Maryland Pearl Tox Screen

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I hope everyone suscribes to the UMEM pearls.

Title: Drug Abuse Screens
Author: Kishan Kapadia
[Click to email author]

Performance Characteristics of Common Drug Abuse Screening Immunoassays
Drug/Class
Detection Interval (***)
Comments
Amphetamines
1-2 days (2-4 days)
Decongestants, ephedrine,l-methamphetamine, selegilene & bupropion metabolites may give False (+) results; MDA & MDMA are variably detected
Barbiturates
2-4 days
Phenobarbital may be detected for up to 4 weeks
Benzodiazepines
1-30 days
Benzos vary in reactivityand potency; False (+) results may be seen with oxaprozin
Cannabinoids
1-3 days (>1 month)
Screening assays detect inactive and active cannabinoids; Confirmatory assays detects inactive metabolite THCA (tetrahydrocannabinoic acid)
Cocaine 
2 days (1 week)
Screening & confirmatory assays detect inactive metabolite BE (benzoylecgonine); False (+) results are unlikely
Opiates
1-2 days; 2-4 days (<1 week)
Semisynthetic opiates derived from morphine show variable cross-reactivity; Fully synthetic opioids (e.g., fentanyl, meperidine, methadone, propoxyphene, tramadol) have minimal cross reactivity; Quinolone may cross-react
Methadone
1-4 days
Doxylamine may cross-react
Phencyclidine
4-7 days (>1 month)
Dextromethorphan, diphenhydramine, ketamine, & venlafaxine may cross react
Propoxyphene
3-10 days
Duration of positivity depends on cross reactivity of metabolite norpropoxyphene
(***)Values are after typical use; values in parentheses are after heavy or prolonged use.
References

Adapted from Goldfrank’s Toxicologic Emergencies, 9th ed; Table 6-10.

Sinus Tach Part 1

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Abnormal vital signs are always something to keep an eye on. Always important to explain it in documentation, but keep an eye on the trend throughout your shift as it’s one piece of information that might tip you off that something else may going on. Try to resolve the vital signs prior to discharge, looks better from a chart buffing standpoint, but also an indication that you have corrected the original problem. And if you can’t, again explain it, or just don’t discharge the patient. You will never be 100% in this job, and your initial impression could be flat out wrong, so putting in little safeguards to protect yourself, from well yourself, can help you not miss things.

Quick case…..47 y/o M, history of 75% TBSA burns, active c-diff, PNA presents to the ED for low Hgb. Had Hgb of 7 at NH, 6.4 when checked here. Was just discharged recently from our ER (by myself, VSS at d/c) with new blisters on L scalp, Hgb was 7.3 at that time, 7-7.8 on prior visits. Wbc count: 11.8. Chronic indwelling foley. Urine dip: blood/wbcs/bacteria, neg leuk esterase/nitrite, already on levaquin for known PNA as well. Sinus tach to 120s. Received transfusion x2 units and initial plan was d/c back to nursing home per initial resident. Checked out to 2nd resident (myself) HR remained tachy to 120. Medicine consulted for admission. He was Afebrile. Blood cultures/urine cultures/ sputum cultured ordered as he did have an elevated WBC. Broad spectrum abx ordered. Rectal temp ordered x2, which were both normal. Medicine consulted for low hgb, sinus tach, and they cancelled cultures and abx, felt it was due to anemia although it did not improve with 2 unit transfusion (they are not always right). Planned for anemia work up and obs.

The patient admitted to the hospital and transfused. Hgb trended down again and patient required transfusion again on 9/26. Neg hemoccult/GI bleeding. Anemia work up not completed, but appeared to likely be of chronic disease vs iron deficiency. Patient became febrile on 9/23, BP dropped (that’s 3 days later…..) Started on broad spectrum abx, pan cultured. Urine grew acinetobacter. Blood cultures neg/c-diff negative. Hypotension was not responsive to fluids. Palliative consulted, patient and family elected to be comfort care. Made DNR. Comfort measures in place, was to be discharged to hospice. Patient subsequently expired prior to discharge on 10/4, etiology believed to be sepsis.

