Hippocratic Medicine No.1: Blood Culture or No Blood Culture, That is the Question.

Welcome to the first installment of our new column here at Everyday EBM - Hippocratic Medicine.  

Modeled after the Do No Harm project pioneered at the University of Colorado, the aim of this (hopefully) monthly installment will be on the avoidance of avoidable care i.e. raising awareness for how medical overuse has the potential to do patient harm.   Because every test or intervention we do has the potential for not just benefit but also harm, we should seek that our patients do better because of the care we provide instead of despite it.  

Clinical Scenario: It is a regular day in the emergency department and along with the regular smattering of chest pain rule-outs, vaginal bleeders, and abdominal pain, you have two patients who need to be admitted for IV antibiotics. One has a diffuse cellulitis of the left leg and the other pyelonephritis, unable to tolerate oral meds. Both have an elevated white count but no other SIRS criteria. When giving sign-out, the inpatient medicine team asks for blood cultures on both patients.  Is there any value for blood cultures in patients with cellulitis and pyelonephritis? Does this value outweigh the potential harms?

Literature Review:The ACEP article [1] “The evidence against blood cultures” presented interesting data regarding cost and benefit of blood cultures. According to the article, in 2010 $151 million dollars was spent on blood cultures. Only 4% to 7% of blood cultures were true positives. Alarmingly, blood cultures are almost as likely to give you a false positive as a true one: 40% of all "positive" cultures are false positives. For cellulitis, only 2% of patients are likely to develop a bacteremia and skin infections are almost always due to Staph or Strep. For uncomplicated pyelonephritis, the urine culture is what is used to target treatment, and if blood cultures are positive, it is almost always with the same organism and does not alter treatment course.
 

With regard to their recommendations for pyelonephritis, the ACEP article draws on a retrospective chart review of 212 patients admitted for uncomplicated pyelonephritis [2] . Blood cultures were performed for 105 of these patients, only 16% of which grew out an organism. Of the 11 positive cultures, all but 2 had the same organism that was identified in the urine and no change was made in treatment. The other 2 were found to have a second infectious source for their bacteremia.
 
With regard to cellulitis, a retrospective review of 710 patients admitted for cellulitis, of which 553 had blood cultures drawn. Of these patients, only 11 cultures (2%) were positive [3]. A 2012 review article in the Journal of infection found 7.9% of patients with cellulitis had positive cultures, all with Staph or Strep identified as the source organism [4]. 

These findings are not limited to the adult population [5].  A retrospective cohort study of blood culture results and microbiology laboratory charges for pediatric cases of community-acquired pneumonia and skin/soft tissue infection found that only 9/279 cultures (3.2%) grew an organism and only 5/9 (55%) were deemed to be true positives.  The main subsequent intervention?  Repeat cultures.  4/9 of these were deemed to be false-positives, leading to a smattering repeat cultures, ID consultation, prolonged LOS, and vancomycin initiation:

Table 2 from Parikh et. al. (Ref 5)

But are there clinical indicators that increase the diagnostic or therapeutic yield of blood cultures? The answer is yes. In a 1996 study, SIRS criteria was found to be 96% sensitive for positive blood cultures and this has been corroborated by other studies [6]. This indicates that in the absence of SIRS criteria aka in the absence of sepsis (2 SIRS + a known infectious source) blood cultures are more likely to be false positives than true positives, and do not meet standards for an indicated test.

As alluded to in the pediatric data, we may be doing more harm than good when ordering blood cultures in patients with uncomplicated [or shall we say SIRS(-) ?] pneumonia, cellulitis or UTI. Just like an incidental finding on an imaging study, false positive blood cultures have the power to beget further testing and intervention. Since we have learned above that the results are unlikely to change treatment course, we know that there are limited benefits. But what about the costs?

- Blood cultures increased cost and hospital length of stay: A retrospective study from Ireland [7] compared "cases" of false-positive blood cultures [defined as a single blood culture set positive for micro-organisms commonly thought of as contaminants or multiple blood cultures positive for different organisms] with "controls" matched for comorbidity via the Charlson index with "true negative" blood cultures. They found an overall false positive rate of 4.7%, and that patients with false positive blood cultures stayed in the hospital for 5.4 days ( 95% CI 2.8 - 8.1 days) longer at a cost of $7502.20 more (95% CI: $4,925.80 - $10, 078.60) compared to counterparts matched for diagnosis and comorbidity. A similar study from Brigham and Women's Hospital published in 1991 [8] found essentially the same results (average increased LOS of 4.5 days and increased total cost of $4,385). 


