Mobile Stroke Unit

My dear BK docs: 

The Mobile Stroke Treatment Unit (MSTU) is operational in Brooklyn now.

So it is highly likely that eventually you will receive a patient who has received thrombolysis in the field for a presumed ischemic stroke. They are operational 9a-5pm and are dispatched by FDNY.

They have been active since June, and respond to 2-3 calls a day along a BLS unit. They are dispatched to the scene if the story is concerning for a critical CVA (CVA-C).

They will push t-Pa and start the infusion if after neurologist assessment they meet t-Pa criteria.

The Brooklyn NYU MSTU crew report pushing t-Pa in the field 15 times since beginning operation.

The crew consist of 2 paramedics, a ct technologist, a nurse, and a neurologists who performs a remote assessment using multiple cameras in the back of the unit.

Please understand that the data supporting use of this technology for the benefit of a patient in an urban setting is controversial and not well studied. The data supporting this approach to stroke management in a rural setting is also controversial. But the primary theory is that it will increase the probability that a patient with a significant stroke will initially be transported to a hospital capable of mechanical thrombectomy or other endovascular approaches. Anything deeper is beyond the scope of this pearl of the day.

Now for a quick review of t-Pa, based on a synthesis of NINDS and ECASS:

Indications for t-Pa:

-acute ischemic stroke with onset less than 4.5 hr

-must have NIH stroke scale <25, but with significant deficit, eg aphasia, RUE paralysis, etc. A caveat here is that a patient with a basilar artery occlusion may have a very high stroke score, but they should get t-Pa (and likely mechanical thrombectomy; again too deep of a topic for a pearl of the day).

-No ICH on head CT

Contraindications to t-Pa:

-stroke or ICH in past 3 months

-Severe stroke NIHSS>25; the thought here is a stroke that is greater than 1/3 MCA territory will have high post-ischemic bleeding potential

-surgery within past 14 days (this has to be “major”)

-Systolic BP > 185 (you can control this prior to t-Pa administration)

-history of ICH

-rapidly improving symptoms

-Combination of previous ischemic stroke WITH diabetes

-minimal symptoms (eg paresthesias in the hand)

-GI/GU bleed in past 21 days

-platelet less than 100k

-arterial puncture at non-compressible site last 7 days (eg, subclavian a-line, extremely rare)

-seizure with onset of stroke

-on anticoagulation

Relative contraindications

-age greater than 80 (I moved this from ECASS III absolute contraindications, mostly because of our patient population)

-recent LP

-Recent MI

-glucose less than 40 or greater than 400 because this suggests metabolic; caveat here, if hypoglycemia is corrected need to more strongly consider stroke.

-post MI pericarditis

-Recent MI less than 3 months ago

-if a patient has a history of veno-hepato/renal occlusive disease or TTP and is defibrotide for treatment of any condition, you should consider witholding t-Pa. This drug is though to enhance plasmin activity, thereby helping to prevent clot propagation and promote reabsorption. FYI: you may never see a patient on this drug.

DOSING:

-t-Pa is dosed at 0.9 mg/kg (max 90), give a 10% bolus with the remainder to be infused over 1 hr.

TOXICOLOGY/PHARMACOLOGY

If and when a thrombolysed patient comes from the field into the ED, you need to be prepared from the complications of administration of these agents.

The mechanism of action of alteplase is to “enhance the conversion of plasminogen to plasmin by binding to fibrin, initiating fibrinolysis with limited systemic proteolysis”. This essentially is the “clot-buster"

Hypersensitivity reaction is also possible. So be prepared to give epi IM if signs of anaphylaxis develop.

However, the most significant and common side effect you must monitor for is HEMORRHAGE, give FFP or cryoprecipitate. Give crossmatched blood if bleeding has stabilized and is indicated. Start MTP if is massive. Rate of GI bleed is as high as 5%.

Other clinically significant hemorrhages include ICH (0.4-1.3%). This may result in herniation (very rare).

Another rare complication is cardiac tamponade. If a patient has an ischemic stroke and has a history of cardiac ablation AND is no longer anticoagulated, you should suspect pericardial effusion/tamponade if there are ANY changes in their hemodynamic status.

