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

Getting ready to intubate? Let’s pray they don’t DESATurate!

You head over to bed 44 to meet the BLS crew as they start telling you about an 82 year old man who has been having trouble breathing and is “confused” as per his family.  His oxygen saturation when you check is 76% and quicker than you can say “sepsis”, the eager resident has popped the grey airway box open and is setting up to intubate.

You slap the NRB on and turn the O2 up all the way.  So why is the resident so focused on finding and placing a nasal cannula too?!

Apneic oxygenation (AO) is used to extend the time until critical arterial desaturation (SaO2 88-90%) following cessation of breathing/ventilation that occurs during intubation.  AO, similar to our other RSI preparation, premedication, and positioning, is used to optimize the patient prior to the first intubation attempt.

First demonstrated by anesthesiologists over 50 years ago, the alveoli of the lungs will continue to take up oxygen even in the absence of active breathing.  AO focuses on increasing a patient’s oxygen saturation through “nitrogen washout” in first the alveoli, and then throughout the circulation.  This effectively replaces the nitrogen one inhales in normal atmospheric air with oxygen and increases the patient’s overall oxygen storage in both the lungs (95% of a person’s natural reservoir) and bloodstream.  Maximizing pre-oxygenation provides us an additional buffer of time for “safe apnea” during oral intubation.  In a 2011 article in the Annals of Emergency Medicine, Weingart et al outline recommendations to reduce the risk of hypoxemia during emergency tracheal intubations which include emphasis on:

Pre-oxygenation for every patient

  • Nasal Cannula set at 15 L/min is the most effective method of AO
  • Non-rebreather mask at rates as high as possible
  • HOB elevated 20-30 degrees or Reverse Trendelenburg in suspected C-spine injuries
  • Minimum of 3 minutes total or 8 deep breaths, if possible

Take home:  Keep in mind the acronym “NO DESAT” which stands for “Nasal Oxygen During Efforts Securing A Tube”.  A nasal cannula with high flow rates should be placed on every patient prior to endotracheal intubation and left in place during attempts in order to reduce the risk of hypoxemia and deterioration.

AMA after Narcan – Is it safe?

In comes a 34-year-old male who is obtunded with pinpoint pupils and breathing at five times a minute; likely due to heroin abuse.  He wakes up after Narcan is appropriately administered, but now he wants to leave.  What is the risk of death if he leaves?  Do we restrain him against his will to monitor him for possible recurrent respiratory depression?

We have some pre-hospital literature that looked into this issue.  The studies looked at patients who refused care after pre-hospital providers administered Narcan for a suspected opiate overdose.  They then searched the death registry to see if those patients later died after refusing care (transport to the hospital).

Wampler et al. looked at 552 patients and found that no one died until at least 4 days later (1).  These deaths four days later were unlikely to be from the initial overdose.  A second study recently published in March of 2016 had 205 patients and showed only one death in 24 hours (2).  Two others died in the 30-day follow up period which again were not likely due to the initial overdose.  Combining the numbers from these two studies equates to 1/757 (0.13%) deaths.

There are limitations with all studies, but death seems unlikely after refusal of care post-narcan administration.  However, our practice should not change as it relates to monitoring patients for about 4 hours to those willing.  Recurrent respiratory depression is a real concern particularly seen in those patients who abuse long acting opiates.  Despite this, some patients who have the capacity to make decisions may not choose the wisest care plan and may leave AMA.  We must still make considerable attempts at providing substance abuse referrals and other appropriate resources as these patients are in great need of help.

Post by: Joe Bove  (@jjbove08)

  1. Wampler D, Molina D, McManus J, Laws P, Manifold C. No deaths associated with patient refusal of transport after naloxone-reversed opioid overdose. Prehosp Emerg Care. 2011;15(3):320-324.
  2. Levine M, Sanko S, Eckstein M. Assessing the Risk of Prehospital Administration of Naloxone with Subsequent Refusal of Care. Prehosp Emerg Care. March 2016:1-4.

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 

 

TLC: Triple Lumen Complications

Placing central venous cathethers, whether under ultrasound guidance or based off of your landmarks can be difficult and still prone to many complications.  With the increased use and now standard of care for placing central lines with ultrasound guidance you would think we are immune to the “catastrophic” complication of an inadvertent arterial cannulation.  But does ultrasound make us infalliable? Are there other methods that we can use to confirm venous placement of these large catheters?