-  Blood cultures increase unnecessary antibiotic use: In addition to adding to hospital length of stay, part of the additional costs incurred by false positive blood cultures are unnecessary antibiotics [8]. 
A prospective, blood culture cohort study [9] evaluated all blood culures positive for skin flora during a three month period at a US medical center.  In this study, they found 59 false positives aka contaminants with Coagulase Negative Staph in 3, 276 collections (compared with 20 cases of "true bacteremia" with the same organism).  Among the 59 patients in the false positive category, 24 (41%) were treated with antimicrobial agents, predominantly vancomycin.  It is unclear from reading the paper if this was a direct result of the positive blood culture, or due to continuation of empiric treatment; however, the results described by Alahmadi [7] and Bates [8] suggest that the culture results are at least in part responsible.  Beyond the aspect of monetary cost alone, there are a number of harms, including renal injury and spread of antibiotic resistance, that make unnecessary antibiotic use particularly troubling.


It has been written [8] that  "The true costs of a blood culture may greatly exceed the costs of the test itself".   How do we change this?  In the same way we make all clinical tests better - by using them in the appropriate situation and maximizing specificity.
 
                I. Decrease blood culture contamination rates:  The nationwide average for blood culture contamination is thought to be in the range of 3-5%.  At our own hospital (BJH), the blood culture contamination rate was within this range, with a rate of 3-4% for the emergency department compared with 1-2% for the ICU for 2014.  Several studies have demonstrated that increased nursing education and standardization of protocols can have significant impact on contamination rates. For example, one study for multiple centers in Sacramento saw a sustained drop from a 12% to 3% after instituting (and intensively educating about) a protocol of chlorhexidine-based skin cleaner and sterile glove technique in which a sterile glove is used for repalpating the site [10].
           
               II.  Use it in the appropriate clinical situation:  If you are admitting a patient with SIRS(-) pneumonia, UTI, or SSTI just don't do it.  However, make sure to send the urine culture before antibiotics (patient has not gone yet?  That's what a straight cath is for!). If the inpatient medicine team asks you to, use it as an opportunity for education.  Floridly septic?  Go ahead.  Think its endocarditis?  Sure.  


Submitted by Alicia Oberle, PGY-3 and Maia Dorsett (@maiadorsett), PGY-3
Reviewed by Ryan Schneider and Stephen Liang. 
Thank you to Maureen Keating and Carey-Ann Burnham of BJC Micro for our own contamination rate data.

References:
1. Lin MP, Schurr JD. Arm Yourself for the “Cultural” Debate: The Evidence Against Blood Cultures. ACEP Now. Sept 2014 Vol 33 Number 9.
2. Pasternak EL, Topink MA. Blood Cultures in Pyelonephritis: do results change therapy? Acad Emerg Med. 2000; 7:1170.
3. Perl B, Gottehrer NP, Raveh D, et. al. Cost-effectiveness of blood cultures for adult patients with cellulitis. Clin Infect Dis. 1999; 29:1483-1488.
4. Gunderson CG, Martinello RA. A systematic review of bacteremias in cellulitis and erysipelas. Journal of Infection. 2012 Feb. 
5.Parikh, K., Davis, A. B., & Pavuluri, P. (2014). Do we need this blood culture?. Hospital pediatrics, 4(2), 78-84.
 6. Jones GR, Lowes JA. The systemic inflammatory response syndrome as a predictor of bacteremia and outcome from sepsis. QJM. 1996; 89:515-522. 7. Alahmadi, Y. M., Aldeyab, M. A., McElnay, J. C., Scott, M. G., Darwish Elhajji, F. W., Magee, F. A., ... & Kearney, M. P. (2011). Clinical and economic impact of contaminated blood cultures within the hospital setting. Journal of Hospital Infection, 77(3), 233-236.
8. Bates, D. W., Goldman, L., & Lee, T. H. (1991). Contaminant blood cultures and resource utilization: the true consequences of false-positive results. JAMA, 265(3), 365-369
9. Souvenir, D., Anderson, D. E., Palpant, S., Mroch, H., Askin, S., Anderson, J., ... & Campbell, D. M. (1998). Blood cultures positive for coagulase-negative staphylococci: antisepsis, pseudobacteremia, and therapy of patients. Journal of clinical microbiology, 36(7), 1923-1926.
10. Denno, J., & Gannon, M. (2013). Practical Steps to Lower Blood Culture Contamination Rates in the Emergency Department. Journal of Emergency Nursing, 39(5), 459-464.

