Antibiotics for chest tubes

Things to keep in mind:

Prophylactic antibiotics for surgical patients in tube thoracostomy is usually limited to 24hrs duration and is 1st generation cephalosporin. It is meant to cover s. aureus the most common organism found in post traumatic empyema

increasing antibiotic use is leading to increase incidence of drug resistance

Potential infectious complications of penetrating or blunt chest trauma:

  • Post Traumatic Empyema
  • Pneumonia

Literature is mixed on whether antibiotics should be given for chest tubes placed for trauma.

In 1998 EAST guidelines gave a level 3* recommendation to give antibiotics prophylacticly to reduce incidence of pneumonia based off of Class I and Class II** data. AND there was insufficient data to give prophylactic antibiotics for post traumatic empyema

This recommendation remains controversial because 

  •    In order for antibiotics to be prophylactic they have to be given prior to a procedure and must reach a steady state concentration in the tissue before an incision is made.
  •    In the case of antibiotics given after a trauma has already occurred, the pleura has already been violated regardless of whether it is penetrating or blunt trauma. Therefore antibiotics do not reach needed concentration before contamination has concerned so these antibiotics are considered presumptive antibiotics.
  •    Non standard definitions of pneumonia and empyema were used, as well as various antibiotics were used in the different studies

In 2012 EAST guidelines reviewed the use of presumptive antibiotics for chest tubes (Tube thoracostomy):

They decided that they cannot make a recommendation for or against the routine use of presumptive antibiotics for chest tubes placed for traumatic hemopneumothorax.

Nor are they able to recommend an optimal duration of antibiotic prophylaxis when antibiotics are administered for traumatic hemopneumothorax because there are insufficient published data to support the routine use of antibiotics.

They concluded:

No single published study has been powered to adequately address the practice of administering presumptive antibiotics in TT for traumatic hemopneumothorax to decrease the incidence of empyema or pneumonia. Until a large and likely multicenter, randomized, controlled trial can be performed, the routine practice of presumptive antibiotics in TT for chest trauma will remain controversial.

If you want to read the article it isn’t a long read:
Post by: Dr. Ashley Guthrie, DO

Case of the Week #1

CC Chest pain and palpitations

HPI Pt is a 23 y/o male with no PMHx presenting with c/o palpitations, chest pain since last night. Pt states the pain is localized to the mid sternal chest wall with radiation to b/l upper extremities at times. Pt states the pain came on suddenly last night and he didn’t think anything of it so he went to bed. He woke up this morning with same pain and now with associated nausea and dizziness prompting the visit to the ED. Pt has never had pain like this in the past. Denies vomiting, F/C, recent illness, sudden cardiac death in the family other than a 70 y/o uncle who was obese. Pt denies drug use and states he was drinking over the weekend 2 days ago.

PMHx: none

Meds: none

Allergies: none

PSHx: none

Social: occasional ETOH, (-) drugs

Pertinent PE and Vitals: BP 90/62 P 186 RR 22 O2 sat 100% RA

General: Awake, alert, mild distress Cardiac: (+) tachycardic; no murmurs Lungs: CTAB, no rales, no rhonchi, no wheezing Abd: soft, nontender, nondistended Skin: diaphoretic; mild pallor

Pertinent Labs (if any) Troponin: 0.439

DDX: SVT with aberrancy vs VTach

ED Course: Pt placed on cardiac monitor immediately and IVF bolus initiated. Adenosine 12 mg IVP given while rhythm strip running with no change. A second dose of Adenosine 12 mg IVP given again with no change. 150 mg Amiodarone given with improvement of HR from 190’s to 170’s still wide complex. Second dose of 150 mg Amiodarone given with improvement of HR from 170‘s to 150’s and eventually converted to a NSR rate 85. Pt remained in stable condition and BP responsive to IVF. Pt admitted to telemetry and Cardiology consulted. While still in the ED, pt reverted back to wide complex tachycardia. 3rd dose of 150 mg Amiodarone given and recommendation from Cardiology was to try a 20 mg IVP of Cardizem. Cardizem given and pt immediately converted to NSR. Pt started on Cardizem drip and upgraded to the CCU. Pt underwent EPS and AV dissociation was noted. Determination was Verapamil Sensitive Ventricular Tachycardia. Pt remained stable throughout hospital course and started on Verapamil. Discharged on hospital day #3 with follow up with cardiology clinic.