Traditionally, we have looked at the color and pulsatility of blood coming from the needle hub before placement of the guidewire, but as you can imagine this is known to not be the most reliable; most of us aren’t going to go through the hassle of checking a blood gas off that blood either.

Troianos et al. found that ultrasound guidance reduced the incidence of arterial puncture from 8.4% down to 1.4% during attempted IJV cannulation.  That’s great that it decreased the incidence, but when looking at the complications such as airway obstruction, hemothorax, pseudoaneurysms, AV fistulas and stroke, 1.4% is not something to sneeze at.  So, keep in mind that although it does reduce the frequency of arterial puncture, it does not eliminate it entirely!

Despite the use of dynamic ultrasound guidance, there are still numerous reports of arterial placement of large bore catheters due to a couple reasons: 1. The needle tip may not be seen in the same plane of the ultrasound and confused with the shaft of the needle.  2. The needle may be in the vein, but the needle may move into the artery during placement of the guidewire after most of us have abandoned the ultrasound visualization.  Ideally, after the guidewire is placed we should make it a habit to confirm the guidewire is in the vein before dilating the vessel.

Management of Arterial Cannulation

Despite our best efforts and even the most astute ultrasonographer there is always the potential for an inadvertent arterial cannulation, but what do we do once we have figured that out?

Option 1: Just old fashioned PULL AND PRESSURE: essentially this is exactly as it sounds. You pull out the catheter and apply pressure, just like any other line that is being removed. This is probably most reasonable for femoral artery cannulations, but there still remains a possibility of false aneurysms and AVF as late as 2 weeks after removal with the pull and pressure technique.  Pull and pressure isn’t supposed to be used for carotid or subclavian arterial cannulations.  One convincing piece of evidence is that there is an immediate stroke risk of 5.6% after removing carotid cannulations with this technique.  Of 11,874 internal jugular vein cannulations, 20 ended up being carotid artery cannulations.  19 of these 20 were removed using the pull and pressure technique; six patients suffered complications and two of the patients died.

Option 2: Surgical ENDOVASCULAR repair:  The more preferable method, especially for removal of carotid and subclavian arterial cannulations, is to involve our vascular surgeon colleagues.  Just leave the line secured to the neck and get them involved. Some are going to request a formal ultrasound of the carotid or even sometimes a CT angio of the neck to check for extravasation, pseudoaneurysms, AVF and the location of the catheter.

Key points to remember

  1. Arterial cannulation can occur despite use of ultrasound guidance
  2. The American Society of Anesthesiologit’s guideline for CVC placement states that color and pulsatility are NOT reliable for distinguishing vein from artery.
  3. The pull/pressure technique is associated with significant risk of hematoma, airway obstruction, stroke, and false aneurysm especially when the site of arterial trauma cannot be effectively compressed
  4. Low IJV placement can injure the subclavian or innominate arteries
  5. Endovascular treatment is safe for management of arterial injuries that are difficult to expose surgically, such as those below or behind the clavicle.
  6. Normal Carotid Duplex after removal of a catheter form carotid artery does NOT rule out the possibility of a stroke
  7. False aneurysms or AV fistulae can occur LATE, up to 2 weeks after the “pull and pressure” technique so close follow up is needed

Post by: Dr. Yenis Paez-Perez, DO

 

 

ALTO at it again

The ALTO program (Alternatives to Opioids) at St. Joe’s has already received national recognition for its work here.  In March we held a legislative summit that was attended by U.S. Senators Bob Menendez, Cory Booker, US Congressman Bill Pascrell, Jr and multiple other members of the local and state government to discuss the opioid epidemic and the ALTO initiative.  Then we were lucky enough to have the New York Times write a story recent story in June on the ALTO program as well.  Not to be outdone, EM Resident recently published a piece to introduce the EMRA readers to the wonders of ALTO and the success we have had thus far with the program, check it out here.

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)

Emergency Medicine Symposium

We are hosting our 8th Annual Emergency Medicine Symposium on May 4, 2016 at the Passaic County Public Safety Academy in Wayne, NJ. This year we are fortunate enough to have Dr. Kevin Klauer, DO, EJD, FACEP (@Emergidoc) as our keynote speaker, discussing Efficiency in the Emergency Department. Dr. Klauer is one of the top speakers in Emergency Medicine today and a true leader in our field. Visit emsymposium.org or call 973-754-2240 to register, CME is available.