Tag Archives: Pharm

Wound prophylaxis – Should lip lacs get antibiotics (and few others)?

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During my review for 72 hour returns we had a through and through lip laceration come in that returned with a wound infection a few days later.  This prompted me to look up current recommendations as I’m pretty sure that I haven’t been giving antibiotic prophylaxis for this.

Searching literature, Tintinalli and UpToDate…… Most superficial wounds do not require prophylaxis, however, through and through lip lacerations were an area of uncertainty and debate….

Tintinalli  – “matter of provider preference.”

UptoDate – no clear clinical evidence to say that these wounds should receive antibiotic prophylaxis , however, due to the pathogens of the oral cavity, they recommend prophylaxis.

Current literature – Review article in 2008, Annals of Emergency Medicine, Mark DG et al – review of studies do not show a statistically significant benefit; however, the only double-blinded randomized control trial showed a trend toward benefit in patient’s that were compliant with therapy.

Some other stats – Rate of infection in wound treated in the ED (Tintinalli)

Head and neck 1-2%

Upper extremity 4%

Lower extremity 7%

Oral wounds – 9-27%

If giving prophylaxis then Pen VK or Clindamycin is recommended for 3-5 days.

For other oral wounds, <1cm, no need to close. Close if large gap susceptible to food getting trapped, and counsel on good oral hygiene.  Dental and OMFS usually recommend d/c with chlorhexidine gluconate oral rinse (0.12%) (Peridex) and will have patients swish and spit after meals to keep the wound from contamination with food particles.

My take away from this is strongly consider antibiotic prophylaxis with through and through oral wounds as they are higher risk for infection with oral flora; however, not an absolute must based on the current evidence.  Be sure to emphasize good oral hygiene, and as always, close follow up with good return precautions.

Other wounds to strongly consider prophylaxis due to increased risk for infection are mammalian and human bite wounds, crush injury, puncture wounds, and wounds with either fresh or salt water contamination, or patients who are immunocompromised, asplenic, advanced liver disease, associated edema (according to the IDSA).

Open fractures and wounds with joint capsule violation should receive antibiotic prophylaxis.

Reminder: Update Tetanus and simple lacerations do not need antibiotic prophylaxis.

Push Dose Pressors

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Are you all tired of hearing about sepsis yet?  How about the fact that we apparently suck at sepsis?  However, I think we can all recognize when someone comes in with severe septic shock.  You know, the sick, hypotensive, altered patient with a source of infection.  With a low blood pressure, we just need to keep pushing more fluids right?  Just keep pushing them until they are in pulmonary edema.

Well, what could we possibly do to improve outcomes?  The longer they are hypotensive, the more end organ damage they are going to sustain, and the worse the outcomes.  I know that most of you all listen to EMCrit.  If you don’t, you should.  So while waiting for that central line to be placed by our intern (and we know that can take a while, j/k interns, I love you) and waiting for the levophed gtt to be started, we can be like Weingart and give some push dose pressors.  Not only could they be used for that septic patient needing a boost in BP, but can also be used for the peri- or post-intubation or sedation patient that becomes hypotensive.

Epi-It’s not ideal to give code dose epi to someone with a pulse.  Instead take a 10 mL syringe and fill it with 9 mL of NS.  Then draw up 1 mL of epi from the cardiac amp.  This gives you 10 mcg/mL of epi.  Now, give 0.5-2mL (5-20mcg) q1-5 min until improved BP.

Phenylephrine- Draw up 1 mL of phenyl from a vial that is 10 mg/mL and put in a 100 mL bag of NS.  This gives you 100mL of phenylephrine at the concentration of 100mcg/mL   Now you draw up 10mL into a syringe at push 0.5-2 mL (50-200mcg) q1-5 min.

And for your convenience, here is a link to a PDF from EmCrit with the instructions on how to mix these.  Take a pic, keep it on your phone.  While doing this, don’t forget patient safety.  Make sure you’re labeling your syringes when you mix up push dose pressors.  Avoiding medication errors is always plus.