This patient had obviously a lot going on. Sinus tach could’ve been from anemia, pain, sepsis, stress, anxiety, etc. The initial thought it was due to anemia. but if this was true, it should come down with fluids and/or blood? Or at least partially respond? But it didn’t budge. He’s obviously had a long in-house history with the history of the burns so he was set up for a resistant bug, odd presentation. And honestly when we start seeing PNA + UTI we should start leaning towards sepsis from 1 agent with seeding, rather than a PNA and a UTI as two different infections going on. But in the end when he was checked out to me and the HR hadn’t budged, that was the tip off that something else was going on.

To expand on this as you can see things weren’t handled as they should’ve been initially. I see some people use the medicine service as a consultant. Which I thoroughly don’t believe in. They practice essentially the same thing as us, except less broad, more in depth, and a hell of a lot more boring (yes offense). When we talk to NES or neurology, or OB, or any of the other sub-specialties we are generally looking for guidance and information about a practice that is beyond our skills, beyond just basic medicine. And they have texts/papers/experience/OR time that allows them to function as a consultant and specialist in their area (especially the surgical services!).

But the medicine service is not all that different from what we do. When we call them, it shouldn’t be, “come see if this guy is ok for discharge.” We know which ones are and aren’t. And if you don’t, read more, use 5-minute EM consult, follow up on the patients you admit, so you can get a better understanding of what happens beyond the ED. You might not know the entire algorithm for hyponatremia and what work up they exactly do, but you should know when to admit one and how to emergently treat it. Or when to transition from insulin gtt to metformin, but you know when the glucose is too high to dispo home. Etc etc……. In their defense, sometimes we call them with patients that can theoretically be managed at home to begin with, but don’t fool yourself into thinking they know exactly what can go home and what can stay, and that they are the almighty, all-knowing doctor (case in point above.) They are residents too, and they don’t have an attending looking into them real time like you do (they have uptodate, which I can only assume why it takes 6 hours to admit asthma or whatever.)

Anyways to get back to my points.
1.Keep a close and scrutinizing eye on those VS.
2.And don’t let medicine pretend to be smarter than you.

Ketofol losing sexiness

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I rarely use ketofol at Jewish, but will let you guys use it at UL when you want. But this article gives a similar opinion to mine: Ketofol does not hold much benefit if any over Ketamine or Propofol.

For quick procedures where you want muscle relaxation (joint reductions or cardioversion), I use propofol. For painful procedures and trauma patients (traction pins, intubating marginal BP patients, chest tubes) I prefer ketamine.

Propofol with the K does NOT seem to decrease emergence reactions. Though Midazolam does so do give 1-2mg midazolam with your ketamine.

My main issue is anecdotally that the ketofol duration of sedation is noticeably shorter than ketamine. I believe this is due to a lower ketamine dose. And we all know that once the dissociative threshold of ketamine is reached, higher doses simply lengthen the duration of effect. You can’t get “more dissociated” just like you can’t be “very unique.”

I don’t even want to mention etomidate here, as I see only one indication for etomidate (as of 2015 where we are on the brink of taking the head injury stigma away from ketamine).

Article is worth a read.

Stress Test

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Another one from Mattu’s Feb review. This article compares psychological stress to physical stress to detect effects on perfusion of the heart. Interestingly mental stress causes ischemia where physical stress does not seem to.

There has always been an intuitive relationship between psychological stress and myocardial ischemia. Bernard Lown, a famous cardiologist, said in EVERY MI patient he had he would find a recent large social stressor in the patient. Of course plenty of hindsight bias occurs here.

Either way, if nothing else with this article remember that emotional stress causing chest pain COUNTS AS exertional ischemic symptoms. The fight with the boyfriend or girlfriend does not allow for blaming the pain on “anxiety.” And perhaps the real stress test in our Chest Pain Center is the 20 hours of sleep deprivation coupled with exposure to yelling, retching and dying that our patients must undergo to make it upstairs for a nice quiet little stroll on the treadmill.

Death of CK-MB?

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Hey guys here is a relevant (albeit 7 years old) article supporting my abandonment of the CK-MB. I had heard Mattu talk about this on some podcasts but this article (along with some newer ones) is the evidence to support that practice. At Jewish I do not obtain a CKMB though when I want a total CK I now have to remember up front. On the POC machines at Jewish the Trop alone seems to error far less than when CKs are running with it. Still watch out for the Trop false positives.

