POTD: LUCAS

POTD: LUCAS

Please watch this 2 min home video made with the assistance of Dr. Eric Roseman on using our LUCAS device.

https://www.youtube.com/watch?v=TZ7YxHzj5sY&t=7s

We’ve all done CPR.  It’s tiring and the pads embarrass you in front of everyone saying they are inadequate compressions even though your hands are pressing against the bed.  To fix this issue, top engineers have developed mechanical compression devices to ease our burden.  There are a few models on the market: LUCAS, LUCAS-2, and AutoPulse device.  At Maimo, we have the LUCAS device. 

The obvious advantage of the LUCAS device is that no one has to do manual chest compressions, which is especially helpful in this COVID pandemic to limit staff exposure.  Another advantage is that LUCAS is a god send for prolonged CPR; there have been many case reports of patients requiring 2+ hours of LUCAS compressions with great neurologic outcomes.  Some examples of cardiac arrest requiring prolonged compressions include TPA patients and hypothermic patients. I noticed when the LUCAS is used, the code is often times much calmer and quieter.

Again, please watch the video demonstrating using the LUCAS.  CPR should be ongoing when placing the LUCAS on the patient.  When placing the LUCAS, inserted it between CPR performer’s arms. The LUCAS should be placed between the patient’s arms and torso.

1. place the back board underneath the patient

2. snap the LUCAS in place, either orientation works

3. turn on LUCAS with green button

4. manually push down the suction cup/compressor to the patient’s xyphoid

5. press button “2” to lock the compressor in place

6. press button 3 to start compressions, both top and bottom do the same thing except the bottom button has a pause for breathes every 30 compressions.  Generally, in hospital you will use the top button.

7. once CPR is complete press button 2 to stop compressions

8. press button 1 to unlock compressor

9. manually retract compressor

10. pull on yellow rings to unlock LUCAS from backboard

How good is the LUCAS? Most studies so far have shown varying results.  One of the earlier studies in 2015 showed that mechanical compression devices are not superior to manual compression in out of hospital cardiac arrest when it came to neurologic outcome and survival (~6000 enrolled)1. Similarly, a study done in 2019 also did not show improved survival2 in out of hospital arrest. There was study done in UK in 2017 for intrahospital arrest that did show improved hospital and 30-day survival (odds ratio 2.34, CI 1.42-3.85), but it was smaller study (689 participants). Another study in 2017 found that LUCAS had a higher rate of adequate compression and decreased hands-off time compared to manual CPR which makes sense4. This final study in 2017 found that the LUCAS and AutoPulse did not cause more serious of life-threatening visceral damage than manual compressions5.

Based on these studies, it seems like the LUCAS is pretty good especially considering it decreases the contact healthcare providers has to possible COVID patients.  Maybe I’m just a LUCAS corporate shill, but I’ve always had good experiences when using the LUCAS, but it is critical to use it properly…so please watch he video or watch another video covering LUCAS usage.

1. https://pubmed.ncbi.nlm.nih.gov/26190673/

2. https://pubmed.ncbi.nlm.nih.gov/31689757/

3. https://www.resuscitationjournal.com/article/S0300-9572(16)00119-2/fulltext

4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391893/

5. https://pubmed.ncbi.nlm.nih.gov/29088439/

POTD: Uric Acid in Urinalysis

POTD: Uric Acid in Urinalysis

What do you make of this “moderate uric acid” in this UA?

I usually just overlooked it whenever I saw it on a UA…I’m sure its fine…but now that I’m on admin, I got a bit of time to take a closer look. For the most part, it doesn’t really mean anything, but there are cases where it can assist in our decision making.

Purine nucleotide (sardines, veal, in basically every proteinaceous food) metabolism produces relatively water-insoluble uric acid in humans. Uric acid level is determined by rate of synthesis, rate of renal/GI excretion, and metabolism. Uric acid has a pKa1 of 5.3 so it’s water soluble at physiologic pH of 7.4. Urine has a wide range of physiologic pH 4-8 and as it gets close to 5.5, it starts precipitating from urine forming crystals. 

By far the most common cause of low urine pH is dehydration especially if the patient is having diarrhea which causes a loss of sodium bicarbonate (hyperchloremic acidosis). This can cause a drop in urine pH beyond 6 into the 5s which will lead to precipitation of uric acid crystals. The patient just needs rehydration and the urine pH will increase resolving the uric acid crystals. Patients can also develop uric acid crystals if their diet is too protein rich so dietary modification can be indicated.  This is why patients with many gout flare ups are often on low purine diets.

