Better to be lucky than good

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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.

IMG_3103

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.

IMG_3105

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.

2015 ACLS GUIDELINES

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The new 2015 ACLS guidelines were published this month!  I love new guidelines!  I’ve highlighted the important drug stuff (you guys are on your own for the rest).

Vasopressin: REMOVED FROM ALGORITHM: This was no surprise to me as vasopressin has never been shown to offer any advantage over epinephrine in studies to date.

“Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest (Class IIb, LOE B-R)”

“Vasopressin in combination with epinephrine offers no advantage as a substitute for standard-dose epinephrine in cardiac arrest (Class IIb, LOE B-R)”

Steroids: I’ve been skeptical of the use of steroids in cardiac arrest since 2009 inhospital cardiac arrest trial (steroids were combined with a vasopressor bundle or cocktail of epi and vasopressin).  Will need much more convincing data before I’ll recommend routine use- and that is exactly what our guidelines endorse as well.  Because: no one in the ICU dies before receiving a course of steroids.  The pre-hospital use of steroids is pretty clear: no benefit.

“In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post-arrest hydrocortisone as described by Mentzelopoulos et al may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy (Class IIb, LOE C-LD)”

“For patients with OHCA, use of steroids during CPR is of uncertain benefit (Class IIb, LOE C-LD)”

Epinephrine: Nothing groundbreaking here.  A few trials did demonstrate ROSC advantage with high-dose epi over standard dose; however, no improvement in survival to discharge (emphasis on good neurologic recover) over standard dose.  There is much concern with adverse effects of higher dose epi in the post-arrest period which may negate potential advantages during intra-arrest period.

“Standard-dose epinephrine (1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest (Class IIb, LOE B-R)”

“High-dose epinephrine is not recommended for routine use in cardiac arrest (Class III: No Benefit, LOE B-R)”

Antiarrhythmics: Really no changes.  Emphasized use of amiodarone over lidocaine (which is not new).

“Amiodarone may be considered for VF/pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy (Class IIb, LOE B-R)”

“Lidocaine may be considered as an alternative to amiodarone for VF/pVT that is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE C-LD)”

“The routine use of magnesium for VF/pVT is not recommended in adult patients (Class III: No Benefit, LOE B-R)”

Circulation 2015:132:S444-64

Antibiotic review

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Maybe it’s because an overhead projector slide scanned and inserted into a powerpoint presentation comprised my medical school antibiotics curriculum (you know what I’m talking about if you went to U of L), but I’ve never really felt comfortable with the nuances of antibiotics. For those who want to understand them a little better, here’s a great review.

The bar is set, Chrissy!

NEXUS in the Elderly

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Hopefully everyone is using the NEXUS criteria or the Canadian C Spine rule in evaluation of patients who have undergone neck trauma. Those familiar with both know one major difference, age criteria. NEXUS does not use age, Canadian C spine does. Using both rules together, like PERC with Well’s, increases sensitivity at expense of specificity.

Well here is a study on falls in the elderly (i.e. low mechanism which is another difference between NEXUS and Canadian) and application of NEXUS. Turns out, probably shouldn’t be using NEXUS in patients over 65. Liberally scan these folks, radiation is less of a concern, and the cost is justified due to morbidity of missed injuries. And of course do not bother with plain films (in adults).

Hot off the Press, Droperidol is Still Safe

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Yet another quality article illustrating the safety of the most magical drug, droperidol. Not sure where people are getting it, as it is not being manufactured currently. We have none at any of my hospitals in Louisville. It is sad but perhaps someday we will get it back. In the same Annals issue an indictment of professional societies, journal editorial boards, and government advisory committees with their misinterpretation of “so-called facts.” Great reading, Dr Newman is the man.

Interesting case from the weekend – thoughts?

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Hey guys, I was hoping to get your input on an interesting case I had at Kosair over the weekend.