Also, until you are comfortable doing this, make sure you are collaborating with your attending and the pharmacist if they are there at the time.

Finally, read this article on safety considerations in push dose pressors.

And for added fun, read all room9ER posts in Danny DeVito’s voice.  It makes everything better.

 

Cool Name, Not So Cool Results

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53yo WM rolls in, wee hours of the am.  C/o HA, onset around 4 days ago.  Wife says “I think he had a seizure in the middle of the night that night”    Def hit his head, has a goose egg middle of the forehead.   “Had some labs done at my primary yesterday, they called me and told me to come in”   No clue as to what labs those might be when asked.   Awesome.  Medical hx only significant for HTN and GERD.   No chronic meds.   Admits to drinking around a case of beer a day.   Probably explains the not so full history he provided.   Nothing else interesting on physical exam and normal vital signs.  So I send labs- CBC, Chem13, Mag, CT his head due to the possible seizure.

Annnnd Na 114, K 2.5, CL 75, Bicarb 32, BUN 12, Cr 1.2, Glucose 111, Ca 8.4.   CT normal.  ETOH and Tox NL.   Serum osmolality 259

So what’s going on here?   Hyponatremia and seizure- needs fixed right.   Normal saline or even hypertonic saline maybe?

Negative ghost rider

Lets look at this a little deeper.

Start with the algorithm

Image result for hyponatremia algorithm

So we will start with the asymptomatic column.   Could argue for the severe side due to the seizure, but he is now 4 days out and asymptomatic.   Went the euvolemic side of things.   No signs of fluid overload clinically and didn’t look dry.  Actually nerded out and ordered urine osmolality.  88.    So where does that land us?

Beer Potomania syndrome.

WTH is that?  Great name.   But too much physiology for my brain.

When patients have poor protein and solute (food, electrolytes) intake, such as in chronic alcoholics, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.

Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load includes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.

However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake … as long as you are not drinking excessive amounts of water.

Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.   

So, we see alcoholics all the time.  Why don’t we see this all the time?   When you think about it, a pretty low percentage of our EXI all star drinkers are beer drinkers.  And most case a day beer drinkers actually have a decent oral food intake.   Making this more rare than you originally might think.

So what do we do about it?  Classic example of ‘dont just do something stand there!’

Fluid restriction, fluid restriction, fluid restriction.

Back to my case.  Admit the patient to my hospitalist, who is half asleep and currently not as excited as I am about hyponatremic management.   Orders in for fluid restriction and serial chemistries.    A few minutes later, I hear my ER nurse arguing with the floor nurse during calling of report.   They are appalled that I am not giving normal saline, and even request hypertonic saline.  I politely pick up the phone and discuss the physiology and reason for my treatment plan.   We were on the same page by the end of the call.

Fast forward to a couple days later.  I come back for another shift, and am checking on my patients from the day before (quick aside, no matter where you are in your career always save the info for 3-4 of your sicker, more interesting patients and look them up on your next shift, by far one of the most high yield learning you can get.   And will help you adjust your practice as indicated).   I look up the serial sodium results.  114, then 119, 123, then………145.   Goooooooo!!!!  Assuming I am about to hear from the Kentucky Hammer due to causing central pontine myelinolysis.  I talk to the hospitalist- apparently the next shift nurse, after the one I talked to, got her way, and they got an order to blast the guy with normal saline.  Hence the huge jump.   Patient did have some transient AMS, but was at baseline and neuro intact once levels stabilized.  Thank god.

Anyway, interesting case.  Beer potomania.   cool name, not so cool results.   Literature states that central pontine myelinolysis happens in over 20% of these patients due to too rapid correction.  So before you pull the trigger on normal saline repletion take a second and scope out the algorithm above.  Sometimes the best thing you can do is nothing.

Reub Strayer – Droperidol and the Dangerous Patient

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Every resident must listen to this podcast (or watch this video) at once. I finally listened to it and was pleased to find it a concise, evidence-based and accurate talk. I avoided watching because I thought he would talk about how much he loves his droperidol and that we should all use it, which would fill me with unbearable envy, since we have not had it in Louisville for years. I have been aware that no US company manufactures it but many EM / FOAMed docs still talk about it. Well Dr Strayer now has no access to the drug and shares his disappointment.