Final Dx:  Idiopathic Fascicular Left Ventricular Tachycardia AKA • Fascicular Tachycardia • Verapamil-sensitive VT • Belhassen-type VT

Discussion:  MC type of idiopathic tachycardia of LEFT ventricle ! It is a reentrant tachycardia typically seen in young patients without structural heart disease ! Verapamil is first line treatment • Dose: 10 mg IVP over 1 minute ! EKG features: • Monomorphic V tach • QRS 100-140 ms (narrower than other forms of Tach) • Short RS interval 60-80 ms • RBBB pattern • Axis deviation depends on anatomical site of re-entry circuit ! Often misdiagnosed as SVT with RBBB ! Keys to dx: • Observe features of VT such as caption/fusion beats, AV dissociation • Usually unresponsive to adenosine, vagal maneuvers, or beta blockers

Post by: Kristen Pena, DO

Recent Pubs

We’ve had a bunch of publications in both peer-reviewed and non peer-reviewed sources over the past few weeks! Check them out when you get a chance:

Traficante and Kashani in the Journal of Clinical Toxicology talking about a Massive Calcium Channel Blocker OD

McGovern and D’Amore in Annals of Emergency Medicine talking about Peds EM Education 

D’Amore, McGovern and McNamee in ACEP Now talking about End-tidal for DKA and COPD

Pena, Mota and McGovern in AAEM/RSA Blog going over the elusive Porphyria diagnosis and management 

DeFranco and McGovern in ACOEP’s Fast Track talking about Isolated Bandemia 


Just because she cannot pee, does not mean “No UCG”

Let’s face it, we’ve all done it. And, believe me when I tell you all the cool cats are doing it, too.  Of course, I am referring to the use of whole blood to determine a woman’s pregnancy status in the Emergency Department using the urine pregnancy test strip. ucg-bcg-photo-brancato

Did you know that the common ICON 25 Beckman-Coulter hCG tests are actually approved for both urine and serum? Don’t feel bad; I didn’t until I read a recent article. Whole blood, which is comprised of serum (54%), hematocrit (45%) and leukocytes/platelets (1%), was rumored to detect a woman’s pregnancy status.  Now, we have research that confirms our suspicions and demonstrates that whole blood pregnancy testing performs quite excellently.

In a study published in 2012, whole blood pregnancy tests were found to be 96% sensitive, 100% specific with a negative predictive value of 98% and positive predictive value of 100%. Translation: Trust a positive test, it will not be wrong.  Can it miss? Yes, it can; however, there’s a good chance that the urine test will be negative at that point, too (5 of 9 that were missed with whole blood testing of the studied 425 pregnancies were also negative on the urine testing—the other 4 of  9 did not undergo urine testing).

As troops on the front lines of medicine, we are presented often with little time to think or to act. We are adroit at putting puzzle pieces together, often with little information. This is our creed and such is our nature.  It is during these critical cases, that the application of using whole blood pregnancy testing has its greatest application.