Worse after antibiotics: Precipitating endotoxin release?

Clinical Scenario:

A middle-aged female patient presents to the emergency department stating she was diagnosed with a urinary tract infection (UTI) several days ago, but does not feel like her symptoms are improving with the ciprofloxacin and subsequent bactrim given.  She is currently complaining of nausea, vomiting, chills, back pain, and dysuria.  In triage, her vitals are normal (no fever, not tachycardic, normotensive).  On exam, she seems uncomfortable, but is fully alert and orientated and giving you her entire history.  You order a urinalysis with reflex culture, some fluids, and ceftriaxone to be given.

After 2 liters of fluid and the antibiotics, the nurse comes to tell you the patient is now not alert nor orientated, and hypotensive with systolic in the 70s.  She has no rash or wheezing and you don't think that is necessarily anaphylaxis. You look at her labs and see a white blood count of 22.  Her lactate returns at 16.  You pressure bag 3 more liters of NS into her, and on recheck her lactate has risen to 18!  She is intubated for airway protection and you find that her arterial pH is 6.52, with her bicarbonate on her basic metabolic panel below the detectable level (less than 5).  CT abdomen/pelvis without contrast (given creatinine greater than 10) revealed bilateral peri-nephric stranding, suggestive of pyelonephritis without a stone.

Clinical Question:

After she is transferred up the MICU, you wonder what had happened.  How did this woman, who came in talking to you, suddenly deteriorate so quickly?

Since most urinary tract infections in women are caused by E. coli, could it be that the treatment with antibiotics caused a lysis of gram negative cells and release a bolus of endotoxins into the circulatory system that caused circulatory collapse?

Literature review:

The idea of antibiotic therapy used in a rational manner can precipitate adverse reactions.  For example, the Jarisch-Herxheimer reaction with the treatment of syphilis with penicillin causes transient worsening of symptoms as the spirochetes are lysed.  With the high mortality and morbidity of sepsis, researches have been examining if certain antibiotics can precipitate circulatory collapse due to lysis of bacteria.

The lipopolysaccharide (LPS) found in gram negative bacteria cell walls has been implicated as mediating an inflammatory response from the body in gram negative sepsis.  LPS triggered inflammation weakens mitochondrial oxidative phosphorylation (which correlates well with high ScVO2 found in some septic patients).  The LPS also triggers a release of TNF-alpha and other cytokines such as IL-6 from macrophages contributing to septic shock from decreased myocardial contractile force and decreased systemic vascular resistance, which leads subsequently to hypotension.  Experimental models where TNF-alpha have been injected into animals have resulted in hypotension, metabolic acidosis, acute tubular necrosis, and ultimately death.

While endotoxins are constantly released into the blood stream during bacteria infection, causing patients to feel sick and become febrile, the administration of antibiotics has been shown to precipitate a large release of endotoxins due to lysis of bacteria.  Compared to bound endotoxin, free endotoxin may have up to 50 fold increase in activity. 

Not all antibiotics release endotoxins equally.  Certain beta-lactam antibiotics appear to liberate a greater amount of endotoxin compared to other antibiotics.  The mechanism of action is theorized to be the interaction of beta-lactam antibiotics with the penicillin-binding proteins (PBP) found in bacteria cell walls.  The inhibition of PBP3 specifically seems to cause a decrease in septum formation in dividing cells, causing long filaments to form.  This increase in biomass with subsequent lysis is theorized to be the cause large increase in endotoxin associated with antibiotics that bind specifically to PBP3.  In contrast, antibiotics that bind to PBP2 seem to form more spheroid cells with rapid lysis, leading to decreased endotoxin release.

Periti and colleagues found that aztreonam, piperacillin, ceftazidime, and cefuroxime seem to have high affinities to PBP3.  With increasing concentrations of these antibiotics, they start saturating other PBP sites, causing less filament formations, suggesting that the larger release of endotoxins associated with these antibiotics may be reduced with higher doses of antibiotics.  Ceftriaxone and cefepime appear to have equal affinities for many of the PBPs causing more spheroid cells and less endotoxin release.  Carbapenems such as imipenem and meropenem showed greatest affinity for PBP2.  Many studies have compared imipenem and ceftazidime, generally demonstrating higher release of endotoxin with ceftazidime therapy.  A study by Arditi and colleagues found that ceftriaxone induced a larger endotoxin release and subsequent TNF-alpha release when compared to imipenem, correlating with the theory that imipenem primarily with PBP2 while ceftriaxone has more equal affinity over all binding sites.  Goscinski and colleagues found that in E. coli treated with cefuroxime, there was higher release of endotoxin after the second dose, supporting the theory of filament formation with subsequent lysis.  They also found that the addition of tobramycin reduced the amount of endotoxin released.

