper and lower GI bleeds.

Upper GIB

An upper GIB is defined as bleeding from a source proximal to the ligament of Treitz.1 Etiologies of upper GIBs include esophageal varices, peptic ulcers, gastritis, Mallory-Weiss tears, arteriovenous malformations, and rarely, Dieulafoy lesions (large diameter, tortuous vessels, protruding through the submucosa of the GI tract).2 Collectively, the annual incidence of upper GI bleeds is 48-180 cases per 100,000 adults, with a mortality ranging from 10-14%.1   Nearly 80% of upper GIBs resolve spontaneously, while 20% require acute intervention.1 Several studies have identified severe gastrointestinal bleeding (GI bleeding resulting in shock, or a decrease in hematocrit of ≥ 6% from baseline) as possessing a mortality rate of nearly 39%.1

While it is clear that patients with severe GI bleeds require inpatient admission, are there methods to determine when it is appropriate to discharge hemodynamically stable patients for outpatient follow-up?

Current literature cites the following scores for use in the mortality risk stratification of upper GIBs: the Clinical Rockall Risk Score,3 the Modified Glasgow-Blatchford Score,4,5 the AIMS65 Score,6 and the PNED Score.7,8 While these scores were initially developed to assess inpatient mortality in the setting of upper GIBs, secondary outcomes included risk for re-bleeds and 30 day mortality, making them useful tools for the emergency physician.3

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Is one of these methods superior to the others? Let’s quickly discuss the statistical method of comparison:

The utility of a scoring systems is determined by calculating the area under the receiver operating curve (AUROC). An AUROC of 1 is a perfect test that when employed, will accurately and precisely predict an outcome 100% of the time. In contrast, an AUROC of 0.5 is of little utility as it precisely and accurately predicts an outcome 50% of the time (i.e. – no better than flipping a coin).

Ideally, to assess the risk stratification methods detailed above, all scores would be applied to one cohort of patients, and the AUROC calculated and compared. To date, there have been no studies performed which directly compare the Clinical Rockall Risk Score, the Modified Glasgow-Blatchford Score, the AIMS65 Score, and the PNED Score. Of the research published:

  • In 2012, Cheng, et al.5 compared the Modified Glasgow-Blatchford Score and the Clinical Rockall Score as applied to 167 patients presenting with GIBs (study endpoint: in-hospital mortality or re-bleeding). An AUROCs of 0.85 (CI 0.72-0.98) for the Modified Glasgow-Blatchford Score, and 0.59 (CI 0.32-0.87) for the Clinical Rockall Risk Score (p <0.0022) was identified.
  • Marmo, et al.8performed a head-to-head comparison of the PNED score and Clinical Rockall Score in 1360 patients (end point: in-hospital mortality) and found respective AUROCs of 0.81 (CI 0.70-0.90) for PNED, and 0.66 (CI 0.6-0.72) for the Clinical Rockall Score (p-value of <0.000).
  • In 2016, Aubougergi et al.6 performed a comparison of the AIMS65 and the Modified Glasgow-Blatchford Score in 298 patients (endpoint: inpatient mortality), identifying an AUROC of 0.85 (CI 0.81-0.89) for AIMS65 and 0.66 (CI 0.61-0.72) for Modified Glasgow-Blatchford Score (p of <0.01).

While it is unclear which mortality stratification method is most appropriate for use by the emergency physician, it is safe to say that the higher the mortality risk as characterized by these scores, the greater the necessity for advanced levels of patient care.

Have any of these scores been directly assessed for utility in predicting the need for ICU admission?

