I’m gonna pump you up…..with heparin

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Another weird one for you all.  42yo wm presents with 2 weeks of intermittent right arm swelling and pain.    Worse with exertion.  Some numbness of the fingertips.    Seen 1 week prior.  No labs done.   US negative.  So I walk into the room and stop in my tracks.    Dude looks like he should be jumping off a turnbuckle in a pro wrestling match.   Absolutely huge.  Second thing I notice is despite being ripped bilaterally,  I can see from 20 feet away, his right arm is almost twice the size of his left.  Third,  I immediately decide this cat gets whatever he wants for pain because there are peanuts in his stool bigger than me.

Start my exam.   Guy states he works out 5-6 hours a day.  Swelling went down with rest and immobilization/elevation .  Started training for a bodybuilding show 3 days ago and it came back with avengence.  Swelling is diffuse and symmetric, extends all the way to the distal pectoral muscle on the lateral chest wall.   Subjective numbness to the digits, non focal.  Cap refill < 2 seconds.  5/5 strength  (more like 9/5) full range of motion.  Lung exam normal.  No neck or supraclavicular masses. Prominent superficial veins of neck and pectoral area.  Bilaterally but right noticeably greater than left. Only other important note, does add he had a history of Non-Hodgkins lymphoma when he was a teenager.

So…….what now?  I decide I am worried about venous outflow or lymphatic obstruction from a mass amongst other things.  Talk to our radiologist about best imaging.  He recommends CTA of chest and ‘I’ll tell them to get the neck too’ .     Lab him up- cbc, bmp, ck.  All normal.  Radiologist calls me with this report ‘i see some schmutz in the axillary region, consistent with superficial thrombophlebitis’.

Go back and check on him.   Looks miserable, states arm feels even tighter.  I decide this seems extreme for superficial thrombophlebitis.  Order a repeat US.    Field the inevitable ‘he just had one a week ago ‘ call.  Lo and behold,  axillary DVT that extends through all the distal venous circulation.

This is called Paget-Schroetter syndrome.  Effort induced thrombosis of the upper extremity.   The axillary vein sits right in between the clavicle and first rib.  Can get a ‘nutcracker’ compression of it.

Then repeated shear force causes fixed intrinsic damage and extrinsic scar tissue formation.   Making the vessel extremely prone to clot formation .    So patients with a tight squeeze on the axillary vein at baseline who are active in exercises that increase shear are prone.  Classic examples are bodybuilders like this guy and baseball pitchers .    For you gunners (nerds) the distention of the chest wall superficial veins association with this condition is called Urschel’s sign.  Treatment consist of anticoagulation and consideration of thrombolysis as most of these patients are young, healthy,  and active .    Surgical first rib resection is an option for refractory cases.

I started him on heparin in case vascular or IR was interested in lysing him.  They weren’t,  and he was discharged home on xarelto in good condition after an obs admission for n/v checks.  Thought about following up by looking him up on Facebook, but that would entail entirely too many pics of him flexing with a spray tan and a Speedo.

Couple of learning points I think .

#1 if you have an index of suspicion for a dvt or a positive d dimer,  repeat ultrasound at 1 week.  Hold your ground if you get pushback.   The data is behind  you and I catch one about 2 times a year.  Initial US too early at times and it propagates later.

#2 if you have a weird case, talk to your radiologist early.  Give them background and get them invested in the test.  You will get a 1000x better read and likely way more timely of a read.  Good rule of thumb in general- better reason for the test, better read.    I see this all the time, we piss and moan about radiology hedging,  then we look back at the indication given and it’s something generic like ‘abdominal pain’

CO Poisoning

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HPI:      57 yo M w/ PMHx of HTN, HLD presents with concern for carbon monoxide poisoning. Pt reports he was using a gas-powered saw in an enclosed bathroom to cut concrete. After some time, he began to feel hot and dizzy. When he stood up to walk out of the bathroom, he reported being unable to walk straight. He then began to feel lightheaded and developed a headache. He has also developed photophobia since. He reports no other problems. Smokes approximately 1ppd.

 

Exam: Vital Signs WNL

GEN: Alert, with no distress

CV: RRR, S1S2 present, No M/R/G

Pulm: CTAB, Non-labored

Neuro: CN II-XII intact, Strength 5/5 in all extremities, Normal Sensation/Coordination

 

Labs:    CarboxyHb lvl 19.3%

ABG showed normal pH, pCO2, pO2, Bicarb

CBC, CMP, Troponin, EKG, and CXR negative for acute process

 

Dispo:  He was placed on a NRB and symptoms began improving. After discussion with Poison Control and Jewish, pt was transferred to Jewish to receive a hyperbaric O2 treatment. He felt much improved after the treatment and was discharged in good condition.