Other antibiotics seem to release less endotoxin by various methods.  Polymyxin actually has a binding effect to endotoxins, inhibiting the biological activity of endotoxins.  Some antibiotics lead to the loss of viability in bacteria without lysis and release of endotoxins, such as quinolones.  Gentamicin, tobramycin, and amikacin have even been shown to neutralize the effects of endotoxins.

While studies have clearly shown a link between antibiotics and the release of endotoxins and the effect of endotoxins and cytokines in precipitating an inflammatory response as well as septic shock, it has remained to be seen if this correlates with clinical outcome.  There have been few prospective human studies into the administration of different antibiotics in the treatment of gram negative sepsis.  One pertinent randomized study by Prins and colleagues of urosepsis patients treated with imipenem compared to ceftazidime found a more rapid defervescence with the administration of imipenem.  Endotoxin and cytokine release also increased after administration of ceftazidime compared to no increase in the imipenem group.  However in other physiological measures and mortality, there were no differences between the two study groups.  Another study by Byl and colleagues examined again the difference between imipenem and ceftazidime in human septic patients.  While both antibiotics did appear to induce endotoxin release and increase cytokine production in a small number of patients, there did not seem to be a difference in the two groups.  Both studies found that the endotoxin rise only appreciably happened to a fraction of their study population that were septic. 

In a review by Holzheimer, he found that clinical significance of antibiotic-induced endotoxin release has only been documented in a few clinical disorders such as meningitis and urosepsis.  In a prospective study by Mignon and colleagues in septic patients in an ICU, there was no significant increase in endotoxin levels after initiation of empiric antibiotic therapy however there was clinical deterioration in 42% of patients 4 hours after antibiotic administration, which correlated with higher endotoxin levels when compared to stable septic patients.  Maskin and colleagues randomized 24 gram-negative septic patients between imipenem and ceftazidime.  All patients showed high levels of LPS, TNF-alpha, and IL-6 compared to controls.  TNF-alpha concentrations were higher in patients treated with ceftazidime compared to imipenem, however LPS and other cytokine production was not significantly different.  Many of these studies were limited by small sample sizes as well as sepsis caused by a wide variety of bacteria.

Severe sepsis is a difficult disease to deal with in the emergency department due to the uncertainty of source combined with the multiple comorbidities of the patient.  It requires fluid resuscitation as well as the quick administration of antibiotics.  While it seems that some antibiotics may precipitate circulatory collapse due to release of endotoxins and subsequent increased production of cytokines in a small subset of patients, there have been no large, randomized studies demonstrating a mortality difference in regard to selection of a specific antibiotic.

Take home points:

-Certain antibiotics cause a greater release of endotoxins and cytokines compared to others, possibly correlated with circulatory collapse

-No large, prospective studies have demonstrated an advantage to selecting certain class of antibiotics over another

  

References:

1. Arditi M, Kabat William, Yogev R. Anitibiotic-Induced Bacterial Killing Stimulates Tumor Necrosis Factor-alpha release in whole blood. J Infect Dis 1993;167:240-4.

2. Byl B, Clevenbergh P, Kentos A, Jacobs F, Marchant A, Vincent JL, Thys JP. Ceftazidime and Imipenem-Induced Endotoxin Release. Eur J Clin Microbiol Infect Dis 2001;20:804-807.

3. Goscinski G, Tano E, Lowdin E, Sjolin J. Propensity to release endotoxin after two repeated doses of cefuroxime in an in vitro kinetic model: higher release after the second dose. Journal of Antimicrobial Chemotherapy. 2007;60(2):328-333.

4. Holzheimer RG. Antibiotic Induced Endotoxin Release and Clinical Sepsis: a Review. Journal of Chemotherapy 2001;13:159-172.

5. Kirikae T, Nakano M, Morrison DC. Antibiotic-Induced Endotoxin Release from Bacteria and Its Clinical Significance. Microbiol Immuno 1997;41(4)285-294.

6. Lepper PM, Held TK, Schneider EM, Bolke E, Gerlach H, Trautmann M. Clinical implications of antibiotic-induced endotoxin release in septic shock. Intensive Care Medicine 2002;28:824-833.

