I’m gonna pump you up…..with heparin

Posted on September 16, 2017 by Eric Yazel

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’

Cool Name, Not So Cool Results

Posted on August 18, 2017 by Eric Yazel

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.

Better to be lucky than good

Posted on November 3, 2015 by Eric Yazel

I was called to a code in the ICU. I roll into the room, 38yo IVDA hx, admitted for sepsis, septic emboli, and ARDS. Stable vital signs 10 minutes previously, now in PEA arrest. Already tubed and had a triple lumen in the IJ. Not a whole lot for me to add for immediate stabilization with a secure airway and access. Already had epi x1. Accucheck was 149 (never, never forget this in a code).

So I immediately get to go to the second phase and start thinking reversible causes. With that hx, all sorts of interesting diagnoses on the playing field. The one major thing I notice was the patient was extremely cyanotic from the upper chest on up. CBC and BMP from a few hours ago essentially unremarkable aside from a white count of 26. Coags normal. Actually starting to kick around the idea of empirically thrombolyzing this dude. All of a sudden, quick run of v-fib, zap him with 200 and voila! we have a pulse. I order a new rainbow of labs, cxr, call his pulmonologist to recite my efforts, and strut back down stairs with a little gangster lean feeling pretty good.

I sit down, take a deep breath, and head to see the next patient. And BOOM! Code alarm goes off once again. Head back into the room, next verse same as the first. Guy suddenly went PEA arrest again, CPR was already in progress. No labs back. I have them pull up the CXR.

Well sh*t, I swear I listened to him during the first code. Bilateral breath sounds (course, but there). I listen again, knowing there is a big pneumo, still can hear. Obvious tracheal deviation on the CXR, but time to get moving. So I ask for an angiocath and a chest tube set up. Deer in headlights, no one moves. Someone finally scurries off to find a pleurovac and tube.

Still waiting for an angiocath, they hand me something that looks like something I’d LP a 10 day old with, not gonna cut it. Finally they roll in with this kit that looked like they pulled off a dusty shelf. Has what looks like a 8 inch spinal needle with a pigail catheter already attached to it. That’s it. nothing else in the kit besides and adaptor to attach to the pleuravac. Don’t have a lot of time to search for anything else so I went with it. Was actually really slick- put the needle into the chest cavity, pulled out the inner cannula, heard the hiss and fed the pigtail. That’s it, working chest tube in place in about the same time it would take to do a needle decompression.

Immediate return of pulse and stable blood pressure. Thank god. That would have been a totally reversible cause of death in a young patient. If I hadn’t ordered or remembered to check that x-ray, would have been on my shoulders.

I post this for a couple of reasons.

#1 Don’t get too cute in your codes. Start with the basics and build from there. I was too busy thinking about lytics etc, and had an easily reversible cause right in front of me. Don’t forget your DOPES mnemonic for ventilated patients.

D- dislodgement, check your tubes, end tidal or even preferably direct visualization. Especially in a patient getting CPR.

O- obstruction, always suction, mucous plugging is an easy removal.

P- Pneumo, already talked this through.

E- Equipment, I recommend always pulling your codes off the vent and bagging through the ET tube to take this one off the radar.

S- stacked breaths. Too much PEEP or high respiratory rates without adequate expiration time can cause air trapping and decreased venous return. Once you pull someone off the vent and bag. Take a second and manually press the chest wall down. Can fix the problem immediately and you look like a total ninja if it works.

For any of you big Pharm conspiracy theorists

Posted on October 5, 2014 by Eric Yazel

I think I’ve shown this to a few of you, but this is an interesting article Droperidol Article

Kind of amazing how some extremely dubious data can affect clinical practice for years, and take a great medicine out of our hands.

Also, do you think these QT concerns that we are now hearing about with Zofran have anything to do with the fact that its now waaaay cheaper than it used to be? No one seemed worried when it was raking in the cash.