 

The suspicion for carbon monoxide poisoning is based primarily on history. Most symptoms are non-specific. Mild to moderate CO poisoning presents with headache (most common), nausea, dizziness. Don’t forget to ask about LOC. Severe CO toxicity can produce neurologic symptoms (seizures, syncope, or coma) and/or end organ damage. If CO toxicity is suspected based on history, a careful and detailed neurologic exam should be performed.

 

If sufficient concern after history and physical, the diagnosis is made by an elevated carboxyhemoglobin level measured off an arterial blood gas sample. Nonsmokers should have baseline level of less than 3% carboxyhemoglobin. Smokers may have baseline levels of 10-15%. Once the diagnosis of CO poisoning is confirmed, an EKG should also be performed. CMP should also be considered to evaluate for electrolyte abnormalities and to assess renal function. Troponin should be obtained in patients with EKG abnormalities, cardiac comorbidities, and older patients.

 

CO binds hemoglobin with greater affinity than oxygen. This results in impaired oxygen transport. CO can also precipitate an inflammatory cascade that results in CNS lipid peroxidation and delayed neurologic sequelae. The half-life of CO can be changed by manipulating O2 delivery to the patient. CO half-life is approximately:

·      250 to 320 minutes on room air

·      90 minutes on high-flow oxygen via a NRB face mask

·      30 minutes with 100 percent hyperbaric oxygen

 

Some evidence suggest that HBO treatment can decrease the chance of delayed neurologic sequelae. Patients can often be discharged soon after HBO treatment is completed.

 

Recommendations for Hyperbaric Oxygen from Rosen’s 9E:

·      Carboxyhemoglobin (COHb) independent of clinical findings

o   >25% with no clinical findings

o   >15% in pregnancy or fetal distress

 

·      Or an elevated COHb with one or more of the following findings:

o   Syncope

o   Coma

o   Seizure

o   Altered mental status (GCS <15) or confusion

o   Abnormal cerebellar function

o   Prolonged CO exposure with minor clinical findings

 

Suggested treatment algorithm from UpToDate:

 

 

 

 

References:

 

Walls, Ron M., et al. “Inhaled Toxins.” Rosen’s Emergency Medicine: Concepts and Clinical Practice, Elsevier, 2018.

 

Clardy, Peter F, et al. “Carbon Monoxide Poisoning.” UpToDate, 28 Feb. 2017, www.uptodate.com/.

Conference Follow Up Info

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Great Blog Posts reviewing LVAD & its complications/management.

Left Ventricular Assist Device


https://lifeinthefastlane.com/ccc/ventricular-assist-device/

Blog Post on REBOA from Life in the Fast Lane:
https://lifeinthefastlane.com/ccc/resuscitative-endovascular-balloon-occlusion-aorta-reboa/

Attached is Dr. Steve Smith’s article for his Equation for Subtle LAD STEMI.

Subtle Stemi- Stephen Smith 2010

IV Metronidazole Currently on Shortage

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Currently, we are using approximately 20 bags/day and at this rate, we have estimated a 14-17 day supply. At this time, please follow the recommendations listed below. We would like to avoid restricting this medication while on shortage. However, a restriction to dedicate remaining supply may be necessary and released as early as mid-next week. The Pharmacy Team is looking at all purchasing options each day. We are buying allocations when they are available and avoiding loaning our current supply.

Please work with your team to facilitate the below options. Please also be aware that, at this time, there is no automatic medication switches or discontinuations. All actions need to be approved with team, except for automatic IV to PO conversions meeting criteria.
PLAN:
Share shortage news with your teams
Be extra diligent with IV to PO/per tube conversions (po metronidazole is available at this time) – Please make this a high priority!
Discontinue unnecessary IV metronidazole and/or duplicate anaerobic coverage
Consider alternative IV anaerobic coverage agents, if needed (examples below – some helpful suggestions)
Anaerobic coverage (non-CNS): IV clindamycin **Reminder: Clindamycin does not penetrate CNS like metronidazole
Hospital acquired infection needing anaerobic coverage (non-CNS): Piperacillin/tazobactam, cefepime + clindamycin
Non-Pseudomonas risk infection needing anaerobic coverage (non-CNS): Ampicillin/sulbactam, cefoxitin, ceftriaxone + clindamycin, fluoroquinolone + clindamycin
Clostridium difficile: PO vancomycin
Please try to reserve IV metronidazole to those with:
CNS abscess
Clostridium difficile treatment in patients with high risk/no gut absorption requiring IV
We would like to avoid using carbapenems, but they are alternatives if the shortage worsens
Contact the ID Pharmacist or ID Team with any questions on substitution or alternatives

Details known on shortage:
Reason for the shortage: Manufacturer delays
Estimated resupply dates: BBraun and Claris are unable to estimate a release date; Pfizer estimates some additional allocation mid-September (not guaranteed)

Building Resilience

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So with the topic of resiliency at the forefront of Emergency Medicine’s fight against burnout, experts are now recommending programs focus on resilience rather than wellness. This is taken from the American Psychological Association.  If you have thoughts about incorporating resiliency into our program or conference, please email me.