Of the mortality risk stratification scores above, only the Clinical Rockall Score has been evaluated for its utility in determining the requirement for ICU-level care. In a study of 565 consecutive patients treated for acute upper GIBs at Wellington Hospital, New Zealand (1988-1991), Phang et al.7 identified an overall mortality rate of 22% in patients presenting with a Clinical Rockall score of 4-7, leading the authors to identify this as a high-risk population requiring ICU level care.7

Publications to watch:

Of note, an abstract by Raemakers et al. was recently published online (prior to the full article in Academic Emergency Medicine), discussing the value of pre-endoscopic risk scores for upper GIBs in the ED. For more information as it becomes available:

Ramaekers R, Mukarram M, Smith C, Thiruganasambandamoorthy V. The predictive value of pre-endoscopic risk scores to predict adverse outcomes in emergency department patients with upper gastrointestinal bleeding — A systematic review. Acad Emerg Med 2016 Sep 19; [e-pub]. (http://dx.doi.org/10.1111/acem.13101)

 Lower GI Bleeding

The majority of life-threatening bleeds originate from the upper GI tract, however profuse bleeding from the lower GI tract often causes hemodynamic instability. Approximately 20-25% of GIBs are distal to the ligament of Treitz, and result in a mortality rate of 2%- 4% (mortality has been demonstrated to increase with advancing age).9 Potential sources of lower GIBs include diverticular disease, malignancy, angiodysplasia, and colitis.9

Unlike upper GIBs, there is far less consensus regarding risk stratification parameters for lower GIBs. Several studies have demonstrated low systolic blood pressure, tachycardia, the use of aspirin, and the presence of medical comorbidities as increasing the risk of mortality in the setting of a lower GIB.9-11

In their study of 688 patients presenting with lower GIBs, Chong, et al.10 demonstrated a lack of reported abdominal tenderness as an independent risk factor for mortality (possibly as pain is often associated with more benign etiologies of bleeding, and could lead to earlier patient evaluation and treatment).10 The authors also identified prolonged bleeding (> 4 hours) as a risk factor for mortality in the setting of lower GIB.10,11

In conducting their study, Chong et al. also utilized a cohort of 410 patients to develop a clinical prediction score (HAKA score) to identify patients most likely presenting with a severe lower GIB. The authors identified severe bleeding as: bleeding requiring transfusion of ≥ 2 units of packed red blood cells, manifesting as a decrease in hematocrit of > 20% from baseline, recurrent bleeding within 24 hours, or readmission for lower GI bleeding within one week of initial presentation. The HAKA score, detailed below, demonstrated a PPV (for scores ≥ 2) of 44% for severe lower GI bleed, and a NPV of 88%.10

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Recognizing the need to investigate risk factors for severe lower GIBs, in 2003 Strate and colleagues published data characterizing presenting symptoms of lower GIBs and their odds of association with severe bleeding (as defined above by Chong, et al.).11 In 252 consecutive patients presenting to Brigham and Womens’ hospitals in Boston, MA from 1996-1999, the following characteristics were associated with severe lower GI bleeding:

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Conclusion

Extensive research has been performed in an attempt to develop clinical decision-making tools for the risk stratification of patients with GI bleeds. Ultimately, patients who are hemodynamically unstable, risk stratify as having a high mortality secondary to GI bleeding, or are at risk for having a severe lower GI bleed, should be admitted to an ICU setting.

Back to the Case

Review of the patient’s electronic health record reveals a history of chronic back pain (prescribed naproxen), hypertension, and hyperlipidemia. Initial screening labs identify a Hgb of 8.1 and BUN of 45. The patient is likely experiencing an upper GIB secondary to NSAID therapy. Utilizing the Modified Glasgow-Blatchford Scale, you quickly identify the patient as having a high risk of mortality. After consulting for ICU admission, you contact gastroenterology. The next morning you open the patient’s record and note the identification of a NSAID gastropathy on endoscopy. The patient ultimately required a blood transfusion, but is hemodynamically stable.