Also I would plug Dr Mattu’s new ECG site. Now he charges a small fee (can pay weekly or monthly but I did the $27/year). Still video based (I prefer to just read a blog with pics) but top notch quality. There is a weekly case and a monthly lit review. The above article is in his Feb review. Might make a one month subscription part of the ECG month. ECGs of course are learned over years and decades, not in a month long elective.

Case #2

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Case #2:

30 yo F h/o morbid obesity and DM2 not well controlled on insulin and metformin presents after high speed MVA vs pole. 5 month old baby in back carseat sent the the Ped’s ED, unharmed. EMS called, prolonged extrication about 30 min, vitals en route stable, BP 120/76 and HR 96 just PTA (hmm?). No IVs established, axox3, talking, calm and cooperative.

On exam, breath sounds normal, seat belt sign obvious on lower abdomen with mild LUQ abdominal tenderness on exam, main c/o left thigh pain. Appears twisted but unsure if broken. Patient is morbidly obese, probably 350-400 lbs, which causes some problems next: placed on the monitor and HR 130, check pulses and does have pulses in distal extremities though weak, BP unable to get multiple times, then manual BP unable to obtain. Ask nurse why no BP, states “cuff not big enough to work properly,” also trying on leg.

IV placed in right AC no problem, placed NS on pressure bag. HR during xrays comes down from 130–>115.

CXR done nothing obvious, PXR done, again nothing obvious and left femur show proximal 3rd shaft fx, traction splint placed by intern, FAST scan neg in cardiac window, but very positive in pelvic window as well and slightly positive in RUQ and LUQ. Level 1 called after FAST and finally a BP obtained 80/40 as trauma walks in the door!!! Patient no longer with palpable peripheral pulses, good central pulses, a&ox3.

Ever feel like an idiot…just watched this lady with HR 130 and BP 80/40 for 18 minutes prior to level 1 trauma call!

Blood, central line, another peripheral IV. Trauma dawdled a little in ED more than should have, repeated the very positive FAST scan, though we did resuscitate her with blood and fluids, central line, trauma attempted a-line (apparently they didn’t trust the very low BP either) and finally went to CT scanner (another 25 min) and thought to have SMV avulsion (yikes) prior to taking her to the OR.

Diagnosis: avulsion of superior mesenteric artery (even worse). left femur fracture.

Patient spent more than one month in the SICU, never extubated, multiple loops of bowel resected for necrosis and never closed her abdomen, family decided to withdraw care after she continued to go downhill and quality of life would have been an issue.

Let me point out the obvious, I should have called a level 1 earlier. 10 min earlier when  had HR in 130s and unable to obtain BP x 2 would have been enough. Unsure if her outcome would have been different, but sure makes me wonder.

Often times it is hard to get a BP on a morbidly obese person, esp when have peripheral pulses and axox3, but it is much better to be safe than sorry, call the level 1 when in doubt. Better for the patient’s sake to feel like an idiot earlier than to feel like an idiot later in the game.

The other thing is, we had her packaged for the OR when trauma arrived, peripheral IV and blood obtained, 1L fluids, HR 110, CXR, PXR and femur, traction splint to femur, FAST done and very positive. Should have gone straight to the OR as soon as trauma arrived. Trauma fellow wanted CT scan and further resuscitation (why try an a-line?) which took time.

Feedback and comments appreciated.

Couple of recent cases…

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One of the most interesting posts recently was Zach’s post about what he could have done differently. Thought I would continue this trend and post a couple of cases that could have gone better and leave some things up for discussion. Case one here and two next post.

Case #1: 90 yo F h/o HTN and arthritis, restrained passenger of moderate speed MVA, driver was unharmed but car was going too fast and struck the back of a semi-truck. Extrication about 10 minutes. Patient c/o right leg pain and right forearm pain, skin tear to right arm and obvious Colles fracture and femur fracture likely as well on initial exam. No chest or abdominal pain. Kept in R9 for the potential femur fracture and age. Vital signs all been stable, patient a&ox3, talkative and despite mild pain appears in good spirits.