10 ways to build resilience:

  1. Make connections. Good relationships with close family members, friends or others are important. Accepting help and support from those who care about you and will listen to you strengthens resilience. Some people find that being active in civic groups, faith-based organizations, or other local groups provides social support and can help with reclaiming hope. Assisting others in their time of need also can benefit the helper.
  2. Avoid seeing crises as insurmountable problems. You can’t change the fact that highly stressful events happen, but you can change how you interpret and respond to these events. Try looking beyond the present to how future circumstances may be a little better. Note any subtle ways in which you might already feel somewhat better as you deal with difficult situations.
  3. Accept that change is a part of living. Certain goals may no longer be attainable as a result of adverse situations. Accepting circumstances that cannot be changed can help you focus on circumstances that you can alter.
  4. Move toward your goals. Develop some realistic goals. Do something regularly — even if it seems like a small accomplishment — that enables you to move toward your goals. Instead of focusing on tasks that seem unachievable, ask yourself, “What’s one thing I know I can accomplish today that helps me move in the direction I want to go?”
  5. Take decisive actions. Act on adverse situations as much as you can. Take decisive actions, rather than detaching completely from problems and stresses and wishing they would just go away.
  6. Look for opportunities for self-discovery. People often learn something about themselves and may find that they have grown in some respect as a result of their struggle with loss. Many people who have experienced tragedies and hardship have reported better relationships, greater sense of strength even while feeling vulnerable, increased sense of self-worth, a more developed spirituality and heightened appreciation for life.
  7. Nurture a positive view of yourself. Developing confidence in your ability to solve problems and trusting your instincts helps build resilience.
  8. Keep things in perspective. Even when facing very painful events, try to consider the stressful situation in a broader context and keep a long-term perspective. Avoid blowing the event out of proportion.
  9. Maintain a hopeful outlook. An optimistic outlook enables you to expect that good things will happen in your life. Try visualizing what you want, rather than worrying about what you fear.
  10. Take care of yourself. Pay attention to your own needs and feelings. Engage in activities that you enjoy and find relaxing. Exercise regularly. Taking care of yourself helps to keep your mind and body primed to deal with situations that require resilience.

 

Xarelto & Eliquis Supply Cards

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All,
On the line of anticoagulation, if you are wishing to send a patient out on Rivaroxaban (Xarelto) or Apixaban (Eliquis), on their website they (or you) can have a card downloaded and printed that can get their first 30 days free. It does require filling out some basic demographic info so you’d have to go through that with the patient.

So if there are any financial/timing issues, this may be an option. Keep in mind that may not fix any financial issues a month later, but could allow them enough time to get that sorted out.

Quick Price Comparison from GoodRx (without these cards):
Cost of 30d of Coumadin (plus ~5d of Lovenox to start): $40-$60 (Coumadin alone for 30d is $4-$10)
Cost of 21d Starter Pack of 15mg Rivaroxaban: $564
Cost of ~28d of Apixaban: $477
Cost of 30d of Lovenox 80mg: $285

https://www.xarelto-us.com/carepath/savings-program
https://www.eliquis.bmscustomerconnect.com/afib/savings-and-support#copaynew

Hope this helps.

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.

Video Links for Fiberoptic and Topicalization

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As promised,
Several links with videos on the process of fiberoptic as well as topicalization. Lots of variations on strategies here, some of which of course are really more applicable for awake Anesthesia patients and may not fit our population but definitely helpful.
The Life in the Fast Lane has a good written summary as well. Hope these help. Email or talk with me for questions!


Good video of topicalization process for awake nasal and oral


Dr. Gallagher discussing the gist of fiberoptic intubation


Rich Levitan’s Video of Fiberoptic Intubation

https://www.youtube.com/watch?v=rljSPu7-vZA
20 min video from Anesthesiolgoist on Fiberoptic- decently covers range of topics

https://lifeinthefastlane.com/ccc/awake-intubation/
LIFTL summary with a couple different videos both on awake intubation and also fiberoptic

https://www.youtube.com/watch?v=c9pAQ3DUKVM
Dr. Ali Diba using aScope on Awake patient—uses spray as you go technique


Narrated Talk on Topicalization: They do both Nasal and Oral for an Oral Fiberoptic for some reason. Also used both viscous Lidocaine and Ointment then sprayed cords.