16 yo F (6 ft, 150 lb…so basically an adult) with a PMH of depression, self injury, and prior suicide attempt presents after ingesting citalopram 40 mg x 90 pills (her prescription, just filled 2 days ago) and concerta 10 mg x 8-9 pills (her brother’s). Patient had been at a party the night before, admitted to EtOH.  Parents found out about the party the morning of admission and they had a big fight, took away car keys, etc. Patient decides to retaliate by swallowing pills, doesn’t tell anyone. Parents find her altered about 10:30, at Kosair at 11:40. Best guess is ingestion occurred sometime around 9-9:30am.  Had one seizure at home per family, and one en route per EMS. Generalized, tonic-clonic, brief.

Initial exam shows a drowsy but arousable patient. Answers orientation questions x3. Initial vitals show HR 147, BP 135/70, RR 25, 93% on some oxygen (can’t remember if NC or nonrebreather). Patient denies CP, palpitations, SOB, abd pain, N/V, weakness/numbness.  4mm, PERRL. MAE equally. Old self injury scars noted on wrists bilaterally. Exam otherwise unremarkable.

We start IVs, get her on a non-rebreather, get IV fluids going. Agree that charcoal seems like a bad idea with her mental status and seizures. Mom has shown up, and as we’re getting some additional history from her, respiratory is placing EKG leads. I’ve talked to poison control. Then, about 20 minutes into her stay, she seizes again. We bag her through the seizure, again generalized tonic-clonic, and just as we’re pushing 2 mg of IV Ativan she comes out of it. She appears post-ictal, but is maintaining her airway. We load her with Keppra, and as I glance at the monitor behind the attending’s head, I notice that her rhythm has changed and she looks like she’s got a wide QRS. We confirm she still has good pulses, still out of it mentally, and since she’s already connected to the EKG leads we grab one (time stamp 12:04):

EKG 1

By the time we get this printed off (!!!!) she appears to have spontaneously converted back to sinus on the monitor. But woah, holy wide QRS/long QT batman! As the attending and I are pouring over the first EKG we get another one immediately (time stamp 12:08):

EKG 2

Thankfully, the QRS appears to have normalized, but we’ve still got a loooong QT, one of the things poison control definitely told us to look out for. Having seen a few similar ingestions at University, I suggest it’s time for bicarb. The attending wants to confirm and we quickly call poison control back, they agree and suggest starting a bicarb gtt, with pH goal of 7.45-7.55.  Now we look back at the monitor and she’s throwing a ton of PVCs, captured here on EKG #3 (time stamp 12:12):

EKG 3

At this point, we opt to push an amp of bicarb while we’re waiting for pharmacy to tube up the bicarb gtt. I have to say, we see it start to work pretty darn quickly. The PVCs slow down, and her rate really starts to head back towards normal. We get an iStat (shot me down when I suggested one earlier), and a few minutes after we’ve pushed the bicarb we get an initial pH of 7.15, pCO2 of 51.5, HCO3 of 18, BE -11, and AG of 21. Electrolytes were WNL. By this time we also know her pregnancy is negative, and her serum tox is negative, no acetaminophen/salicylates on board.  At this point, we talk about intubation as the patient’s mental status is still waxing/waning and she’s breathing shallowly with brief periods of apnea, almost like an opiate overdose. Attending wants to hold off, so I go off to call the PICU resident…and end up having to hang up the conversation halfway through when he changes his mind.

So we intubate her (finally got a peds tube…in an adult), the bicarb gtt comes up from pharmacy, they’re cleaning the PICU bed her, the last EKG looks 1000x better, and all’s well that ends well (time stamp 13:08):

EKG 6

So I’m curious to see what your all’s suggestions/thoughts are on this case.  Looking back at that first EKG, how would you classify it? We’ve got a wide complex, monomorphic tachycardia that to me looks like sustained V tach (with a pulse).  The long QT doesn’t surprise me, but this rhythm does as you’d typically you’d worry about it devolving into Torsades, but that’s not what this is.