Post by: Raphael Brancato, DO (@DrRayFields )

Tox Box Journal Club

In this installment of the Tox Box Journal Club we are going over three articles reviewed at the NYC Poison Control Center in Manhattan last week.  Two of the articles discuss utility of lipid emulsion therapy in animal models and a third on the deleterious effects of methotrexate dosing errors in Australia.
Background: LAST = Local Anesthetic Systemic Toxicity is a well described phenomenon which can occur from accidental intravenous administration of anesthetics during peripheral nerve blocks or other procedures. Seizures are often described following accidental intravenous administration, which can then lead to cardiovascular collapse in the setting of severe acidosis and hypoxia. This study was designed to see if there exists a role for lipid emulsion therapy for LAST. Prior animal models did not account for the acidosis / hypoxemia that is known to occur, and this model was able to simulate these settings
Methods: 20 pigs separated into 2 groups of 10. All were anesthetized/paralyzed/intubated. Then infusions of levobupivicaine were administered to each at a dose of 3mg/kg, then five minutes of hypoventilation, then 1mmol/kg of lactic acid infusion (to simulate aforementioned settings). One arm was given Lipid emulsion, the other arm was given Ringer’s acetate. Mean arterial pressure / HR / EKG/QRS/ and plasma concentrations of the anesthetic were all monitored and compared. 
Results: The data show that there was no effect of lipid emulsion compared to that of the ringer’s acetate. QRS took similar amounts of time to narrow in both arms. Pharmacokinetics of Levobupivicaine were the same in both groups. 
Bottom Line: Although there have been case reports describing successful resuscitation of patients who suffer from LAST who were given lipid emulsions during resuscitation, this particular model which simulates acidosis and hypoxemia in pigs, does not support the use of lipid emulsion therapy for local anesthetic toxicity. There seems to be a growing body of lack of support based on this study and others like it. 
Background: Intravenous lipid emulsion (ILE) is a potential antidote for severe overdoses and its use in cocaine toxicity has been suggested; however, it is not well characterized. Its potential use as an antidote during cocaine toxicity was the focus of this study to see if cocaine-induced cardiac arrest in rats was able to be reversed using this therapy.
Methods: 12 rats were given lethal doses of cocaine IV over 30 seconds, and mechanical chest compressions were initiated once asystole was noted. One arm was given ILE, while the other arm was given a similar bolus rate of 0.9% NS. 
Results: The data show that ILE had no affect in the terminal outcome in cocaine-induced cardiac arrests in this particular rat model, suggesting that this is not an appropriate toxin/antidote pairing. Only 1 of 12 rats received ROSC and was found to be statistically not significant. This rat was in the ILE arm of the study.
Bottom Line:  This article demonstrates some potential design flaws including small sample size,  and withholding ACLS medications post cardiac arrest which potentially would have aided in resuscitation. 
This was a retrospective review article which sheds light upon the fatal errors which can occur as a result of accidental, improper dosing of methotrexate (MTX).  After looking at the Australian database for reported poisonings, errors occurred for a number of reasons and the ones most commonly identified were: 
  •  mistaking medication for another medication
  •  care-giver/nursing home error
  •  MTX was newly prescribed medication
  •  pharmacy dosing packet error
  •  misunderstood directions
  •  patient believing it would improve efficacy
  •  prescribing error by physician
  •  dispensing error
  •  labeling error 
As a result there were 22 deaths noted to be linked to MTX administration errors
Bottom Line:  These medication errors are not uncommon, and because MTX is a high risk medication which can become fatal if taken incorrectly, further care is warranted in dealing safely with this medicine. A multi-faceted approach should be considered and suggestions are still ongoing. Some recent suggestions have been to change packet size, to increase education/awareness, mandatory weekly dosing labeling on packaging, including software alerts for prescribers and dispensers
Post by: Dr. Ray Brancato (@drrayfields)

Fat embolism syndrome

Typically when we start talking about anything related to fat embolisms our minds go immediately to trauma and long bone fractures as the cause, but this isn’t always the case. The constellation of signs and symptoms of respiratory insufficiency, neurologic dysfunction and petechial rash which are typically associated with fat embolism syndrome can also be caused by pancreatitis, sickle cell disease and liposuction; all of which show up regularly in the Emergency Department. With mortality rates as high as 20%, despite the fact that FES usually doesn’t present for at least 12 hours after the initial event, it should be something that we are aware of.