Take home points:

  1. Droperidol is a magical, wonderful drug and we need it back.
  2. The end

No but seriously many great points related to managing the combative patient. From the mildly disorganized schizophrenic, all the way to the truly medico legally dangerous excited delirium, Strayer gives inarguable advice. I love the “shove an O2 mask on the patient who is being restrained by 6 security guards.” He notes that this will often calm the patient, it will protect from spitting, and it will oxygenate the patient. Many other practical pearls here that you WILL USE pretty much every shift at UofL.

Post your favorite tips in the comments.

Can you give Vasopressors through a PIV?

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I looked back and couldn’t find a post about this topic in the last year or so but forgive me if it has already been posted. I have been following R.E.B.E.L. EM for a few months now  and I would recommend it to everyone who has the time and wants quick summaries on the latest EM literature.  They have short written summaries of papers including pros/cons of the study and what they feel are the most important take away points. It was founded by Salim Rezaie with Rob Rogers, Matt Astin and Anand Swaminatham serving as editors.

Occasionally they will have a “mythbuster” post looking at common myths in the ED and the most uptodate literature available on the topic. (their latest mythbust is on “safe” glucose levels before ED discharge but I digress)

 

Back in May they reviewed the safety of vasopressors through a PIV. The topic paper was titled “A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters”

What the review found was very interesting: of 318 events, 204 results in local tissue damage, 114 were only extravasation events and 7 events involved the use of a CVC (so clearly not completely safe). Interesting, of the 204 local tissue events 85.3% involved PIV distal to the antecubital fossa and 96.8% involved administration of >4hrs.

REBEL EM’s take away points were:

In critically ill patients, with hemodynamic instability, vasopressor infusion through a proximal PIV (antecubital fossa or external jugular vein), for <4hours of duration is unlikely to result in tissue injury and will reduce the time it takes to achieve hemodynamic stability.

What I feel like this means for us is simple: If you have a crashing, hypotensive patient who needs a pressor without a CVC but good proximal PIVs, start the pressor immediately, stabilize the patient as best you can, then take the time to properly place a CVC.

Continue to monitor the PIV until it can be switch to the CVC and stop the pressor immediately if there is any suspicion for local extravasation. I am sure this will make some people nervous but I think this is better then placing a “crash line” that is less then sterile which will expose an already ill patient to infection or other complications secondary to a hastily placed CVC.

I highly recommend read their review and how they came to this conclusion along with their other posts. I have included the link to this study at the bottom.

http://rebelem.com/mythbuster-administration-of-vasopressors-through-peripheral-intravenous-access/

Managing Migraine

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As mentioned on R and R in the Fast Lane. This article by Friedman is a welcomed update to evidence-based migraine management. Some people love treating migraine patients, some hate it. But we all have our cocktails we believe in.

I am a fioricet/neurontin/IM compazine, escalating to IV compazine/benadryl/decadron/toradol OR if they want to drive home IV MAG/decadron/toradol … kind of guy.

This article starts with criteria for delineating migraine from other headache forms. Then provides a succinct algorithm for treatment, starting with reglan or compazine +/- benadryl, then another dose plus toradol, then dihydroergotamine, then occipital nerve blocks (very fun), then as a last resort, opioids. I would encourage you to attempt a few other methods before the blocks and especially before the opioids.

Many other medications can be used (keppra, depakote, propofol, etc). But this is a solid overview of the EM approach. Also of note, see the Oct 2016 EM-RAP paper chase of the reglan +/- IV fluids in migraine article which showed no real benefit to the addition of IVF.

1.4% Observed Adverse Reaction Treated With Flumazenil

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Flumazenil (Rx: Romazicon) has recently been described as coming into favor for two unique purposes: (1) hepatic encephalopathy and (2) paradoxical reactions to benzodiazepines.