Looking back, things I would have done differently:  get a temperature sooner/order a total CK (serotonin syndrome could have been a factor and we don’t have a recorded temp until she’d almost 2 hours into her stay, no one ever ordered a CK), intubate sooner, loading her with keppra when she hit the door after 2 witnessed seizures, maybe could have prevented the 3rd?

Also, if you’re curious, I found this “Toxicology Conundrum” on LITFL that specifically discusses citalopram overdose. Has some good info, citalopram is definitely one of the more potent SSRIs, and QT prolongation is dose dependent and can be seen after ingesting >600 mg (this chick took 3.6 GRAMS). Seizures are also fairly rare, only seen in 2-3% of cases.

Intractable Pain

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I’ve seen about 3 cases now that presented with intractable pain. One was leg pain, put him in Room 9 much to the dismay of nursing, dude ended up having an acute arterial clot and received an amputation. One was acute on chronic back pain (history of chronic norco use, no change in quality) that ended up with an infected ulcer on his aorta (died later). And now this case….

67 y/o M presents with hip pain. Reports he was riding on a mower, hit a bump, had mild pain afterwards in his hip, but overall did well. He ambulated inside, took a shower, and after he sat down to do his business on the toilet he started to worsen. Especially when he stood up. No numbness/tingling/weakness/nausea/vomiting/fevers/chills/bowel or bladder incontinence. VSS. He has pin point tenderness behind his R hip. Worse with palpation. NO pain with axial load, internal/external rotation of leg. Pain with movement of torso. Pain isn’t nearly as bad when he’s just laying there. Appears in pain though at all times. Like TOO much pain.

Skip the XR knowing it won’t satisfy me, go straight to CT pelvis w/o contrast. It is normal. Decide to check labs at this point because I forsee an admission. He has a WBC count of 12. Cr of 1.8 (which is old) I admit him to the hospital for pain control as the idea of ambulation wasn’t happening, let alone just sitting up in the bed.

He is discharged the next day after MRIs of the L spine and hip are showing degenerative changes and lumbar stenosis and he is walking now (with the assistance of PT)

He presents again today and sees one of my partners. Again appears in pain, uncomfortable. Now has abdominal pain in the LLQ as well CT shows DIFFUSE pneumoperitoneum. He’s in the operating room at this moment…..

Sorting out theatrics/drama from reality can be a fine line we walk. Opiate abuse complicates things, and we often meet plenty of actors. But keep in mind pain out or proportion is almost always bad and delineating that can be difficult!

Always have your radar up, don’t be afraid to work up patients (regardless of what your ancillary staff and colleagues say)….. and don’t be afraid to be patient advocates and put them in the hospital to allow things to develop…..Remember One EKG, one CT, one lab draw, they are all stand still pictures of one moment in time and don’t always tell the whole truth. Certainly didn’t here in this case…..

Chest Pain Admission Dilemma

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Hey guys here is an interesting article with actual patient oriented outcomes related to admission for chest pain.

Several take home points:

1. From highest quintile of admission rate to lowest (81% to 38%) the rate of MI and death went up by 3.6 per 1000 and 2.8 per thousand. This correlation implies that when you admit more patients you save lives.

2. It is VERY IMPORTANT to note the patient population. These are Medicare patients with average age of 71 years. So we ARE NOT talking about low risk chest pain ED patients.

3. Even though it looks impressive to save these lives, the NNT or number needed to admit to prevent one MI is 250 and to prevent one death is 333. Thats a lot of admissions. And admitting geriatric patients is often not a good thing for them. May be why the decrease in deaths is less than the decrease in MIs. They were dying because of a hospital acquired infection or deconditioning or something else.

4. It is striking to see how different the practice patterns are at different hospitals regarding admission of a fairly homogenous cohort of patients.

Appreciate any further comments.