There are two competing theories as what causes FES. Some believe more in the mechanical-obstruction theory where the fat globules act similarly as other embolic events, showering throughout the end organs and wreaking havoc by those means. The new challenger to this theory is the biochemical theory where proponents support the notion that the fat is broken down into free fatty acids and the damage is caused by the endothelial damage and subsequent increased vascular permeability. No matter which theory you support, the clinical diagnosis is going to be equally as challenging. There are a few criteria/scores that have been developed in the past that are non-specific diagnostic tools to identify patients with FES, but they have not been compared head-to-head in their accuracy. In the Emergency Department we are limited with the tests that we can routinely order. Unfortunately, CXRs are going to be essentially useless in diagnosing FES, but MRI may hold more promise. The starfield pattern seen on MRI is not specific to FES, but has been seen routinely in patients who have disease processes associated with FES along with neurologic symptoms. Otherwise, in the ED this is going to essentially be a clinical diagnosis with a good history and a little bit of luck. There is some evidence that earlier fixation and specific orthopedic surgery techniques may decrease the rate of FES, but from an EM point-of-view it is essentially supportive care. Research seems to be lacking into the non-trauma causes of FES, so maybe there is somewhere for us to intervene in those patients…

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Time for Terlipressin?

Correct, we don’t have terlipressin in the US, yet… Hopefully, sometime in the not so far off future we’ll have the chance to play around with it. Essentially it’s a synthetic analog of vasopressin which we are more familiar with. There’s some written about its use in variceal bleeds and here is a cool little study from Egypt using it for refractory septic shock.

They enrolled 80 ICU patients that were in refractory septic shock; meaning that they had to meet sepsis criteria and have the following three criteria:

  1. SBP < 90mm Hg or MAP < 70
  2. Received at least 1000ml of IVF or CVP 8-12cmH2O
  3. Necessitated more than 0.5 mcg/kg/min of norepinephrine

The 80 adult patients were split into two, pretty well matched groups, of 40. One group received adrenaline (0.2ug/kg/min) as their second-line vasopressor and the other group received a continuous infusion of terlipressin (1.3ug/kg/hr). This study was interesting because it only lasted for the next 6 hours after the second vasopressor was started. Unfortunately, they really didn’t look at patient related outcomes, but instead their primary endpoints were:

  1. MAP > 65 mmHg
  2. Systemic vascular resistance index > 1300 dynes s/cm5/m2
  3. Cardiac index > 4 L/min/m2
  4. Oxygen delivery index (DO2I) > 550 ml/min/m2

From an Emergency Medicine point-of-view the MAP is probably what we are most familiar with and is an easy enough measure to monitor in the ED.  After initially starting with a statistically equivalent MAP before the start of the second vasopressor, to having a statistically significant difference (p<0.001) after the 6 hours is hard to ignore despite the lack of reported clinical outcomes. This was in addition to showing improved hemodynamic measures and decreased doses of norepinephrine needed in the terlipressin group. This by no means is the do-all and end-all for terlipressin, and doesn’t mean we start throwing it at everything with hypotension when it gets approved in the US. Might as well get familiar with it now though, so when it does show up there are no surprises.

Post by: Terrance McGovern DO, MPH (@drtmcg13)


It’s difficult to miss a raging STEMI or a CVA with unilateral flaccid paralysis, but there are other, less-sexy diagnoses that we have the opportunity to make in the Emergency Department that can be as important and impactful to the patient’s health.  Endophthalmitis is a difficult word to spell and equally as difficult to diagnose if you’re not looking for it.  Check out Dave Traficante’s recent post on EM Resident on Endophthalmitis.

Fixed dose PCC?

In the past, vitamin K and FFP were the mainstays of reversing warfarin, but now we have fancy new drugs like four-factor prothrombin complex concentrate (4F-PCCs).  4F-PCCs can rapidly reverse the INR of warfarin induced coagulopathy with less volume and quicker than FFP.  Many of the dosing regimens base the dose on the patient’s presenting INR and body weight, with ranges from 25-50 IU/kg.  A few problems arise with this approach, first the INR is not immediately available.  Second, 4F-PCCs are not cheap; costing up to $7,000 per patient in some cases.  Is there a fixed-dose regimen that we can give to patients on vitamin K antagonists without having to wait for the INR?