Video on the LMA MADgic

Pantoprazole on Shortage

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See below: The gist is, 40mg IV Pantoprazole (Protonix) on shortage until August or so. Consider using Pepcid instead.

Medical Staff,

Pantoprazole 40mg inj vials is on national backorder. The anticipated availability is in early August. To ensure continuity of patient care, Pharmacy, supported by P&T plan to substitute pantoprazole 40mg IV push daily to famotidine 20mg IV push BID for the indication of stress ulcer prophylaxis. And pantoprazole IV push to esomeprazole IV push for all other indications.

Pantoprazole 40mg inj vials will be reserved for existing PPI drip protocols.

The good news is that we do not have to adjust existing protocols or infusion pump library settings. Pharmacist will manually change the order from pantoprazole to alternative upon verification. We expect that this shortage will be relatively short.

Please call pharmacy with any questions or Michael Nnadi at 336-817-5265.

Narcissus: A Case Presentation

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11 month old Chinese female brought with concern for two episodes of emesis after family dinner. Via interpreter phone the father explains that everyone in the family vomited after dinner at home. He states the adults all vomited once and feel fine now, but the child vomited twice and he wants to ensure she is well. He is concerned that she is sick from “the onions”. When asked to clarify he explains he made a noodle dish for dinner – every ingredient has been used previously for the same recipe except for “the onions”. He then holds up a Kroger bag of what initially appear to be green onions, with the typical long green stalks and a white bulb base – but these are covered in dirt. He explains that he found them growing in their backyard and thought he’d use them for dinner, but now suspects they have made everyone sick. A brief intradepartment search procured a gardener RN who readily identified the plants – daffodils, “they just haven’t flowered yet”.

 

Kentucky Regional Poison Control advised that all parts of the daffodil (genus Narcissus) cause self-limited gastrointestinal symptoms for approximately 3 hours after consumption, and that care is largely supportive. There are reports of massive consumption causing CNS symptoms in dogs, but similar presentations have never been reported in humans.

 

Take home points:

  1. Green onions and unflowered daffodils are quite similar in appearance – the classic onion odor and tearing following incision differentiates the two
  2. Daffodil toxidrome is self-limited, with predominantly gastrointestinal symptoms (nausea, vomiting, diarrhea). Supportive care with oral rehydration fluid is warranted in pediatric patients.

References:

  • National Capital Poison Center – http://www.poison.org/articles/2015-mar/daffodils

Limping toddler

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Nothing crazy here, just some EM bread and butter. I’ve had a couple of these at Children’s, and each time (with two different attendings), I’ve been told that the adult EM residents seem to overlook this, or not have any idea that it’s a thing, which is kind of embarrassing.

The patient is a 22-month-old male who presents with difficulty walking. Mom states that the child was walking fine until this morning. Since then, he has not been wanting to put weight on his right leg. Mom does not recall any injury. The child is otherwise well, no signs/symptoms of illness, and he has no medical problems.

On exam, the child will not put weight on his right leg when forced to stand. The extremity is well perfused, and there are no signs of trauma. He has no point tenderness, so it is not clear where he is hurting, but does seem to have pain when the foot is grasped and rotated internally and externally.

Discussion: In the toddler with a possible lower extremity injury, it may be difficult to localize where the child is having pain. If there is a question, the entire extremity should be imaged (though you should try to localize the problem area if possible). In this case, we suspected a toddler’s fracture, so a 3 view tib/fib was obtained. This is an important learning point: many times, the fracture line will only be visible on the oblique view, so it is necessary to get 3 views. In this patient, the xray was negative (as were other films of the leg). We diagnosed the child with a toddler’s fracture, placed him in a short leg splint with stirrups, and discharged him with orthopedics follow up.

A toddler’s fracture is a spiral fracture of the distal tibia which usually occurs by the same mechanism as an adult spraining an ankle. Sometimes it is a clinical diagnosis, not visible on X-ray. There is debate in the literature about immobilization in this case; some say it is necessary, some say it’s not. The culture at Norton Children’s seems to be immobilization. Regardless, the child should follow up in 1 week for definitive diagnosis, either with repeat plain films, or possibly MRI or bone scan. If there is a visible fracture on plain films in the ER, the child should be placed in a short leg splint with knee immobilizer and follow up with orthopedics in 72 hours.