Uric acid stones make up 5-10% of all kidney stones in the US.  The thing is that in the most common calcium oxalate stones, there is often urate excreted as well so sometimes uric crystals are not always diagnostic. Uric acid crystals are radiolucent on XR but easily visible on non-contrast CT, but who is trying to find stones with an XR anyway? The treatment is just hydration and at most diet modification.  It’s interesting that in desert/arid regions of the world, up to 40% of all renal stone are due to uric stones.  The patient might have a condition causing hyperuricemia leading to recurrent uric acid stones (gout, malignancies, hemolytic disorders, obesity, G6PD, purine overproduction genetic disorder).  The next step would be alkalization of the urine; most commonly daily potassium bicarbonate or potassium citrate can be given to dissolve the stones, but this is not really an ED concern. PMDs/urologists can do serum and urine uric acid testing if these stones do not resolve to identify if the hyperuricemia is from overproduction or underexcretion.  I could not find a study finding the correlation between uric acid crystals and the likelihood of kidney stones.  There are studies linking lower pH to increased chance of kidney stones but there were no specific numbers given.

One of the patient populations where uric acid crystals is more concern are cancer patients are chemotherapy.  Chemotherapy/radiation can induce rapid cell lysis leading to hyperuricemia in tumor lysis syndrome. This can lead to acute uric acid nephropathy when uric acid precipitate on the nephrons causing acute uric acid nephropathy. Sometimes these patients need to be on rasburicase, allopurinol, or febuxostat to reduce uric acid production. The problem with uric acid crystals in urine is that it can be negative this in case if they become obstructed in the nephrons.  It does not always correlate with uric acid level, which is a much better indicator of hyperuricemia. Indication for dialysis in tumor lysis syndrome is serum uric level > 10, renal failure.

Gout is characterized by extracellular fluid urate saturation leading to hyperuricemia.  These patients have 2x likelihood of having kidney stones but the most common stone is still calcium oxalate. In these patient’s uric crystal in urine is still not correlated to uric acid level. Gout is diagnosed with arthrocentesis of the synovial fluid. Urine uric crystals are not useful in diagnosis in this case as the uric acid is precipitated in an acute attack and the patient’s uric acid levels are often (70%) normal. Serum uric acid levels are not even very helpful in these cases.

Overall, seeing uric acid crystals in urine is generally just a sign of urine pH < 6 likely due to dehydration. It can help guide the management by the urologist or primary care doctor after the visit but it is of low utility to the ED provider.  It can tip us off for tumor lysis syndrome or a gout attack, but I wouldn’t depend on it.  Serum uric acid level are much more useful from a diagnostic perspective.

POTD: Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVC)

POTD: Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVC)

Case: 22M presents unconscious in VTach.  The patient was exercising and suddenly passed out.  ACLS performed and after defibrillation, ROSC was achieved. Epsilon wave was seen on EKG, pt was admitted to MICU, which did MRI showing arrhythmogenic RV dysplasia.

Arrhythmogenic Right Ventricular dysplasia:

Inherited myocardial disease where R ventricular myocardium is replaced by fibro-fatty tissue

Typically autosomal dominant but there is recessive form caused Naxos Disease with wooly hair and skin changes

3:1 men to women, more in Italian or Greek descent, 1:5000 people overall

Second most common cause of sudden cardiac death to HOCM (causes 20% of sudden cardiac death in pt < 35yo)

Presentation: 30-50s with syncope or dysrhythmias including PVCs, VT, VF, CHF, or sudden cardiac death

EKG:

Epsilon waves are the most specific finding on EKG (30-50% spec) but there are other findings as well, the most common being TWI in V1-V3. The epsilon wave occurs because conduction is slower through fattier tissue, and there is a post-excitation wave. 

It can be difficult to pick up epsilon waves, a different set of lead placement can be used

RA over manubrium, LA over xiphoid, LL in V4 position, I/II/III will be denoted as FI/II/III in the image

Imaging:

Echo – dilated hypokinetic RV with prominent apical trabeculae and dilated RV outflow tract

MRI – will see fibrofatty infiltration, RV dilation, wall motion abnormalities

Treatment:

Betablockers preferably Sotalol or amiodarone

ICD placement if patient has sypmtoms, some pathways can be ablated

Some patients will develop heart failure and will require standard CHF treatment, other might need heart transplant

Disposition:

If patient is asymptomatic and abnormal EKG is found incidentally, the patient can be discharged with cardiology f/u

The patient should be admitted if concerning symptoms likely syncope, chest pain, arrhythmias or has a family history of sudden death/cardiac arrest