Regarding the first, flumazenil’s use in hepatic encephalopathy has been well described recently in a Cochrane review of 113 RCTs with a total n = 805, wherein flumazenil had a significant beneficial effect on short term improvement of hepatic encephalopathy.1 This is thought to occur physiologically secondary to reversal of the origin of hepatic encephalopathy—i.e., an accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition1 (principally GABA receptors which are forefront in the stimulation of sedation). Therefore GABA receptor antagonists (such as flumazenil) can be used to directly oppose this mechanism. Effect on full recovery and survival has still not been proven with flumazenil administration.1

Secondly, flumazenil can be used for paradoxical reactions to benzodiazepines2,4 and in a 10 year review of its use, published in the Journal of Emergency Medicine,3 the real safety of this drug has once again come into question, as there were relatively few adverse outcomes even in the highest of seizure provocation risk—which occurred with co administration of pro-convulsant (e.g., TCAs) at a 2.7 % incidence (8/293)—the total incidence including all subjects bore a rate of 1.4% of seizure activity (n = 904).3

I present an example of administration in the second of indications above. I took care of a 26 yo WF with PMH of asthma, a prior severe dental cavity pending root canal and an IV heroin addiction, currently sober and progressing through the the 12 Steps program at the Healing Place. She presented in sepsis, afebrile with qSOFA of 0/3 (Labs: WBC 21.2 with left shift, procal 1.33, ESR 83, CRP 201, lactic acid 0.8 s/p 2 L NS IVFs), and AKI (Cr. 1.6) with dental as well as urinary possible sources. She was eventually discharged on day 3 with Dx of urosepsis, creatinine returned to normal, and had a negative echo for routine endocarditis rule out in the setting of PMH of IVDA.

During her ER stay she was uncomfortable, diaphoretic, pale, GCS of 15, but anxious and in pain, professing severe insomnia for 3 days, stating, “I just want to sleep”. A trial of oral Ativan 2 mg was given, as she did not want any pain medication due to her prior addiction. She noted a small temporary improvement; however 2 hours later this beneficial effect was absent. By now she had received cefepime 2g and vancomycin 25 mg/kg (for potential osteomyelitis coverage), and was requesting more anxiety medications, having already received 50 mg IV Benadryl 30 minutes prior with no improvement noted. Clinically she was GCS 15, pleasant in interaction, increasingly pale, uncomfortable, wide awake at 0445, and subjectively in pain. She was then given 2 mg IV Versed.

Immediately following the administration of midazolam she became altered to GCS 12 (E4, V3, M5), eyes wide, extremities tremulous, pulled out all of her IVs, and was trying to jump off the bed. It was clear she was paradoxically agitated and hyper-aroused. Rather than reversing her (though we doubted history of benzodiazepine use), we opted to watch and see if this reaction would subside without intervention since she responded favorably to the oral Ativan; however the rarely seen but well known paradoxical reaction to Versed was suspected. She was observed 1:1 and thereafter 3:1 for 40 minutes, at which time she appeared to be steadily worsening rather than improving. The decision was made to give an IV push of 0.2 mg of flumazenil (Rx: Romazicon). Within 30 seconds after administration she once again returned to her pleasant self, she was GCS 15, appropriate, and had no recollection of the previous hour, and had no seizure activity noted throughout her stay. She maintained a healthy mental status of GCS 15 and was AAOx4 for the rest of her evaluation and admission.

In 2010, Kreshak et al. reported a similar case and treatment. This paradoxical reaction to Versed in their report is thought to occur at less than 1% incidence, however it is described as commonly as 1.4 %.4 In the reported literature this reaction is described as a patient becoming acutely agitated, restless and aggressive2. Stiffening and jerking of the extremities, and shaking of a part of the body are also noted. When observing a patient with this reaction, after ruling out other etiologies of agitated AMS, Kreshak et al. (2010) opted to administer flumazenil 0.5mg IV, and “…immediately after which the patient became conscious, oriented and calm, the paradoxical reaction was terminated”. The patient had no recollection of the events,2 similar to the patient observed in the ULED.

