Diabetes Insipidus in Intracranial Injury/Trauma

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During a string of nights, I had two separate patients that despite having different injuries presented me with an interesting question. The first was a man in his 50s with a large intracranial hemorrhage, mass effect and the beginning of herniation; the second was a young male that was the victim of a GSW to the head. However, despite the different etiologies of their injuries, they both presented to Room 9 literally yelling for water. One became so combative in his demands for water, he had to be restrained.

This got me thinking; in the setting of very serious injuries, why is the only thing that concerns these men oral hydration?

The most concise information I found comes from Life in the Fast Lane. While it is referring to TBIs, the pathology relates to both of my patients as well. Thirst is controlled mostly by ADH released by the hypothalamus and transported to the posterior pituitary. Any disruption in this production chain can decrease ADH, leading to central diabetes insipidus.

In the setting of trauma, this can be caused by direct damage to the hypothalamus or posterior pituitary, disruption in their vascular supply or increased intracranial pressure/herniation that can compress these structures. Whether by a large hemorrhage or direct trauma like a GSW, intracranial injury can damage the ADH supply, leading to diabetes insipidus and the extreme thirst felt by these patients. Endocrinopathies have been associated with 30-50% of TBIs with the most common disorder being diabetes insipidus.

 

Just another overdose…..right?

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20 yo M with unknown PMH comes in to room 9 with AMS and tachycardia to the 180s. Per EMS, he had been found down in his apartment, with crack cocaine pipes and other drug paraphernalia around him. He was found to be tachy as mentioned, as well as febrile with a temp of 103 axillary.

When he arrived in room 9, his HR was still in the 170s-180s. Blood pressure normal. He was pale, diaphoretic, and looked sick. He was speaking inappropriate words and would localize pain, GCS 12. Pupils dilated and briskly reactive. Rectal temp 104.1. CXR normal. Started IVF bolus and placed ice packs to the groin and axillae. Also gave Ativan as this was likely a stimulant overdose.

First EKG showed SVT at 180 BPM. After 2L of crystalloid and ativan, a repeat EKG showed sinus tachy at 140. The pt’s mental status was unchanged. The iStat showed a lactate of 13.

The plan was to place a rectal probe and monitor his temp, give him more fluids and Ativan prn, and re-assess later. I thought this was 100% an overdose. No problem.

About 2 hours and who knows how many room 9s later, I go to review his labs. I haven’t heard anything from nursing other than him continuously pulling out his rectal thermometer probe, so all must be well…Turns out he has a WBC of 44,000. Lactate has trended down, but he is still febrile to 102. This is when it hits me that maybe the guy who I’ve been treating for stimulant overdose is actually septic? His CXR and UA were normal, but maybe he has meningitis or encephalitis and that’s the reason for his mental status? Maybe I’m now 2 hours late with ABx?

I suppress the awful feeling in my stomach and go re-evaluate the pt. His mental status is unchanged from when I saw him in room 9. At least now his HR is in the low 100s. Given his mental status and tenuous vital signs, I know this patient is going to have to come in to the MICU. He’s going to need a head CT and an LP to rule out meningitis. I gave him antibiotics and called MICU. They evaluated the patient, and they agreed.

I chart checked the patient the next day. His LP was normal. His mental status improved overnight and he was transferred to the floor. Turns out this actually was likely all tox-related, but I thought it was a good learning point nonetheless. Sometimes it’s convenient to go down the path you’re led to by EMS or by nursing. Not only is it easy, but it’s usually the right path anyway. The stroke buzzer goes off and you immediately get your quick assessment over with so the patient can go to CT and stroke can do their thing. EMS tells you they found the patient in a house with drug paraphernalia, so you run with that.

But it’s important to keep the differential wide open when you first see a patient. At least consider less likely and less obvious possibilities. At some point, you’ll catch something that you otherwise would have missed until it was too late.

Just say NO to DESAT

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I was about to spend a lot of time on a post here about pre oxygenation, specifically re: apnea oxygenation with nasal cannula. I was inspired be yet another favorable article in this month’s Academic EM (which by the way is going to be online ONLY as of Jan 2017).

Then realized Weingart had of course already posted a ridiculously good synopsis of what was out at the time.