7. Maskin B, Fontan PA, Spinedi EG, Gammella D, Badolati A. Evaluation of endotoxin release and cytokine production induced by antibiotics in patients with Gram-negative nosocomial pneumonia. Critical Care Medicine. 2002;30(2):349-354.

8. Mignon F, Piagnerelli M, Van Nuffelen M, Vincent JL. Effect of empiric antibiotic treatment on plasma endotoxin activity in septic patients.

9. Periti P, Mazzei T. New criteria for selecting the proper antimicrobial chemotherapy for severe sepsis and septic shock. International Journal of Antimicrobial Agents. 1999;12(2):97-105.

10. Prins JM, van Agtmael MA, Kuijper EJ, van Deventer SJ, Speelman P. Antibiotic-induced endotoxin release in patients with Gram-negative urosepsis: a double-blind study comparing imipenem and ceftazidime. J Infect Dis 1995. 172:886–891

Submitted by Steven Hung (@DocHungER), PGY-2

Faculty reviewed by Richard Griffey

Pediatrics: Refusal to use arm

Clinical Scenario:

A 5 week old infant presented to the Emergency Department (ED) with refusal to move right arm for the past 3 days. No significant past medical history; the pregnancy was uncomplicated, and born via Cesarian-section due to failure to descend at full term at 40 weeks.  The patient has otherwise been feeding well and moving all of his other extremities. No history of trauma or fever. The arm and shoulder have no erythema, no swelling, however the patient screams in pain whenever you move the arm. 

X-rays of the right shoulder and entire right arm were unremarkable. Laboratory tests demonstrated a slightly elevated white blood cell count (WBC), however the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were both elevated.  You admit the patient for further work up.  The following day (actually a few hours later since was a late admission) the patient underwent a sedated MRI, which revealed humeral osteomyelitis with associated septic arthritis.

Clinical Question:

What are common causes of osteomyelitis/septic arthritis in a newborn?  What is the best tests/imaging to diagnose it?

Literature review:

Osteomyelitis can cause significant morbidity and mortality in a neonate/infant and can be difficult to diagnose.  In one small study, Wong and colleagues found that only 10 of the 30 babies studied demonstrated any systemic signs of infection, such as fever.  This study also found that more than half of the infants affected were born pre-term, and 70% of the patients with osteomyelitis had extended contact with the healthcare system (eg prolonged stay in the hospital).

A review by Montgomery and colleagues found that Staphylococcus aureus (S. aureus), to be the most common cause of osteomyelitis, with cases of Methicillin resistant S. aureus rising nationally.  In infants and children specifically, other common bacteria causing osteomyelitis are Group B Streptococcus, Ecsherichia coli, Kingella kingae usually spread hematogenously.

In a review of septic arthritis with concomitant adjacent osteomyelitis, such as this particular case, it was found that the shoulder was the most likely of all the joints (elbows, hips, knees, ankle) to be infected, as it was in this patient.  S. aureus again was the most common organism to cause a simultaneous osteomyelitis with associated septic arthritis.

In osteomyelitis, the WBC is often not a sensitive marker. One study in the journal of Pediatrics found that only 35% of children with osteomyelitis had an elevated WBC.  In contrast, ESR and CRP elevations were more sensitive, at 92% and 98% respectively.  Combined together, ESR and CRP offered the greatest sensitivity in detecting osteomyelitis.  After initiation of treatment, the ESR usually normalized within 24 days and the CRP in 10 days.

The recommended imaging modality for acute osteoarticular infections is magnetic resonance imaging (MRI) with contrast given the superior imaging it provides of bone as well as the soft tissues when compared to other imaging modalities.  In follow up after treatment, positron emission tomography (PET) or commuted tomography appears to be better imaging modalities. 

Take home points:

-Osteomyelitis/septic arthritis needs a high degree of suspicion for diagnosis given paucity of other symptoms such as fever.

-WBC can be normal, ESR and CRP together are more sensitive.

-Patients can have no other symptoms besides from joint pain.

-Preferred imaging is MRI with contrast.

References: 

1. Montgomery NI, Rosenfeld S. Pediatric Osteoarticular Infection Update. J. Pediatr Orthop. 2014.

2. Unkila-Kallio L, Kallio MJ, Eskola J, Peltola H. Serum C-reactive protein, erythrocyte sedimentation rate, and white blood cell count in acute hematogenous osteomyelitis of children. Pediatrics. 1994;93(1):59

3. Wong M, Isaacs D, Howman-Giles R, Uren R. Clinical and diagnostic features of osteomyelitis occurring in the first three months of life. Pediatr Infect Dis J. 1995;14(12):1047-53

Submitted by Steven Hung (@DocHungER), PGY-2

Faculty reviewed by Joan Noelker

Antibiotics for Mandible Fractures?

