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Jabbed

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Cyclist who lost sight after fast food meal targets Paris Paralympics

Inspiring story, but I’m scratching my head over the medicine.

Patients eats at ________ fast food restaurant and contracts ________ e coli. Develops multi system organ failure due to __________. Receives expensive/experimental treatment __________ and survives, but is now blind.

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Am I supposed to supply answers to the mab libs?
Yeah, I don't get this. I'm not sure what we're supposed to do with this sorta mad-libs thing.

Also, I read the original article and it quotes her saying she got a rare and experimental drug. No, she got ECMO (Source: Woman woke up blind after food poisoning from fast-food restaurant).

I'm assuming the blindness is just due to anoxic brain injury when she was critically ill with terrible hypoperfusion to the point that she needed ECMO. I'm assuming it was VA ECMO anyway as I don't know how e.coli would nuke her lungs.
 
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Septic shock from E. coli leading to ARDS is well known in the ICU. It may start as pyelo, ruptured appy, and even PID (not all pid is std) in previously healthy young women - especially in pregnancy. Often they are bacteremic but certainly not always.

On the other hand, E. coli is not a particularly uncommon cause of HAP/VAP in ICU long haulers. The normal skin and oral flora gets replaced by GNRs like E. coli, Klebs, Pseudomonas, etc. after a week or so in the hospital which then get aspirated, make their way past that ET cuff or down the ET tube, etc.

When it comes to ECMO, most patients with severe PNA/ARDS will need VV-ECMO. While they may also have septic shock requiring pressors, the VV circuit provides gas exchange support to patients with ARDS with some indirect circulatory benefit by supporting the RV (ie preventing hypoxia and hypercarbia),

Interestingly, VA-ECMO is notoriously ineffective in septic shock and other mostly distributive states. VA-ECMO is ideal for providing more flow to patients in cardiogenic shock with low CI and high SVR. Septic patients often don’t need more flow since their is CI often elevated, and their low SVR makes the ECMO circuit flow problematic. It’s not uncommon for a distributive patient with a CI of 5 get put on VA-ECMO providing another 4 LPM yet have the BP go nowhere because the SVR plummets.

Moreover, patients with ARDS are prone to a unique problem on peripheral VA-ECMO called differential oxygenation (aka north-south or harlequin syndrome). It is not seen in VV configurations. This happens when the super-oxygenated ECMO blood traveling retrograde up the aorta mixes with deoxygenated native blood coming down the aorta from the bagged lungs. This mixing cloud will fall somewhere along the aorta that is determined by the amount of ECMO flow and native LV cardiac output. A strong LV may land the cloud somewhere in the aortic arch so that the brain is getting mostly deoxygenated native blood while the rest of the body appears well oxygenated. This is why we keep an a-line or pulse ox on the right hand so that we can make sure that the entire brain is getting oxygenated blood. Differential oxygenation can be fixed by 1) going up on the vent (if you can) to better oxygenate the native blood, 2) go up on the ECMO flow to drive the mixing cloud toward the aortic root, 3) beta block the heart to lessen deoxygenated blood coming out of the heart (yeah, weird right), 4) split your ecmo circuit arterial limb to a VAV configuration to deliver oxygenated blood into the RA.
 
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Septic shock from E. coli leading to ARDS is well known in the ICU. It may start as pyelo, ruptured appy, and even PID (not all pid is std) in previously healthy young women - especially in pregnancy. Often they are bacteremic but certainly not always.

On the other hand, E. coli is not a particularly uncommon cause of HAP/VAP in ICU long haulers. The normal skin and oral flora gets replaced by GNRs like E. coli, Klebs, Pseudomonas, etc. after a week or so in the hospital which then get aspirated, make their way past that ET cuff or down the ET tube, etc.

When it comes to ECMO, most patients with severe PNA/ARDS will need VV-ECMO. While they may also have septic shock requiring pressors, the VV circuit provides gas exchange support to patients with ARDS with some indirect circulatory benefit by supporting the RV (ie preventing hypoxia and hypercarbia),

Interestingly, VA-ECMO is notoriously ineffective in septic shock and other mostly distributive states. VA-ECMO is ideal for providing more flow to patients in cardiogenic shock with low CI and high SVR. Septic patients often don’t need more flow since their is CI often elevated, and their low SVR makes the ECMO circuit flow problematic. It’s not uncommon for a distributive patient with a CI of 5 get put on VA-ECMO providing another 4 LPM yet have the BP go nowhere because the SVR plummets.