Per Kreshak et al. (2010), there exist “…different theories concerning the mechanism of paradoxical reactions, involving a central cholinergic effect or the serotonin imbalance”.2 Unfortunately the exact mechanism of paradoxical reactions remains unclear.

Although difficult to locate literature, if seizures develop following flumazenil administration, pharmacology guidelines recommend Valium 20-30 mg IV then immediately switching to barbiturates; some soft EM sources also suggest going straight to propofol.5

Thank you for reading my post.

References

  1. Als-Nielsen, B., Kjaergard, L., & Gluud, C. (2001). Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy. The Cochrane Database of Systematic Reviews (Complete Reviews). doi:10.1002/14651858.cd002798
  2. Cabrera, L., Santana, A., Robaina, P., & Palacios, M. (2010). Paradoxical reaction to midazolam reversed with flumazenil. Journal of Emergencies, Trauma, and Shock J Emerg Trauma Shock, 3(3), 307. doi:10.4103/0974-2700.66551
  3. Kreshak, A. A., Cantrell, F. L., Clark, R. F., & Tomaszewski, C. A. (2012). A Poison Center’s Ten-year Experience with Flumazenil Administration to Acutely Poisoned Adults. The Journal of Emergency Medicine, 43(4), 677-682. doi:10.1016/j.jemermed.2012.01.059
  4. Tae, C. H., Kang, K. J., Min, B., Ahn, J. H., Kim, S., Lee, J. H., . . . Kim, J. J. (2014). Paradoxical reaction to midazolam in patients undergoing endoscopy under sedation: Incidence, risk factors and the effect of flumazenil. Digestive and Liver Disease, 46(8), 710-715. doi:10.1016/j.dld.2014.04.007
  5. (n.d.). Retrieved August 23, 2016, from http://www.goodfriendem.com/2013/05/flumazenil-romazicon-is-probably-safer.html

Hypertonic Saline vs Mannitol

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Research and Reviews in the Fast Lane (which is a must for anyone consuming FOAM) just covered a SR and meta-analysis on hypertonic saline. Relevant after our discussion in conference this morning.

Berger-Pelleiter E, et al. Hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials. CJEM 2016. PMID: 26988719

  • Hypertonic saline seems to be recommended more and more often for intracranial hypertension. What is the evidence in traumatic brain injury?
    This is a systematic review and meta-analysis that identified 11 RCTs covering 1820 adult patients with traumatic brain injury comparing hypertonic saline to either mannitol (½ the studies) or another solution (often normal saline, or even hypotonic saline.) Hypertonic saline did not decrease mortality (RR 0.96, 95%CI 0.83-1.11). It didn’t lower intracranial pressure (weighted mean difference -0.39, 95%CI -3.78 – 2.99). And it didn’t improve functional outcomes (RR 1.12, 95% CI 0.92-1.36). Maybe we shouldn’t be rushing to adopt hypertonic saline in the management of traumatic brain injury.
  • Recommended by Justin Morgenstern

A Mysterious Death in a 21 yo Healthy White Female, and the Larson Maneuver

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My wife is at work at a hand surgery pre-op care clinic. It is her birthday. In walks a middle-aged male who is about to have tendon reconstruction after he sustained a crush trauma, and is excited about the possibility of returning to work. He is slightly abrasive and somber, despite the prospect of receiving the surgery.

My wife asks him if he is concerned about the procedure, asks if he is feeling well, asks if there is anything she can do to help. With a quiet manner he states all is well. To make discussion my wife states today is her birthday and she is excited to celebrate when she gets home. He smiles and states today is also his daughter’s birthday. She was born the same year as my wife. He states today is always a rough day for him because she passed away in an emergency room 7 years ago at 21 years of age.

We can never fully understand where those we treat are coming from, their life experiences, or what their home situations, thoughts, fears, dreams, and worries entail; and this was a reminder for me. He stated that his daughter was healthy,woke up without issue on that day, but later developed difficulty breathing and wheezing. She was diagnosed with an acute asthma attack. She had one episode in the distant past but was not on any routine medications. She was given albuterol and experienced a negative reaction to the albuterol and completely stopped breathing. She was brain dead by the time she was intubated. They withdrew care in the emergency department.