FINAL CAVEAT: ask the stroke EMS crew for labs if they drew them. They should be drawing them because coagulation studies may become deranged after t-Pa administration.

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Electrophysiology 102: modes of pacing

Avid learners: 

As promised: part 2 on electrophysiology. The emphasis here will be modes of pacing and what they mean. Please note, I am not an electrophysiologist,

so if anything here is wrong, please respond ALL. 

This topic may require multiple reads, and I encourage you to seek out other sources. 

Please take this POD with a grain of salt.

Electrophysiology super-fellowships recently were extended to 2 years because this is a complicated topic.

We will focus on what the EP provider needs to know. 

Typically a pacing mode is described in letters. For simplicity sake, we will stick to the old fashioned 3 letters. 

A typical appearance is VVI [OO]. Most pacemakers will be reported with an omission of IV and V and will be just be the first 3 letters out of 5, in this case VVI. 

Position 1 is what is Paced

Position 2 is what is Sensed

Position 3 is what is the action of the device. 

Position 4 is rate modulation

Position 5 is for atrial, ventricular, or both pacing 

For this case (VVI), the ventricle is paced. The ventricle is also sensed, and if the pacemaker senses a ventricular beat, the pacemaker’s delivered beat will be inhibited.  So: if the rate of the pacemaker is set to 50 bpm, and the ventricle is beating at 60 bpm without pacing, every sensed beat actually inhibits the pacemaker from firing. However, if the ventricular rate all of sudden drops to 25, there are half the beats to sense, and the pacemaker will then start pacing. 

In short, for patients with an old school unipolar lead in the RV (VVI), if the ventricle does not beat faster than the programmed rate, the transvenous pacer will depolarize the RV. As I mentioned in my previous POD (Electrophysiology 101), this is why we see a LBBB morphology. 

Here is a key:  

miller_pacing_schema.png

reproduced from above source.

As per my review of the literature; the most confusing thing about pacing schema is the 3rd position: 

If a pacemaker is in DDD mode (most common mode), it will pace both chambers (if necessary) AND senses both chambers. So, if the atria does not spontaneously fire at the programmed rate, it will trigger an electrode signal causing pacing the atria; and subsequently, it will do the same for the ventricle. If an atrial depolarization occurs spontaneously, it will ensure there is a subsequent atrial beat. In short, DDD mode automatically senses which chamber(s) is/are not firing and makes them contract in synchrony. 

If a pacemaker is in DDI mode, “AV synchrony is provided only when the atrial chamber is paced.” Basically, this means the if the atrial chamber is not being paced because it is depolarizing on its own, the pacemaker will not depolarize the ventricle(s). But, if the atrial chamber needs to be paced, it will also subsequently pace the ventricle.

As mentioned previously in my POD, Cardiac Synchronization Therapy (CRT) expands the pacing to both ventricles in an attempt to improve cardiac output in the setting of reduced ejection fraction. 

By far the most important mode of pacing that we utilize emergently in the ED is VOO. In this mode we just overdrive pace the ventricle. Typically these are patients with bradycardia and/or hypotension/AMS. Occasionally, you may see intermittent asystolic events due to profound heart block. Both of these patients need to have transvenous pacing until electrophysiology can place a permanent pacemaker. You can let them figure out the mode that best suits them. 

Penultimate final point for patients with a pacemaker who come in unstable: if you a put a magnet on the pacemaker it will default the pacemaker to AOO, VOO, or DOO (all overdrive pacing). No response to this means dead battery or lead displacement, which means they need a revision. 

Final point: as I mentioned in my last POD on electrophysiology, putting a magnet on a pacemaker is substantially different than putting a magnet on an AICD. 

Magnet on pacemaker=overdrive mode

Magnet on AICD=inhibition of defibrillator

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Contrast induced nephropathy

Dear pearl of the day readers,

I suppose you could consider this is a part 2 on side effects/toxicity of Iohexol (omnipaque™). This pearl of the day comes at the personal request by one of my coresidents to cover this topic.

Epidemiology

Contrast induced nephropathy (CIN) is an increase in serum creatinine > 25% after administration of IV contrast.