References / Further Reading

  1. Barkun A, Bardou M, Kuipers E, Sung J, Hunt R et al. International concensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2010; 152:101-113.
  2. Baxter M and Aly E. Dieulafoy’s lesion: Current trends in diagnosis and management. Ann R Coll Surg Engl. 2010; 92(7): 548-554.
  3. Monteiro S, Goncalves T, Magalhaes J, Cotter J. Upper gastrointestinal bleeding risk scores: Who, when and why? World J Gastrointest Pathophysiol. 2016; 7(1):86-96.
  4. Blatchford O, Murray W, Blatchford M. A risk score to predict need for treatment for upper-gastrointestinal haemorrhage. Lancet. 2000; 356(9238):1318-1321.
  5. Cheng D, Lu Y, Sekhon H, Wu B. A modified glasgow blatchford score improves risk stratification in upper gastrointestinal bleed: a prospective comparison of scoring systems. Alimen Phamacol Ther. 2012; 36(8): 782-789.
  6. Abougergi M, Charpentier J, Berthea E, Rupawala A, Dheder J, et al. A prospective, multicenter study of the aims65 score compared with the Glasgow-blatchford score in predicting upper gastrointestinal hemorrhage outcomes. J Clin Gastroenterol. 2016; 50(6): 464-469.
  7. Phang T, Vornik V, Stubbs R. Risk assessment in upper gastrointestinal haemorrhage: implications for resource utilization. N Z Med J. 2000; 113(1115):331-333.
  8. Marmo R, Koch M, Cipolletta L, Capurso L, Grossi E, et al. Predicting moratlity in non-variceal upper gastrointestinal bleeders: validation of the Italian pned score and prospective comparison with the rockall score. Am J Gastroenterol. 2010;105(6):1284-1291.
  9. Qayed E, Dagar G, Nanchal R. Lower gastrointestinal hemorrhage. Crit Care Clin. 2016: 32(2):241-254.
  10. Chong V, Hill A, MacCormick A. Accurate triage of lower gastrointestinal bleed (LGIB) – a cohort study. Int J Surg. 2016; 25:19-23.
  11. Strate L, Orave E, Syngal S. Early predictors of severity in acute lower intestinal tract bleeding. Arch Intern Med. 2003;163(7):838-843.

Human Trafficking in the ED: Pearls and Pitfalls

Authors: Shannon Findlay, MD (EM Resident, University of Iowa), Daniel Runde, MD (EM Attending, University of Iowa), and Christopher Buresh, MD (EM Attending, University of Iowa) // Edited by: Jamie Santistevan, MD (@Jamie_Rae_EMdoc, Admin and Quality Fellow at UW, Madison, WI) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)  

 Background Information

Human trafficking (HT) affects individuals of all ages, genders, races, sexual orientations, and socioeconomic levels. This pervasiveness makes it difficult to identify potential victims. Human trafficking is not limited to overseas’ brothels or the rough inner cities of America. Trafficking occurs every day throughout America and involves individuals manipulated and coerced into exploited roles.

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Image 1: Locations of potential human trafficking cases in 2015

Nearly 21 million people are affected worldwide.1,2 It is estimated that 18,000 victims of HT are brought into the US annually, a number that does not account for the numerous individuals already in the US who are victims of HT.3

HT has significant mental and physical health effects. Emergency Medicine (EM) physicians are in a unique position to identify, treat, and assist victims of HT with their medical needs and connect them to safe houses, counseling support, legal assistance, and additional resources as needed. Studies have shown that between 28-88% of victims of HT seek medical care during the time when they are being trafficked. Conversely, only 5% of EM physicians feel comfortable identifying and treating possible victims of HT. 4-8

Awareness and education about both labor and sex trafficking are critical in understanding the complex needs of this difficult to identify population.

 At Risk Populations

Being aware of populations and persons at risk is the first step in identifying potential victims of HT.

Marginalized Populations9 Psychosocial Risk Factors9
·      Child welfare or juvenile system

·      Runaway youth and homeless youth

·      Children working in agriculture

·      American Indians and Alaskan Natives

·      Migrant laborers

·      Foreign national domestic workers

·      Employees of business in ethnic communities

·      Populations with limited English

·      Person with disabilities

·      LGBT

·      Previous physical, sexual, or emotional abuse

·      Poverty

·      Limited education

·      Substance misuse

 

Concerning Signs

Emergency physicians should have heightened suspicion for HT when patients present with the following signs/symptoms.