After my wife shared this with me, I searched to find any case reports of paradoxical reactions to albuterol. Below are three related cases, however bronchospasm becoming worse with beta-blockers is exceptionally rare.

Case reports of paradoxical bronchospasm to inhaled beta agonists:

What I think more probable, and possibly related to the above case reports, is acute laryngospasm. The albuterol she received may have further irritated her vocal cords potentially worsening, rather than relieving her vocal cord dysfunction. Both Resus.me and LITFL (Life In The Fast Lane) have very useful articles describing management (see below for links). Here is a brief synopsis:

Laryngospasm

What is it?: a potentially life-threatening closure of the vocal chords (can occur spontaneously). Often misdiagnosed as asthma—especially exercise-induced asthma (more common in white females).

How to diagnose (and differentiate from asthma):

  • Stridorous sounds are usually loudest over the anterior neck, beware wheezing sounds transmit throughout the lungs
  • Typically, albuterol has minimal to no beneficial effect.
  • Subjectively more difficulty on inspiration than expiration

   Clues in history: recent exercise, GERD, ENT procedures, or extubation

   Common causes & some that are not-so common:

  • Post extubation
  • Exercise
  • GERD
  • Medications (e.g., (1) ketamine sedation, incidence 1-2 %; (2) versed (very rarely), which can be reversed with flumazenil)
  • Near drowning/ aspiration
  • Inhalants (smoke, ammonia, dust, cleaning chemicals)
  • Related to anxiety
  • Strychnine (plant based poison, sometimes used as a pesticide for birds and rodents, also the poison reportedly used to kill Alexander the Great in 323 BC)

Treatment of laryngospasm:

Initially:

  1. Jaw thrust with Larson Maneuver
  2. CPAP/ NIPPV
  3. Heliox might be helpful if available, (also topical lidocaine can be applied to larynx if available)

If conservative measures fail:

  1. Low dose propofol (0.1 mg/kg) ~ give 10 mg
  2. Low dose succinylcholine (AKA: suxamethonium) 0.1-0.5 mg/kg IV
  3. All else fails: intubation with succinylcholine 1.5 mg/kg IV
    • If no IV access, then succinylcholine IM (3-4 mg/kg). Experts advocate IM injection into the tongue.
    • Perform chest thrust maneuver immediately preceding intubation to open the vocal cords and allow passage of the ET tube.
    • Monitor for negative pressure pulmonary edema—(from patient pulling hard against closed glottis in the setting of acute asphyxia).

Flow chart from Resus.me

Larygospasm_flow_high_res

What is the Larson Maneuver? (Published 1998 in Anesthesiology)

It is a manipulation jaw thrust technique targeted at the ‘Larson’s point‘, AKA: laryngospasm notch.

  • Place middle finger of each hand in the laryngospasm notch, located behind the lobule of each ear, between ascending ramus of the mandible and the mastoid process.
  • Press very firmly inward toward the base of the skull with both fingers
  • At the same time lift the mandible at a right angle to the plane of the body (perform jaw thrust).

Reportedly will convert laryngospasm within one or two breath cycles to laryngeal stridor, and in after a couple more breath cycles, to unobstructed respirations. As proposed by Larson, it is likely that the painful stimulus relaxes the vocal cords by way of either the parasympathetic or sympathetic nervous systems through the glossopharyngeal nerve.