Moreover, patients with ARDS are prone to a unique problem on peripheral VA-ECMO called differential oxygenation (aka north-south or harlequin syndrome). It is not seen in VV configurations. This happens when the super-oxygenated ECMO blood traveling retrograde up the aorta mixes with deoxygenated native blood coming down the aorta from the bagged lungs. This mixing cloud will fall somewhere along the aorta that is determined by the amount of ECMO flow and native LV cardiac output. A strong LV may land the cloud somewhere in the aortic arch so that the brain is getting mostly deoxygenated native blood while the rest of the body appears well oxygenated. This is why we keep an a-line or pulse ox on the right hand so that we can make sure that the entire brain is getting oxygenated blood. Differential oxygenation can be fixed by 1) going up on the vent (if you can) to better oxygenate the native blood, 2) go up on the ECMO flow to drive the mixing cloud toward the aortic root, 3) beta block the heart to lessen deoxygenated blood coming out of the heart (yeah, weird right), 4) split your ecmo circuit arterial limb to a VAV configuration to deliver oxygenated blood into the RA.
In addition to @ShockIndex's excellent explanation, I just read through this (https://www.ahajournals.org/doi/full/10.1161/CIRCHEARTFAILURE.118.004905) which helped me visualize what he was talking about vis-a-vis north-south syndrome.

The article also talks about central cannulation VA ecmo which obviates the north-south issue and how you can achieve the same effect outside of the OR using different cannulation sites (e.g. the subclav artery) albeit with different potential issues there.

I also wound up going down a rabbit hole and started reading about how instead of doing IJ - Fem VV ECMO they will sometimes do a single cannulation, dual lumen V-V ECMO solely in the IJ/SVC for certain patients like severe CF patients who are awaiting lung transplant but are otherwise ambulatory and could get out of bed while on ecmo. Crazy stuff.
 
In addition to @ShockIndex's excellent explanation, I just read through this (https://www.ahajournals.org/doi/full/10.1161/CIRCHEARTFAILURE.118.004905) which helped me visualize what he was talking about vis-a-vis north-south syndrome.

The article also talks about central cannulation VA ecmo which obviates the north-south issue and how you can achieve the same effect outside of the OR using different cannulation sites (e.g. the subclav artery) albeit with different potential issues there.

I also wound up going down a rabbit hole and started reading about how instead of doing IJ - Fem VV ECMO they will sometimes do a single cannulation, dual lumen V-V ECMO solely in the IJ/SVC for certain patients like severe CF patients who are awaiting lung transplant but are otherwise ambulatory and could get out of bed while on ecmo. Crazy stuff.
There are 3 unique complications that can occur with peripheral VA-ECMO, and understanding them means that you understand the physiology of the support.

1) Differential oxygenation / north-south: previously covered.

2) LV distension: It turn out that VA-ECMO is great at perfusing your body but terrible for a weak heart -ironic since it’s weak hearts that go on ECMO. The retrograde blood being blown up the aorta is a big afterload on the LV’s native CO. If you look at the pressure-volume loop of a heart on peripheral VA-ECMO, it’s almost identical to what is seen in aortic stenosis with a tall pressure spike needed to overcome isovolumetric contraction. This is no bueno for a stunned, hypocontractile myocardium as it increase stroke work (ie the area under the pressure-volume loop curve). You know there is a problem when the pulse pressure is <10 , PA pressures are rising from backward congestion, the AV valve is opening less than every 3rd beat, and the LV looks distended on echo. Thus, you often need an LV venting strategy; something that off loads the LV. That can be an IABP or percutaneous LVAD (ie Impella) that pulls blood out of the LV and injects it into the aorta. The Impella makes tons of physiologic sense but there is no evidence that it’s better than an IABP…yet. You can even do a surgical carheter vent to the LV if the patient came out of the OR peripherally cannulated (rare).

3) Lower extremity ischemia: That arterial cannula in the femoral artery threatens perfusion to the leg. A reperfusion cannula to the distal leg lessens the risk significantly but I’ve seen plenty of legs lost.