Clinical Scenario:

You’re working a busy Saturday overnight, and the traumas are rolling in. You’ve just finished packaging up your patient with an abdominal GSW for the OR, and they’re bringing back a new patient before the stretcher is even flipped over. He’s a 25 year-old male, presenting to the ED after being in an altercation with some friends of friends. He was hit in the face during the fistfight. He is complaining of left-sided jaw pain and facial swelling. He is able to open his jaw to a reasonable degree, but uncomfortably. There is no apparent intra-oral injury. CT max/face shows multiple minimally-displaced fractures of the left mandibular ramus and paramental region.

Luckily for you the ENT consult resident is still in the department from seeing your last patient with a complicated ear lac. She evaluates the patient with her senior and looks over the images. The patient will need surgical repair, but is OK for discharge with close pre-op follow-up next week. They recommend mouthwash, nasal spray, analgesia, and antibiotics.

Clinical question:

When are prophylactic antibiotics indicated in mandibular fractures, and how effective are they are preventing infection?

3D CT recon of minimally-displaced mandible fractures. Image from MD Consult.

@WUSTL_EM FOAMed Digest #7: Best of the Best of the Best Sir! ...With Honors

To build on my “Intro to FOAMed” lecture from Tuesday, I thought I would use the Digest this week to highlight some of the highest-quality resources out there for those of you just dipping your toes into the FOAMy goodness. You can’t go wrong adding these to your Feedly. Well-referenced, expert review, open discussion with prompt response – they’re really setting the bar for the FOAMed world.

And don’t worry – in the spirit of FOAMed the lecture and slides will be posted as soon as the video editing is done.

Now come on in, the water’s fine!

Three Stars:

1. Academic Life in EM (ALiEM) continues to be one of the paragons of the FOAMed community. Check out this “Diagnose on Sight” case from this week – don’t want to give it away, but you will see it time and time again during your Children’s shifts. Make note of the reference list and pre-publication review from a practicing clinician. Supremely high quality.

2. I must credit my inspiration for this FOAMed Digest – the LITFL Review from Life in the Fast Lane. Curated by some of the sharpest tacks around, it’s a great way to get familiar with the variety of resources out there. Lots of good stuff this time around, including links to Amal Mattu’s EKG video review of QT prolongation, the latest edition of FOAMCast (all about the spleen!), and the St. Emlyn’s view of the new NICE guidelines for managing acute heart failure.

EXTRA CREDIT: If you need help keeping up with the EM primary literature, the Research & Reviews in the Fastlane segment is a great place to start!

3. EM Lyceum takes the “flipped classroom” concept to the next level. Every month or so, they publish a series of clinical questions focused on a particular topic. This time, it was trauma. The point is to ponder those questions, discuss them in a group, and maybe even do your own research. The EM Lyceum group then publishes the best evidence-based answers they could find in an exceptionally well-referenced summary. Pearl from this month: Bust out the PCC for ICH on warfarin, but no good evidence for PCC in your “average” coagulopathic trauma patient.  

Sour Milk: Antibiotic Coverage For a Breast Abscess

Clinical scenario:  

Your patient is a middle-aged female who was brought in from home for altered mental status.  As EMS is moving her over to the stretcher, they say: "this lady has some kind of infection on her breast ... I saw it when I went to do her EKG".  The patient is febrile to 39.3, tachycardic in the 120’s, but maintaining a blood pressure of 150’s/80’s.  She has a large, right- sided breast abscess with some spontaneous drainage.  Clearly, this patient has severe sepsis and she needs IVF, antibiotics, and source control.

Clinical Question:  

What is the most appropriate antibiotic choice for coverage of a breast abscess?  Obviously, the patient needs an I&D, but in the meantime, what typically is growing in there?  Should anaerobic coverage be routine?

#FOAMed Digest No. 6: Ain't Nobody Got Time For That

Welcome back, FOAMheads! My apologies for the delay this week. I ended up being a bit busier than I expected, which not coincidentally brings me to the theme for today's entry.