Diagram from LITFL

Larson_man

References:

  1. Resus.Me: http://resus.me/laryngospasm-after-ketamine/
  2. LITFL (Life In The Fast Lane): http://lifeinthefastlane.com/ccc/laryngospasm/
  3. UpToDate: https://www.uptodate.com/contents/paradoxical-vocal-fold-motion?source=machineLearning&search=Laryngospasm&selectedTitle=1~150&sectionRank=1&anchor=H3#H3
  4. Larson, Philip, MD. Laryngospasm-The Best Treatment. Anesthesiology. 1998. http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1947036
  5. Paradoxical bronchospasm: a potentially life threatening adverse effect of albuterol. South Med J. 2006 Mar;99(3):288-9. http://www.ncbi.nlm.nih.gov/pubmed/16553105
  6. Paradoxical response to levalbuterol. J Am Osteopath Assoc. 2008 Apr;108(4):211-3. http://www.ncbi.nlm.nih.gov/pubmed/18443029
  7. Paradoxical reaction to salbutamol in an asthma patient. Pneumologia. 2012. Jul-Sep;61(3):171-4. http://www.ncbi.nlm.nih.gov/pubmed/23173379

Hypotension

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Late 70s year old female with chief complaint of dizziness and fatigue. Patient has a medical history of HTN and recent cataract surgery.  In triage patient was hypotensive with BP of 70\35 and Bradycardic with a heart rate ranging from 55-60, O2 sats 100% on room air and afebrile.

I found the patient to be lethargic. Otherwise her exam was unremarkable with no focal neurologic deficits, cardiac and pulmonary exam unremarkable, and no abdominal pain. Her husband was in the room and states that they were on their way to their grandson’s high school graduation and she began complaining of feeling dizzy and she started to become lethargic. She had not been sick recently and before this morning she was completely at her baseline. To note yesterday her blood pressure was 180/95 when she checked at home so she typically runs high. No new changes to her medications which consisted of metoprolol Succinate 100mg QD and a Baby Aspirin.

As I talked to the husband he went on to explain that she had recently had cataract surgery on her left eye and that this morning she had a follow up appointment with her ophthalmologist. While at the ophthalmologist appointment the doctor said that the pressure in her eye was high and she received some drops in her eye to bring the pressure down but the husband could not remember the name of the drops.

So I started by getting CBC, CMP, TSH, Urine, Chest xray, EKG, Troponin and a head CT to complete my little old lady AMS workup. Obviously the differential diagnosis for AMS in the elderly is vast so I was considering a lot of different possibilities.  While I waited for her results to come back I called her Ophthalmologist that she had seen that morning to see what drops she had received. Ends up she got Alphagan which is an alpha agonist, Trusopt which is a carbonic anhydrase inhibitor, and 3 drops of Timolol. I discussed with him the possibility of the Timolol on top of her morning metoprolol 100mg as potentially causing her hypotension and bradycardia. He stated he had never seen that happen in his 16 yrs of practice but it is theoretically possible. A quick Uptodate search confirmed that hypotension can occur in as many as 10% of patients using Timolol eye drops which to me was a surprisingly high number.

So I’ll go ahead and cut to the good stuff. All of her labs and imaging returned unremarkable and her EKG just showed sinus bradycardia with a rate of 57.  Ultimately she got 2L of Normal Saline and we watched her for about 5 hrs. Throughout her stay her blood pressure steadily increased and at the time of her discharge she was 135/86 with a heart rate of 74 and she was back to her baseline and much more awake.

I thought this was an interesting case as it seems relatively rare for topical eye drops to result in systemic side effects however in the right patient population it can result in severe side effects. A quick literature search brought up multiple case reports of patient’s having symptomatic bradycardia and even syncope resulting from Timolol use.

So definitely something to keep in mind if you have a elderly or frail patient with acute angle glaucoma who is already on beta blocker therapy. Maybe trying other drops first instead of Timolol or at least be sure to make the patient aware of the possibility of side effects including hypotension, bradycardia, fatigue, and even syncope so they know what to watch out for.

Treating BB/CCB overdose

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Systemic review article on treating BB/CCB overdose

CCB poisoning A systematic review

Key points:

1) High dose insulin 1u/kg bolus and then 0.2-0.3u/kg/h in conjunction w a vasopressor improves survival.

2) No mortality benefits with glucagon or atropine

3) In animal studies , lipids, levophed and dopamine improves survival

4)Consider ECMO for pts in cardiac arrest or refractory shock.