If you plan at anytime in the future to intubate a human patient, STOP what you are doing and read the Emcrit post before your next intubation.

Add to his post the new article. And the common sense that a nasal cannula has no risk to the patient. There is just no reason not to place a 10L or greater nasal cannula on all patients during intubation.

Just finished writing the post and noticed EMLitofNote just reviewed this article, also linked to a LITFL post and a Rebel EM post. Their conclusions are similar, though they call for an RCT. Not sure we need to spend a bunch of money on an RCT. I say just use the cannula for 5 minutes while you intubate.

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:

FullSizeRender

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.

Phrenic Nerve Paralysis after intrascalene nerve block

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This was covered in the opening of the February EMRAP however not something that I was at all familiar with.  Here are the basics and something that is probably rare but worth knowing about:

 In the episode they presented a case of  70 year old female that was brought in with a complaint of shortness of breath. RR = 28 and SA02 – 88%. The patient presented three hours after a right shoulder arthroscopy.  

ECG : normal

CXR: elevation of the right hemidiaphragm

 Dx:  paralysis of right hemidiaphram after intrascalene nerve block

There are two major complications associated with intrascalene nerve blocks: 1. pneumothorax

2. unilateral phrenic nerve paralysis.

The patient likely had a transient phrenic nerve dysfunction causing unilateral diaphragmatic paralysis.  Younger patients can compensate, older patients with co-morbid conditions may not be able to tolerate this as only one lung is effectively ventilating.

The patient in this case was managed with supplemental 02 until the buvipicane wore off.  Some patients with underlying lung disease and this complication may require BiPAP/CPAP or intubation.  

Things that I took away:

  •  be aware of this procedure and this complication
  • this may be done for patients with same days surgeries to the upper extremity and this is important history to have from Pt or family.
  • It may be missed prior to d/c.  This was an example of one that was missed by Anesthesia prior to d/c of the patient. 
  • May look clinically like PE (tachypnea, tachycardia, post-op patient), however,  history will help make the dx as well as CXR.

 

A little more about the block:

Interscalene nerve block is typically performed to provide analgesia for upper extremity surgeries and may or may not be combined with mild general anesthesia.

 Example of Surgeries this may be used for:

-Shoulder surgery, such as rotator cuff repair, acromioplasty, hemiarthroplasty, and total shoulder replacement

– Humerus fracture

Dr Huecker Stayin’ Healthy

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As I was catching up on my weekly EM/pharmacology blogs, I stumbled across an article featuring our very own Dr Martin Huecker on the Academic Life in Emergency Medicine (ALiEM) website.  It is a great article about staying healthy and balancing life in EM. I’ve attached the link for your viewing pleasure.

https://www.aliem.com/2016/martin-huecker-healthy-in-em/

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.

Urine Drug Screen

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So while on my ICU months this year, I had upper levels that were very insistent that we needed to get a urine drug screen on everyone.  I would try to make the point that it most likely was not going to change our management of the patient at all.  My point was often ignored and after countless urine drug screens obtained during those months, most if not all proved to be of no utility.

Interestingly, Foamcast just put out a podcast about false positives and false negatives on the UDS.  What I found most interesting was that ibuprofen can cause a false positive for just about anything under the sun including cocaine, PCP, THC, and barbiturates.  Also, the benzos tested on this really only test for oxazepam which is a metabolite of diazepam.  So Ativan, Klonopin, and Xanax won’t show up.

Here is the link if you want to read the whole thing.   https://foamcast.org/2016/04/26/episode-48-urine-drug-screen-cocaine-and-pcp/

Must-Read Resuscitation

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Folks,

I know I am incessantly encouraging people to follow Dr. Smith’s EKG blog, but the most recent post is too good to not tell you all about. In it, there is a write up of a fantastic resuscitation.

Highlighted in it are double-defibrillation, Head up CPR, hypokalemia bolus dosing, ultrasound for stemi and VFib (!), esmolol bolus for refractory vfib,  cath lab availability and MDM, hypothermia discussion, and prognostics in cardiac arrests.  I mean, this case report has it all, and it is referenced and discussed for our enjoyment.  Read it.

The resuscitation you wish you had run IS HERE!

Read it. I’ll buy you a drink if you do.

Zach