EKG Changes in Hyperkalemia

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I have had a couple of good EKG’s in the setting of hyperkalemia that I thought I would share.

The first case is a 68 y/o female with ESRD on dialysis presenting with “back pain”.  Turns out that her back pain was actually chronic and at baseline, but she had missed her last two dialysis appointments.  She denied any chest pain or SOA.  I ended up getting an EKG while waiting on labs.

Initial EKG:

Screen Shot 2015-08-04 at 2.46.53 PM

Previous EKG (~6 months ago)

Feb

 

What says you?  New onset LBBB?  After seeing this we gave Calcium Gluconate and asked one of our wonderful techs to grab a quick iStat as labs were taking forever to result.  Potassium was 6.8.  Gave insulin + D50 and bicarb.  EKG was repeated after Hyperkalemia treatment:

post

Renal consulted for emergent dialysis and medicine admitted.

 

 

Here’s another EKG that I had recently from a DKA patient who had an initial potassium of 7.8:

Hyper-K

 

Here’s a couple of good hyperkalemia resources:

Hyperkalemia EKG Basics

Treatment of Hyperkalemia

Just get a walking O2 sat

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In patients with some suspicion for PE, even with a negative d dimer, I have often ordered a walking O2 sat and HR. This was not really evidence based, but maybe now could be. Below is the abstract for a prospective cohort study of patients known to be with and without PE. Interesting data even if only 114 patients. Cannot get full text yet.

Take home point. Combined sensitivity of HR increase of 10 BPM AND Sat decreased of >/= 2% was 100%.

ie if HR does not go up by 10 or more AND sat does not drop by 2 or more they are very unlikely, based on this small study, to have a PE.

 

 

CJEM. 2015 May;17(3):270-8. doi: 10.1017/cem.2014.45.

Ambulatory vital signs in the workup of pulmonary embolism using a standardized 3-minute walk test.

Amin Q1, Perry JJ1, Stiell IG1, Mohapatra S1, Alsadoon A1, Rodger M2.

Author information

Abstract

OBJECTIVE:

Diagnosing pulmonary embolism can be difficult given its highly variable clinical presentation. Our objective was to determine whether a decrease in oxygen saturation or an increase in heart rate while ambulating could be used as an objective tool in the diagnosis of pulmonaryembolism.

METHODS:

This was a two-site tertiary-care-centre prospective cohort study that enrolled adult emergency department or thrombosis clinic patients with suspected or newly confirmed pulmonary embolism. Patients were asked to participate in a standardized 3-minute walk test, which assessedambulatory heart rate and ambulatory oxygen saturation. The primary outcome was pulmonary embolism.

RESULTS:

We enrolled 114 patients, including 30 with pulmonary embolism (26.3%). A ≥2% absolute decrease in ambulatory oxygen saturation and an ambulatory change in heart rate >10 beats per minute (BPM) were significantly associated with pulmonary embolism. An ambulatory heart rate change of >10 BPM had a sensitivity of 96.6% (95% confidence interval [CI] 83.3 to 99.4) and a specificity of 31.0% (95% CI 22.1 to 45.0) forpulmonary embolism. A ≥2% absolute decrease ambulatory oxygen saturation had a sensitivity of 80.2% (95% CI 62.7 to 90.5) and a specificity of 39.3% (95% CI 29.5 to 50.0) for pulmonary embolism. The combination of both variables yielded a sensitivity of 100.0% (95% CI 87.0 to 100.0) and a specificity of 11.0% (95% CI 6.6 to 21.0).

CONCLUSION:

In summary, our study found that an ambulatory heart rate change of >10 BPM or a ≥2% absolute decrease in ambulatory oxygen saturation from baseline during a standardized 3-minute walk test are highly correlated with pulmonary embolism. Although the findings appear promising, neither of these variables can currently be recommended as a screening tool for pulmonary embolism until larger prospective studies examine their performance either alone or with pre-existing rules.