 

 

 

Sick PEs

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We had a very ill patient recently. She was found down upstairs visiting her family member. She was calmly altered, not agitated but was in mild distress. Consciousness fluctuated. Tachycardic and hypertensive initially, then had more labile BP and some hypotension.

We had to intubate her due to poor MS and clinical condition. She coded in CT, we placed a central line on the CT table between her noncontrast head CT and her CT chest. We pushed an amp of Epi and ran out of the room for the CT chest. We were worried about dissection and PE in equal amounts. We could not get good cardiac windows on bedside Echo in room 9 prior to the CT.

She continued to intermittently lose her pulse and drop her BP. We confirmed bilat PEs on the CT when we saw NO contrast left her right ventricle. The CT tech noticed first and became worried the patient had no cardiac output (ie pulseless).

We rushed the patient back to room 9 and gave a tPA bolus (50mg) followed by infusion of 40mg. She was on pressors and heparin and improving. Dr Smith accepted her to Jewish for possible EKOS or even ECMO if needed. On arrival to Jewish a few hours later she coded and died.

I was surprised when I found out she had died. Her O2 sat was improving, HR was decreasing, blood pressure was stable (though dependent on pressors). She received a large amount of crystalloid IV which according to some data might not have been optimal management. She also had the following ECG:

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I think she was infarcting her myocardium. She likely had pulmonary infarction considering her poor oxygenation. She had coded a few times. She had a lot of strikes against her. Her BEST SHOT was going to a place with catheter assisted treatment for PE and ECMO if needed.

I am posting the case to let everyone know:

  1. How to manage sick PE patients (see post below)
  2. To use tPA in massive and in many cases of submassive PE
  3. TRANSFER sick PE patients to Jewish for EKOS/ECMO
  4. The decision to diagnose PE with RV strain on BEDSIDE Echo with no formal Radiologic testing will depend on your attending

This post from EmCrit / PulmCrit is a beautiful summary with potential dogmalysis related to PE management (see take home points below but do read the post).

In addition, here is a nice review article on catheter-based reperfusion treatment for PE with nice references for further reading.

Take home points from the Emcrit post:

  • The only evidence-based intervention that seems to improve mortality in massive PE is thrombolysis.   The primary goal of therapy should be administration of thrombolysis as soon as possible to patients without contraindication.
  • Consider early stabilization of blood pressure using a norepinephrine infusion, administered peripherally if necessary.
  • Volume administration may facilitate dilation of the right ventricle and hemodynamic deterioration.
  • Intubation is very hazardous and should be avoided if possible.   Patients die from cardiovascular collapse, and intubation may worsen this.
  • For a coding PE patient consider 50mg alteplase bolus as well as an infusion of epinephrine.  Patients can do well despite requiring CPR and high dose vasopressor infusions.

Valsartan/sacubitril use likely to increase significantly

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So I just came across that the Valsartan/sacubitril (Entresto) was given a strong class 1 recommendation by the American College of Cardiology for heart failure.  I haven’t seen much of it in med-recs yet, so I just wanted to post a couple of high points that I think we need to know from the ER side. From what I’m reading this drug will start to replace ACE-Inhibitors in the treatment of Class II-IV heart failure. It’s also prescribed in slightly odd dosing in the combination (51 mg/49 mg or 26 mg/24 mg).

Sacubitril is a prodrug that converts to sacubitrilat. Sacubitrilat is responsible for the benefits of this drug as it inhibits the enzyme neprilysin and stops it from degrading atrial/brain natriuretic peptide.

Ultimately the main thing you need to know are the contraindications with other drugs. Basically there are 3: Lithium, ACE-Is, and Aliskiren. Lithium levels have the potential to increase with this drug, while the other 2 can lead to significant hypotension in combination with Valsartan/sacubitril.

Here’s the ACC release: http://www.acc.org/latest-in-cardiology/articles/2016/05/20/11/30/societies-release-focused-update-for-hf-management?wt.mc_id=fb

Would be appreciate if someone with a stronger background in pharmacy or cardiology than I can chime in.