On initial exam, HR 96 and regular, 125/70, RR and temp normal. Pain controlled as long as not moving. Good breath sounds, minimal chest tenderness on palpation of sternum, abdomen and pelvis unremarkable. Placed in traction splint in R9 for significant pain and shortening of right leg. CXR normal, PXR normal, and R femur with proximal femur fx minimally displaced. FAST neg. Give tdap and bag of LR. Further eval shows pain in right leg from femur/knee/tib/ankle and also left femur/knee/tib. As mentioned obvious fx right Colles, with pain in right elbow/forearm/wrist/hand and  also pain left forearm and wrist. That makes for man scan + a whole ton of xrays in all extremities.

Spoke with ortho on the phone in R9 due to known femur fracture. Vitals on R9 exit unchanged. To the CT scanner. Nurse calls from xray after CT done and asks for small amount pain meds as patient now c/o more pain, especially in right leg and arm. Dilaudid 0.5mg ordered. Patient comes into main ER literally 90 minutes after initial presentation due to so many xrays! (This is my fault). Labs unremarkable, Hgb 11. I see the CT scans but nothing obvious to me, no head bleed, no c-spine fx, no PTX, no obvious free fluid in belly. See patient as she as she comes back bc ask for more pain meds. HR now 120s, irregular?, BP 95/65. Ask nurse how long this has been going on, states “oh, just the last 30 min or so.” Ortho at bedside as well, wants to do sedation.

EKG done, show afib rate 120s (no h/o afib). BP cont to be 90/60s. Giving 2nd L LR, nurse start 2nd IV and get L NS going. Patient still talking and states she feels ok other than the pain in her leg. Call to Trauma (should have called earlier in 90 yo with known femur fx), but by now its been more than 100 min total time in ER. Trauma arrives pretty quickly, patient now been here 2 hrs. Agree with fluid boluses, talk about patient condition with fellow and wedge and all agree think likely due to trauma in afib and that why BP sucks.

Tell ortho that too high risk patient and unstable to do sedation. Does hematoma block right Colles fracture with reduction as well and leaves the femur in traction. Admitted to SICU after just over 2 hours in ER. CT head and c-spine only scans back and are neg at admission. About 30 min later rest of man scan comes back. Small nondisplaced sternal fx and very small hematoma (but possibly active bleeding) to right retroperitoneal area. Again speak to trauma about this. Asked about the retroperitoneal bleed and fellow states it very small and should wall off without intervention based on place. Possibly afib due to contusion? Cards was consulted by Trauma who saw patient and said to control pain, resuscitation and other trauma factors (unhelpful but true, not much for them to do).

Brings up a question I had, in setting of trauma, what medicines should be given for afib with RVR? Cardiac contusion? Or just let it ride? Trauma asked the nurse to give metoprolol but this was never given mainly due to nursing concerns about BP.

Ok, long story short, HR cont to be 120-130s, afib, BP 90/60s, after being ICU hold for about 2 hours patient had decreasing mentation. Trauma placed central line and a-line and ABG showed pH 6.8! Istat Hgb 8.0. Blood given, minimal response.

Patient intubated by trauma, arrested during intubation, one round CPR and came back, went to SICU same vitals, called in IR and intervention showed minimal bleeding, thought to likely be venous, but did have several coils placed. More blood and then pressors through the night. Arrested 2 more times throughout the next 6 hrs, family still wanted all interventions. Finally about 12 total hrs after ER presentation, arrested for about 20 min and TOD called.

Couple of main points from this case that I learned and hopefully helpful for you all:

1. As Coleman says, old people go down hill quickly, be on your guard no matter how good they may look on presentation.

2. Be careful of ordering too many xrays, me not seeing the patient for over an hour while in xray is unacceptable, I should have known the change in her vitals either by seeing it directly or have nursing tell me.

3. I knew this was a trauma admit as soon as she hit the door being 90 yo and femur fx, but I didn’t call them for a long time, why? Bc I didn’t have much to tell them (couple xrays, stable VS, man scan taking 3 hrs to get read). But just be sure to get them involved early.

4. We don’t typically repeat labs or get istat too often, but for someone like this who takes a turn for the worse, would have been worth it to get hgb after her vitals became unstable.

5. Her mentation decreased after admission, but I could have been more aggressive with central line and resuscitation (blood), she got 4L crystal but needed products.