Central cannulation circumvents these issues because the cannula is placed in the proximal aorta and blood flows anterograde down the vessel. There is no mixing cloud, LV afterload, or big catheter in a little leg. However, central cannulation is more invasive and must be done in the OR by a CT surgeon. We mostly see central cannulation in patients coming out of cardiac surgery who couldn’t be separated from bypass. The ECMO is an extension of the bypass circuit minus a blood reservoir.

VV-ECMO is a different beast and none of these complications occur. While most of us trained on the 2-cannula technique (venous drainage from a femoral cannula with return to the RA via the IJ), we are increasingly using the dual lumen cannulas (Avalon and Crecent) for all of our VV cases. Here, a single long cannula is placed under fluoro into the IJ and extends across the RA with the tip near the hepatic IVC. Blood is drawn from holes in the distal tip and proximally through a hole in the SVC. The blood is pumped through one lumen to the oxygenator that delivers it via the other lumen to the RA where it is ejected out of a hole aimed at the TV.

These single cannulas has theoretic advantages such as less recirculation. This occurs when the oxygenated blood delivered by the return cannula is taken up by the venous drainage cannula instead of going to the patient. When using a 2-cannula method we see this when the cannulas from above and below migrate within 6-10 cm of each other. The single cannulas do not eliminate the problem as recirc can still happen- especially if the cannula rotates and ejects the oxygenated blood away from the TV.

FWIW, I was once an EP but now this is most of my day. During covid I had 14 patients on VV at one time. Now, I typically have 4-5 on VA and a VV here and there with tons of IABPs and Impellas. 3 years ago, I crashed a COVID peripartum cardiomyopathy onto VA ecmo while OB yucked out her baby via perimortum c-section. I had her on off and on my service for 9 months before she was finally discharged with a new heart. Watched her meet her 9-month old neurologically intact baby for the first time at discharge. Since then, no desire to work another ED shift. All the 60-hour work weeks, time away from family, etc - WORTH IT.
 
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ECMO has become popular of late, but does the average community EP need to know about it? The answer to that is maybe. Here is my take on ECMO uses in the ED.

1) Cardiac Arrest / Extracorporeal CPR (ECPR): This is where a patient in cardiac arrest is placed on ECMO and maintained, often with long periods of non-pulsatile flow (ie the ECMO circuit provides the preponderance of flow), until native circulation is restored. This has been a thing in Europe for more than a decade and many of you may have seen pictures on the net depecting a cardiac arrest victim being cannulated on a subway platform. However, the EMS system in Europe is very different than the US, and the data in the US is unconvincing. We all got excited with the ARREST Trial which seemed to show improved outcomes from ECPR initiated in the ED followed by cardiac cath in v-fib arrest. However, this study was stopped early for efficacy and likely benefited from a champion primary investigator supported by a unique system capable of selecting ideal patients who were most likely to benefit. The EROCA trial was unable to show a benefit in OOHCA, and was spun as a feasibility trial to soften the blow to the ECPR acolytes. The final nail in the coffin of ECPR came last January with a large European trial (INCEPTION) published in NEJM that showed no benefit. Bottom line, routine ECPR should not be attempted outside of the protections of a clinical trial and should be viewed as an experimental therapy.

2) Peri-cardiac arrest: So, your partner spent the entirety of the last hour of their shift doing CPR (because Betsey gotta live) before finally getting a pulse, and is now trying to sign it out to you. However, the patient is on rocket fuel and trying to meet Jesus. Should you put them on ECMO? Maybe. There are select patients who may benefit from ECMO if they have a brief cardiac arrest and are at risk of coding again. One population is patients with profound hypothermia. ECMO is very effective at rewarming a corpse; so is dialysis if you don’t have ECMO. Massive PE is another that does pretty well if you cannulate them with a pulse. I suggest that you get any PE patient that you lyse to an ECMO-capable center because ECMO should be considered as a salvage if their hemodynamics don’t improve. In fact, a number of us are starting to think that ECMO, if immediately available, may be preferable to lyrics if your center has a pro at sucking out clot via thrombectomy. However, this is an evidence free zone, and a lot depends on local culture and resources. Just understand that there is a lot of heterogeneity around the approach to massive PE and ECMO may fit select post-arrest patients depending on the center.