Sometimes you have a lot on your plate and may not be able to set aside a large chunk of time to watch/listen to a 30-minute-plus podcast. But that doesn't mean you don't have time to get your learn on! This time around, we'll highlight some of the best FOAMed sources of short-and-sweet educational pearls. Easily digestible for the highly-distractible mind of the EM trainee.

There is no moment like the present -- let's get started!

#FOAMed Digest No.5: But This One Goes to 11

Time once again for your mid-week blast of FOAMy goodness from around the interwebs. There’s no particular subject today; instead we’re going to highlight some of the better podcasts/vodcasts that updated this week. Podcasts are great. They break up the monotony of reading (and the monotony of mundane things like laundry, grocery shopping, training for this damn marathon…). For the more distractible among us, they usually come in easily-digestible 20-30 minute morsels. They expose you to different presentation styles, and allow you to match a face and a voice with the big names in FOAMed. Most of them also feature written show notes with references as well, which allows you both to reinforce the things you learned while listening, and also to dig deeper into topics you’re interested in.

Fun for the whole family!

Three Stars:

1. I think FOAMcast, authored by residents and EM social media savants Jeremy Faust and Lauren Westafer, might be the first example of “metaFOAM.” They peruse the FOAM world for interesting recent posts, then integrate that information with relevant material from the most popular EM textbooks (i.e., “Rosenalli”), other relevant blogs/podcasts, primary literature, and even Rosh Review questions. This week they use a post from ALiEM on calcium channel blockers vs beta blockers for A-Fib as a jumping-off point for a discussion on ED management of A-Fib and A-Flutter. There’s links to vodcasts from Scott Weingart and Amal Mattu on narrow-complex tachydysrhythmias, and plenty of cited references from the primary literature (including one from our own Brian Cohn!). It’s good stuff.

2. Speaking of the Godfather of ED EKG, Dr. Mattu has two quick cases for you to ponder. Remember: T-wave inversion does not always mean cardiac ischemia!

Remember: Gotta think tox in a seemingly unprovoked wide complex tachycardia!

3. Steve Carroll at EM Basic provides an excellent analysis of the ED management of asymptomatic hypertension, including references to the relevant ACEP Clinical Policy document and other FOAMed resources.

Oldie But Goodie:

Chris Nickson, creator and administrator of Life in the Fast Lane, gave an excellent talk at the original SMACC conference in March 2013 with the confidence-inspiring title, “All Doctors are Jackasses.” Why are we jackasses? Because we don’t do enough to understand how we think and how we make decisions, and this leads us to make errors. Watch Nickson’s lecture and begin to understand how to remedy this situation.

(EXTRA CREDIT: Links in the show notes to the other SMACC talks in the “Mind of the Resuscitationist” plenary by Weingart, Cliff Reid, and Simon Carley.)

F(FN)OAMed:

By this point you guys all know how awesome EM:RAP is, but this week is particularly relevant because Herbert & Co. just released an “EM:RAP Mini” segment about the newly-published “Ultrasonography versus Computed Tomography for Suspected Nephrolithiasis” trial in the New England Journal. For those of you that aren’t familiar, this was a study in which we participated, and our own Drs. Aubin and Griffey are authors on the paper! An excellent summary of this paper is found on the Emergency Medicine Ireland blog, with a link to download the EM:RAP Mini segment in the show notes.

The Gunner Files:

1. Time to synthesize the knowledge you gained about non-surgical management of pediatric appendicitis at Journal Club last month. Dr. Cohn is back with another excellent EMJClub podcast along with Drs. Trehan and Horst, summarizing the primary literature.

2. EMin5 is back at it with a review of the four types of shock, in a little over four minutes.

3. From the Maryland Critical Care Project, an excellent lecture from Neuro Critical Care and ED intensivist Dr. Wendy Chang describing the ED management of status epilepticus. She covers the gamut from first-line benzos to second-line AEDs and third-line agents for initiation of therapeutic coma.

4. The good people at the All NYC EM blog posted a lecture given during their conference day by the FOAMed superstar Dr. Haney Mallemat. He covers all the basics of ultrasound evaluation of pericardial effusion and tamponade, even ultrasound-guided pericardiocentesis.

5. In case you’re not familiar, US Air Force Pararescuemen, a.k.a. “PJs,” are the ultimate badasses. Just look at it this way: think becoming a SEAL is tough? PJ training has an even higher failure rate. But I digress.