6. This one was pretty clear cut that should not do sedation, but don’t be afraid to tell ortho ‘no’ if you’re worried about their safety.

7. I’m sure there is more, would appreciate your thoughts and comments…

Fever from Africa…..

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Just stop right there. It’s not ebola.

It’s malaria (unless the patient is uncontrollably vomiting blood or has participated in the cultural burial practices of West Africans within the past couple of weeks).

Seeing as I’ve had two patient’s with malaria, I thought it’d be nice to share some of the great resources I’ve come across (had med students look up), while treating these guys.

1. First off is the CDC malaria map: http://cdc-malaria.ncsa.uiuc.edu

You can see where malaria is endemic, and you click on different countries to see speciation and resistance.

2. Next is the CDC treatment recommendations: http://www.cdc.gov/malaria/resources/pdf/treatmenttable.pdf

Get a good history and know where the patient has travelled. This has doses for adults and children, so it can be useful at Kosair or out in the community too.

3. Clinical Pearls

  • Transmitted by the Anopheles Mosquito
  • Classically will have fevers/symptoms spiking every 24/48 hours
  • Severe Malaria (ICU admission): AMS, severe anemia, DIC, parasitemia >5%, metabolic acidosis, AKI/liver injury, hypoglycemia
  • Probably best to admit/observe all patients until you have a viral load and get treatment started at the hospital. Some of the antimalarials can be hard to come by and these patient’s can get sick.

The competition

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It turns out that the Mayo EM program has a little room9er of their own… except it’s public… and updated frequently… and has a fellow generating content for it. Truthfully, it’s a great site. Quite a few reviews on topics that don’t pop up on the other FOAMed sites (the killer rashes, retroperitoneal hematoma, tumor lysis syndrome). Worth a look if you’re stuck at Jewish South with a broken CT scanner).

Mayo EM.

 

Ultrasound IVs

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We are pretty spoiled at UL with our nurses being the best in the hospital, and being savvy with ultrasound-guided IVs. But when you leave UL to moonlight or graduate and start a new job, don’t expect your nurses to be able to place USN IVs. At Jewish the docs do them all. Nurses in places other than UL are quick to call IV therapy, very quick.

Here is a nice article, one of the simplest but

How do they do it?

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Really cool article with commentary attempting to investigate how experienced docs walk into a room and smell the diagnosis and dispo in a few seconds. Looks like most of the “reasoning” is done before even seeing the patient. Read the RN notes!

As a resident I made a comment about Dr Mallory’s knowing the unteachable. I think this diagnostic skill is learnable but maybe not teachable. It can be called intuition. Pattern recognition. Etc.

Stroke or seizure?

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A middle age male with history of HTN, smoking, and seizures presenting with “mini seizures” since last night. History of a TBI and subsequent seizure disorder back in 1998. Takes phenytoin for it, used to be on phenobarb as well but was taken off of it 1.5 months prior. His seizures have been of the generalized, tonic/clonic variety in the past. Since last night he has had L sided numbness on his face/arm. They have been episodic, coming every 10 min, and they last 2 min. He feels some “clumsiness” in that arm during these episodes but no reported weakness. No difficulty in speech/vision/swallowing. No fevers/chills/LOC/convulsive activity noted.

Phenytoin Level: 14.7
Labwork unremarkable
CT head: negative for acute pathology

Stroke or seizure? I wasn’t sure and I had the attending meet the patient as well. Both of us felt like these were probably seizures. Now I very rarely call neurology about seizures but you can make the argument that this is status so I called them. However, they informed me that isolated sensory symptoms for a seizure is VERY rare and that you are dealing with a possible stroke until proven otherwise. That was news to me, but to his point this was the first case I’ve seen. Anyways, we got the MRI/MRA and they were negative. His EEG showed multiple R sided epileptiform discharges. Loaded him with keppra in the ER, and a repeat EEG improved the seizure activity noted symptomatically and on the EEG. So yay, no stroke!

Main reason I point this out there is to avoid the pitfall of missing a stroke, as Neurology themselves were highly suspicious. Our initial thought process ended up being right, but in order to get there, the point here is to rule out stroke first! Same thing with a Todd’s paralysis BTW. Rule out stroke before you start making that assumption!

For any of you big Pharm conspiracy theorists

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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.

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