Signs of Abuse/Exploitation9-13,15 Sex Trafficking9-15 Labor Trafficking9-13,15
·      Sleep deprivation

·      Bruises, lacerations

·      Malnutrition

·      Untreated chronic illness

·      Anxiety, depression, suicide attempts

·      Overbearing accompanying person

·      No self-identifying documents

·      Lack knowledge of surroundings

·      Substance abuse

·      Multiple STDs, urinary symptoms

·      Ob/Gyn Concerns

·      Unintended pregnancies

·      Trauma to the vaginal or rectal area

·      High number of sexual partners

·      Limited use or access to contraception

 

·      Heat related illness

·      Musculoskeletal injuries

·      Lack of appropriate protective clothing at work

·      Chemical exposures

·      Chronic respiratory Illness

·      Chronic skin conditions

 

Case 1:

Worried, Anxiety, Women.

A 17-year-old female with history of drug/alcohol abuse along with depression and previous suicide attempt presents to the ED with the complaint of urinary symptoms and nausea. She is not very cooperative during the examination. She states that she has been seen in the past for similar symptoms and just wants antibiotics so that she can get back to work. She works to support herself and cannot afford to miss work.

When asked if she could be pregnant, patient says that she has not been able to buy birth control the past few months. Her LMP was about 1 months ago and reports barrier protection is rarely used. The patient refuses a pelvic exam and to give a urine sample because she states it’s a waste of time since she has already answered your questions. On visual inspection, you notice a thin tired appearing female with several bruises along her extremities. She has poor eye contact and appears anxious. She refuses to be examined further.

Vitals: T: 37 HR: 70 BP: 110/60 RR: 12 spO2: 99%

SH: High school student. Currently in the Foster Care System, but reports living with a friend presently.

Case 2:

migrant-worker-kort-duce

A 40-year-old male who does not see doctors presents with syncope from work. He is Spanish speaking and accompanied by a co-worker. He is able to speak simple English and states he is seasonal worker. His co-worker speaks over the patient to answer questions about the event and work environment. Patient states that he fainted after working in the field all day. Prior to this, he felt very hot and thirsty.

He further explains that he has a cough with bloody sputum production and extremely irritated eyes. Blood sugar by EMS is 400. Patient does not have any identification with him and does not have insurance.

Vitals: T: 39 HR: 115 BP: 90/60 RR: 20 spO2: 98%

Physical Exam:

Constitutional: Appears fatigue. Strong chemical smell present

HEENT: Dry mucus membranes and cracked lips. Red, watery, irritated eyes

Heart: Tachycardic with regular rhythm

Lungs: Normal breath sounds bilaterally

Skin: Hot and dry. Dermatitis on hands

Abdomen: Soft and non-distend. Non-tender

Extremities: Atraumatic

Neuro: CN in tact, moves all extremities spontaneously

Review of the Cases

Many of us have seen cases similar as those described above. The important thing is to recognize potential victims of exploitation. Below are concerning signs of human trafficking from the cases. No single sign guarantees that a person is a victim of human trafficking. Instead, concerning signs should prompt you to ask patients about their well-being and offer assistance as appropriate.

CASE 1: Suspected Sex Trafficking CASE 2: Suspected Labor Trafficking
·      Unexpected demeanor

·      Foster care background

·      Mental health history

·      Previous history of urinary infection /STD

·      Potential concerning work history

·      Limited use/access to contraception

·      Multiple bruises

·      Poor eye contact

·      Language barrier

·      Overbearing accompanying individual

·      No self-identifying documents

·      Migrant worker

·      Untreated or poorly controlled health conditions

·      Heat-related illness

·      Possible chemical exposures

Approach to Suspected Cases of Human Trafficking

  1. Remember that human trafficking can affect anyone, anywhere, anytime. You need a high level of awareness to identify potential victims of human trafficking. Treat the patients immediate medical and basic needs first.15
  2. Use a well-informed and culturally sensitive approach when interviewing your patients. Ask open ended questions about safety, employment, living environment, documents, and youth-specific questions.11,12,15
  3. Use a multi-disciplinary approach that involves social workers, those trained in medical evidence collection, interpreters, community resources, and law enforcement only when appropriate and with the consent of the individual. Exceptions include mandatory reporting laws in your area.10-12,15
  4. Recognize that your patients may not be ready to leave their situation for a wide variety of reasons including fear for themselves and loved ones. It often takes several visits for an individual to disclose their situation to healthcare providers.11 Your responsibility is to build a trusting and safe environment where individuals feel comfortable returning. This also includes safety awareness for not only the patient during the encounter but also healthcare staff.
  5. Call the National Human Trafficking Hotline 24/7 for assistance and reporting of potential cases of HT. You may also Text BeFree from 3PM-11PM EST. 