Former PJ and critical care flight retrieval medic Mike Lauria is now in medical school, and is making a bit of a splash in the FOAMed community as an expert on training, thinking, and operating in high-stress environments. Scott Weingart recently interviewed him on EMCrit about the concept of “mental toughness,” how that translates from the combat realm to the ED, and how to incorporate it into physician training. Really interesting stuff.

That Others May Live,

Sam Smith, PGY-3

#FOAMed Digest No. 4: Butter My Biscuit, Baby

Welcome back, to the brand new edition of the WUEMR FOAMed Digest. Get out your Tintinalli’s and strap in, because we’re going back to basics today. It’s all about the bread and butter. The things any PGY-2 setting off to an overnight Saturday shift in the Deuce should have down cold…yet us seniors still screw up on the daily.

FOAMed…ENGAGE!

Three Stars:

1. If my last shift at Children’s is any indication, the season is upon us – pharyngitis in every exam room. Casey Parker over at Broome Docs (a blog authored by EPs & GPs practicing in rural Australia), presents a magnificent summary of the data surrounding rapid strep swabs, antibiotic use for symptom relief, and antibiotic use for preventing secondary complications of strep. As always, be sure to check out the original literature for yourself. And don’t miss Minh Le Cong’s excellent counterpoint in the comments, which is also well-referenced.

2. What’s your record for most C-collars cleared in one shift? (When you hit double-digits, then we can talk.) The best tools in our arsenal for clearing C-spine in low-risk patients remain the Canadian C-spine and NEXUS instruments. But which one should you use? Do you even remember which criteria belong in each rule, or do you find yourself trying to apply the “Canadi-EXUS” criteria, like I do? Luckily for us, Alayna Hawling at BoringEM authored an excellent rundown and comparison – with a pretty flowchart!

3. As much as you want to start the fist-pumping and beer-chugging as soon as you drop that tube past the cords, your work with the intubated patient is not done, my friend! We’ve already touched on our persistently poor rates of achieving adequate analgesia & sedation in the intubated patient. Another part of quality post-intubation care is knowing what to do if your ventilated patient acutely decompensates. Check out Chris Cresswell’s summary of the DOTTS mnemonic over at EM Tutorials.

(EXTRA CREDIT: He also included a link to Scott Weingart’s notes regarding care of the crashing ventilated patient, which are well worth a look.)

Oldie But Goodie:

There’s been some e-mail discussion lately among our attendings regarding the best way to clean lacs prior to closure. Back in February, Ken Milne at the Skeptic’s Guide (along with Eve Purdy, a rockstar med student and creator of the excellent Manu et Corde blog) published a piece dedicated to breaking down the dogma of management of simple lacerations. Tap water vs sterile water, sterile gloves vs clean gloves, to sew or not to sew…it’s all covered here. Plus there’s links to other excellent FOAMed resources regarding wound care dogma.

F(FN)OAMed:

The good folks over at EB Medicine recently published a stem-to-stern guide to UTI diagnosis and management in the ED, all based on best available evidence. A bit lengthier than your average blog post, but incredibly high-yield and well worth your time. It’s a bit difficult for me to place a direct link here, but you can find it simply by logging into your account at EBMedicine, following the link to browse issues of Emergency Medicine Practice, and opening the July 2014 issue on UTI.
(As always, contact your friendly neighborhood Social Media Committee member if you need help obtaining access to EB Medicine resources.)

The Gunner Files:

1. Hard to get through a Deuce shift without breaking out the prochlorperazine at least once. We’ve all seen patients get jittery, agitated, or downright whacky following its use. Does Benadryl help? A PharmD expert at ALiEM has a good lit review of the topic.

2. Short and sweet: some diabetic medications are more likely to cause harmful hypoglycemia after overdose than others. Quick table-based rundown over at ALiEM.

3. It is asthma season, and you may find yourself in the worst-case-asthma-scenario of impending need for intubation. Check out this post from The Kings of County regarding care for the sick asthmatic, including intubation and mechanical ventilation issues.

4. FOAMed is taking the world by storm! Does the UK College of Emergency Medicine launching a dedicated FOAMed site mean it’s officially gone mainstream? Don’t worry – we were all into FOAMed before it was cool. But seriously, check out this vodcast on diagnostics in EM, and not feel quite so much increase in sphincter tone when Carpenter or Cohn pimp you on likelihood ratios or Bayesian analysis.

5. Another classic from the Skeptic’s Guide, this time addressing another oh-so-common ED complaint: renal colic. Fluids? Flomax? Any good evidence for either? In news that will surprise no one, Ken Milne is skeptical.

Never stop learning,

Sam Smith, PGY-3