3) Post-MI cardiogenic shock: Another tough one. The most recent evidence this year suggests no benefit (ECLS-SHOCK). However, this study came out of Europe and may not be applicable to the US since only 5% of the patients in this study got a LV vent (see my earlier post). Bottom line, I do it every day for this population but cannot say that it’s any better than inotrops, IABP, etc. The truth is that most of these patients will not do well and we need more studies since we rare use just ECMO in this population.
 
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One population is patients with profound hypothermia. ECMO is very effective at rewarming a corpse; so is dialysis if you don’t have ECMO.
Well, that came from cardiopulmonary bypass; ECMO is like "CPB lite". And, I can conceptualize that about HD. Anything that can rewarm the blood rewarms the body. It's the most efficient way, I would guess (vs full body immersion in warm water, or peritoneal lavage).
 
ECMO has become popular of late, but does the average community EP need to know about it? The answer to that is maybe. Here is my take on ECMO uses in the ED.

1) Cardiac Arrest / Extracorporeal CPR (ECPR): This is where a patient in cardiac arrest is placed on ECMO and maintained, often with long periods of non-pulsatile flow (ie the ECMO circuit provides the preponderance of flow), until native circulation is restored. This has been a thing in Europe for more than a decade and many of you may have seen pictures on the net depecting a cardiac arrest victim being cannulated on a subway platform. However, the EMS system in Europe is very different than the US, and the data in the US is unconvincing. We all got excited with the ARREST Trial which seemed to show improved outcomes from ECPR initiated in the ED followed by cardiac cath in v-fib arrest. However, this study was stopped early for efficacy and likely benefited from a champion primary investigator supported by a unique system capable of selecting ideal patients who were most likely to benefit. The EROCA trial was unable to show a benefit in OOHCA, and was spun as a feasibility trial to soften the blow to the ECPR acolytes. The final nail in the coffin of ECPR came last January with a large European trial (INCEPTION) published in NEJM that showed no benefit. Bottom line, routine ECPR should not be attempted outside of the protections of a clinical trial and should be viewed as an experimental therapy.

2) Peri-cardiac arrest: So, your partner spent the entirety of the last hour of their shift doing CPR (because Betsey gotta live) before finally getting a pulse, and is now trying to sign it out to you. However, the patient is on rocket fuel and trying to meet Jesus. Should you put them on ECMO? Maybe. There are select patients who may benefit from ECMO if they have a brief cardiac arrest and are at risk of coding again. One population is patients with profound hypothermia. ECMO is very effective at rewarming a corpse; so is dialysis if you don’t have ECMO. Massive PE is another that does pretty well if you cannulate them with a pulse. I suggest that you get any PE patient that you lyse to an ECMO-capable center because ECMO should be considered as a salvage if their hemodynamics don’t improve. In fact, a number of us are starting to think that ECMO, if immediately available, may be preferable to lyrics if your center has a pro at sucking out clot via thrombectomy. However, this is an evidence free zone, and a lot depends on local culture and resources. Just understand that there is a lot of heterogeneity around the approach to massive PE and ECMO may fit select post-arrest patients depending on the center.

3) Post-MI cardiogenic shock: Another tough one. The most recent evidence this year suggests no benefit (ECLS-SHOCK). However, this study came out of Europe and may not be applicable to the US since only 5% of the patients in this study got a LV vent (see my earlier post). Bottom line, I do it every day for this population but cannot say that it’s any better than inotrops, IABP, etc. The truth is that most of these patients will not do well and we need more studies since we rare use just ECMO in this population.
With regards to how much an EP should know about ECMO itself I feel like you hit the nail on the head - really not much of the mechanics because it’s beyond what happens in the ED and the evidence doesn’t support it’s use for any one hard indication in the ED population yet (unlike strokes, stemis, etc)

I do think in broad strokes EPs should know generally what the capabilities and limitations of mechanical support are, and what the indications for transfer to a center capable of doing mechanical cardiac or pulmonary support are. Because getting these people transferred to a center that has that capability quickly is very important in the dispo from the ED ultimately.

The challenge is some systems have great hub-spoke type models where you can Identify a patient that may need ECMO from the ED and get them transferred to the mother-ship where mechanical circulatory support is available quickly. But many smaller systems won’t have a process for that in place and arranging the transfer would be impossible from the ED.

In the future I imagine a world where MCS looks a lot like trauma. EPs know stabilization and when to recognize the person needs transfer to a trauma center - and every hospital has some system in place to get those patients out of the ED and to an MCS center in a reasonable time frame.
 
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