Hotline number: 1-888-373-7888. Text: BeFree 233733

References / Further Reading

  1. United Nations Office on Drugs and Crime. Global Report on Trafficking in Persons 2014.
  2. International Labour Organization. Profits and Poverty: The Economics of Forced Labour. May 20, 2014.
  3. Department of Health and Human Services. Human trafficking into and within the United States: a review of the literature. 2009. Available at: https://aspe.hhs.gov/basic-report/human-trafficking-and-within- united-states-review-literature. Accessed January 4, 2016.
  4. Lederer L, Wetzel C. The health consequences of sex trafficking and their implications for identifying victims in healthcare facilities. Ann Health Law. 2014;23:61-91.
  5. Baldwin SB, Eisenman DP, Sayles JN, et al. Identification of human trafficking victims in health care settings. Health Hum Rights. 2011;13:e36-e49.
  6. Family Violence Prevention Fund; World Childhood Foundation. Turning Pain Into Power: Trafficking Survivors’ Perspectives on Early Intervention Strategies. San Francisco, CA: Family Violence Prevention Fund; 2005.
  7. Chisolm-Straker M, Baldwin S, Gaigbe-Togbe B, et al. Healthcare and human trafficking: we are seeing the unseen. J Health Care Poor Underserved. In press.
  8. Viergever R, West H, Borland R, et al. Heath care providers and human trafficking: what do they know, what do they need to know? Findings from the Middle East, the Caribbean, and Central America. Front Public Health. 2015; http://dx.doi.org/10.3389/fpubh.2015.00006.
  9. United States Department of State. Trafficking in Persons report. July 2015. Available at: http//www.state.gov/j/tips/rls/tiprpt/
  10. Zimmerman C, Borland R. Caring for Trafficked Persons: Guidance for Health Providers. Geneva, Switzerland: International Organization for Migration; 2009.
  11. Alpert EJ, Ahn R, Albright E, et al. Human Trafficking: Guidebook on Identification, Assessment, and Response in the Health Care Setting. MGH Human Trafficking Initiative, Division of Global Health and Human Rights, Department of Emergency Medicine, Massachusetts General Hospital, Boston, MA and Committee on Violence Intervention and Prevention, Massachusetts Medical Society, Waltham, MA. September 2014.
  12. Becker H, Bechtel K. Recognizing victims of human trafficking in the pediatric emergency department. Pediatric Emergency Care. 2015; 31: 144-150.
  13. Zimmerman C. Trafficking in Women. The Health of Women in Post-Trafficking Services in Europe Who Were Trafficked into Prostitution of Sexually Abused as Domestic Labourers.
  14. Raymond JG, Hughes DM. Sex Trafficking of Women in the United States: International and Domestic Trends. New York, NY: Coalition Against Trafficking in Women; 2001.
  15. Jamie Shandro, MD, MPH; Makini Chisolm-Straker, MD, MPH; Herbert C. Duber, MD, MPH; Shannon Lynn Findlay, MD; Jessica Munoz, MSN, FNP-BC; Gillian Schmitz, MD; Melanie Stanzer, DO; Hanni Stoklosa, MD, MPH; Dan E. Wiener, MD; Neil Wingkun, MD. Human Trafficking: A Guide to Identification and Approach for the Emergency Physician. Annals of Emergency Medicine. October 2016; 68. 4. 501-508.

 

Images Obtained from the following

  1. Image 1. Accessed Nov 13, 2016. Image available from: https://polarisproject.org/sites/default/files/2015-Statistics.pdf
  2. Case 1. Accessed Nov 13, 2016. Image available from: http://docorman.com/anxiety-and-telling-the-truth/
  3. Case 2. Accessed Nov. 13, 2016. Image available from: http://images.fineartamerica.com/images-medium-large/migrant-worker-kort-duce.jpg