2-10% of patients who received iodinated contrast media suffer acute kidney injury (AKI). The peak of AKI is seen 2-3 days later.

A caveat here is that many times patients will develop AKI from other etiologies after receiving contrast. This makes sense because they needed a CT scan for some clinical indication.


Patients who have pre-existing renal disease or elevated serum Cr are at higher risk for CIN. There are scoring models to see who is at higher risk, but this applies more to interventional procedures requiring higher contrast loads. If you are curious about the scoring systems they can be found here: http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf

Side note I found interesting: in patients who had no protein in the urine, only 1% had a Cr>1.7 mg/dL. So no protein in the urine means they probably do not have kidney disease.

Mechanism

The putative mechanism of injury to the kidneys is renal vasoconstriction and direct toxicity to the renal tubular cells, possibly through increased reactive oxygen species.

Chance of recovery

Patients who develop CIN have higher odds of mortality, 1.9. If the CIN requires dialysis, in hospital mortality at one institution increased from 7.1% to 35%.

One British study found that 0.9% of patients developed CKD within 6 months of receiving a contrast loads, compared to 0.17% of patients who developed CKD during the same time period.

So the chances are good the patient will recover.

Treatment

There is no proven treatment; however, pre-treatment with IV or PO fluids is the mainstay practice. In the sense that dehydration is bad for the kidneys, it is reasonable to try to avoid a second hit. However, conflicting data show that there was no difference between fluid pretreatment or not.

Several controversial studies may show that pretreatment with sodium bicarbonate was superior when compared to normal saline (NNT=10); theoretically, this effect is due to decreased free radical formation.

Also theoretically, N-acetyl cysteine (NAC) can help reduce oxidative stress on renal tubular cells. The official journal of the international society of nephrology actually recommends pretreatment in patients at increased risk for CIN with ORAL NAC. High dose oral NAC was shown to decrease the incidence of CIN by 76% in one study. Data is also conflicting here, but trends toward favoring the use of oral NAC in patients at risk for CIN.

Lastly, preliminary data also shows that statins may some how be protective through an unknown mechanism.

Final take home points

Be cautious:

-if the patient is on other nephrotoxic agents

-if the patient has a slightly elevated creatinine compared to baseline (even if it still normal)

-if there is protein in the urine

-if they have a history renal disease

-if eGFR<60

Balance the risk of contrast against the risk of not-performing the correct radiology study. This will be different for every patient.

TR,

W

References

http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf

Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA. 2004;291(19):2328-34.

Patschan D, Buschmann I, Ritter O. Contrast-Induced Nephropathy: Update on the Use of Crystalloids and Pharmacological Measures. Int J Nephrol. 2018;2018:5727309.

Reuben Strayer's response to my post is quite poignant and definitely worth a read:

Despite how penetrated the notion of CIN is in our teaching and practice, and how much time and energy we spend on its supposed prevention, there is considerable controversy as to whether CIN actually exists/occurs.

paper

audiocast

Farkas’ blog post

Morgenstern's blog post

I’ve pasted conclusions from the latter below. The most important point is if you have a high concern about a dangerous condition and require an IV contrast-enhanced CT scan to rule it in/out, the patient’s creatinine should factor minimally if at all in your decision around whether or not to do the scan. Do the scan.

It is not clear whether contrast is a significant cause of acute kidney injury. According the the American College of Radiologist, “at the current time, there is very little evidence that IV iodinated contrast material is an independent risk factor for AKI in patients with eGFR ≥30 mL / min/1.73m2”. (ACR manual 2017)

We need some large RCTs to settle this issue. There is clearly equipoise on this issue and there should be no barriers to running a RCT.

We should stop using the term “CIN or contrast induced nephropathy” as it implies a degree of causation that simply is not supported by the literature. Post contrast acute kidney injury more appropriately describes what is occurring.

If a patient needs contrast to make an important diagnosis and there isn’t an easily available alternative test, just do the scan. Even if contrast causes acute kidney injury, true patient oriented harms are only seen in a very small number of patients. There is a balance, but as long as the pretest probability of important pathology is higher than the chance of harm (probably less than 1%), the patient will still benefit from the contrast CT.

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