Some studies have looked at using 500 IU and 1000 IU fixed dose regimens for reversing the INR.  The 500 IU only corrected the INR in 43% of the patients, whereas the 1000 IU fixed dose study showed better clinical outcomes in 83.5% of the patients, but there is concern that the obesity epidemic in the United States will dilute the IU/kg concentration of the 4F-PCC and not be as efficacious.  Klein et al looked at using a fixed dose of 1500 IU of 4F-PCC for reversal of warfarin in 2015.  It was a relatively small sample of 38 patients on warfarin with the vast majority of them presenting with an intracranial hemorrhage.  Each patient had their INR drawn and then 1500 IU given before the result of the INR returned.  92.3% of the patients had their INR lowered to less than 2.0 after the 1500 IU of 4F-PCC and they reported no thrombotic events within the subsequent 7 days.  The presenting INR median was 3.3 (2.5-4.0) which was reduced to 1.4 (1.2-1.6) after administration of the 4F-PCC.  Additionally, this saved $40,273 dollars when compared to the typical INR and weight based dosing regimen for their patient sample.

We’ll have to figure out whether this fixed dose regimen of 1500 IU is the way to go, or should we base the dose solely on the patient’s weight and not worry about waiting on the INR.  Does waiting the extra 20 minutes for the INR lead to improved clinical outcomes?  And if we are going to start using a standard dose, is there a role for pre-hospital administration of the 4F-PCCs?

Post by: Terrance McGovern DO, MPH (@drtmcg13)


Lower abdominal pain in women can be challenging diagnostic dilemma in the Emergency Department. We had a case of a 50-year-old woman that had been previously seen by her PMD 3 days prior and diagnosed with a “small kidney stone” without any imaging, but did get the ever-reliable percocet prescription. Needless to say, she came to the ED because her pain wasn’t getting any better and now she was having increasing lower abdominal pain with high fevers. In the ED she was febrile (T: 104.5) and tachycardic (HR: 120s), but her BP was normal. She ended up having a WBC: 17k/mm3, bands: 20% and a pretty nasty UTI. Her pain persisted and we ended up doing a CT abd/pelvis with contrast to see if she had anything brewing. From the images below you can see that she had bilateral tubo-ovarian abscesses causing bilateral hydronephrosis seen on CT and confirmed with ultrasound. She was started on ampicillin, clindamycin and gentamicin and her abscesses were drained with CT guidance, yielding 400cc of thick, brown, purulent fluid. Yum

Figure 1 Figure 2

Up to one half of all cases of tubo-ovarian abscesses occur in patients with a history of pelvic inflammatory disease (PID). The theoretical etiology of tubo-ovarian abscesses is thought to revolve around an ascending infection arising in the lower reproductive tract, into the uterus and subsequently the fallopian tubes and ovaries. While Neisseria gonorrhea and Chlamydia trachomatis are commonly associated with PID, TOAs are typically polymicrobial and rarely grow either chlamydia or gonorrhea when cultured. As with most pelvic pathology, ultrasound remains the initial diagnostic modality of choice for tubo-ovarian abscesses to best visualize the upper reproductive tract. Ultrasound remains very specific (86-98%), whereas the sensitivity ranges between 56-93%. There is evidence however that computed tomography of the pelvis with contrast may provide better sensitivity than ultrasound in evaluation of TOAs. In the Emergency Department, a triple coverage antibiotic regimen (i.e. ampicillin/clindamycin/gentamicin) should be initiated despite whether the patient is going to need surgical exploration, percutaneous abscess drainage or conservative management. If the patient’s clinical status has either worsened or not improved after 48-72 hours the gynecologist will likely proceed with minimally invasive drainage procedures that have become more readily available, similar to our case.

Post by: Terrance McGovern DO, MPH (@drtmcg13)