Kenny0471

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5 hours ago, Off Label said:

You might be drifting into the tall weeds here. To break it down, "crush injury" for the purposes here is distinct from blunt trauma, although blunt trauma is obviously a major component in the crush syndrome. Crush syndrome or injury or whatever you want to call it is a constellation of problems that are superimposed on the blunt trauma problem, and, as your question suggests, does not require blunt trauma to set in motion. So....the problems we've identified so far...

1. Massive liberation of muscle protein, myoglobin, into the vascular space leading to renal damage/failure (rhabdomyolysis)

2. Sudden release of severe, blood flow restricting limb/pelvis compression after an extended period of entrapment. Accumulation of anaerobic metabolites and cellular release of potassium from cell death, (to say nothing of vascular injury and thrombus formation) is capable of causing sudden and catastrophic cardiovascular collapse via sudden and profound metabolic acidosis and hyperkalemia.

 

How can these present through a medical mechanism?

1. Rhabdomyolysis can occur when a poorly conditioned athlete attempts an activity that is far out of his depth, ie a marathon. Hyperthermic emergencies, diabetic emergencies, drug reactions, certain infectious diseases can all have the same effect.

2. As far as this goes, a scenario will be instructive...Say a poorly conditioned alcoholic is on a binge one weekend and  spends the weekend on the couch drinking and goes into a fib (maybe has a history of p-afib). He ignores it and continues to drink until Monday when he sobers up. As the week progresses he notices pallor pain in both legs which he ignores for a couple of days until the pain is unbearable. He's admitted to the hospital for pulseless lower extremities 2/2 embolization of thrombus most likely caused by is immobility and a fib. Several days of no flow to both legs from a clot does the same thing as a two ton concrete block on the pelvis.

When the surgeon fishes out those clots and reperfuses the lower half of the body, that "acid wash" will occur and the consequences are the same as if he were extricated from a building collapse...get it?

Obviously, the severity of the syndrome with vary with the situation. While these things can occur, most times the degree to which they present are not clinically significant and resolve on their own with no treatment except rest and fluids.

 

This is perfect. I believe this is my exact form of thinking but put into words that I can digest and fully understand.

Thanks so much!

6 hours ago, Just Plain Ruff said:

The fact that you are still asking these awesome questions are going to get you props from all of us here brother.  Shows that you want to learn and just don't want to get it spoon fed to you.  

 

I would definately put the obese patient down as a candidate, especially an extremity that gets caught under their weight after they fall and are unable to get up on their own.  

 

Depressed patients, I'm not so sure.  

What about the stroke patient who falls, lands on the affected extremity and is not found for 2-3 days or even 6-8 hours?  

Hey Plain,

You are right my friend I see not benefit it getting an "answer anyone can cut and paste but it doesn't help me to learn. Imagine showing upto treat a patient and being like huh? Where my cut and paste treatment haha.

Stroke patient is definitely a candidate I think anyone that can be immobilized without help is something that is a potential candidate for crush syndrome.

Thanks

I put a question to all of you here.

When speaking in regards to immobilized patients and the compression of muscle tissue  in a specific area causing crush syndrome that will release  toxic metabolites/enzymes.

Would you consider the following as potential candidates for crush injuries. 

Obese patients who can't walk but and are alone in their homes?

Chronically depressed patients who mentally cannot move and live independently?

Please bear with me As I am still learning so if my answer are incorrect please just correct my constructively

On ‎7‎/‎27‎/‎2017 at 0:04 AM, Just Plain Ruff said:

I don't think there are really any set medical conditions that cause crush injuries or syndrome, your question is difficult to understand but here is one link. This better not be for a paper that you are having to write and you are wanting us on this site (like many have before) to write your paper for you or do your research.  Yes this has happened before by people who are to freaking lazy to do a Dr. Google search.  

but if you are truly seeking understanding about crush injury look at this link and then take what you learned from this link and expand your search and knowledge. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919827/

But be warned - if the regular members of this site figure out that this was just a Help me do my paper post, your rep here will be ruined and you won't get any future help from anyone especially me.  

Hi.

Just want to thank you for your answer. Crush injuries and their associated causes and effects on the body formed a portion of a test paper that I have already finished.

What I found was that Mosbys Paramedic textbook didn't provide me with enough information to actually fully understand the effects behind crush injuries further than the aspect of natural disasters and obvious crush.

What I want to know and understand is how can a crush injury be caused by a not so obvious MVA, Building collapse and so forth.

I have read ncbi and found it to very useful in digging further into the whole "pre-cursor" for crush injuries. Especially in relation to crush caused by an excessively overweight patient who has suddenly become immobilized, this was a very interesting read.

I do appreciate your help in pointing me in the direction of additional information.

On ‎7‎/‎27‎/‎2017 at 2:44 AM, Off Label said:

Good article, Ruff...

there are "medical" v. "traumatic" causes of the syndrome, which is actually a misnomer, IMO, because while the syndrome can be caused by crush or blast injuries, the actual cause of end organ damage isn't exclusive to trauma. It'd be like calling the effects of acute, significant blood loss a "syndrome" like "penetrating hepatic trauma syndrome". You can have the same "syndrome" from an acute GI bleed.

Might be kind of splitting hairs, but there is a lot in medicine that is confusing that doesn't have to be...so to the OP, the cause of the end organ damage that is caused by blast or crush injury is identified in the posted link.

Hi Off Label.

I agree with your reasoning. However would the end organ damage exist if the crush didn't occlude the anatomical process that would have taken place without the obstruction.

From my understanding the end of organ damage is caused by the release of the crush object or by an occlusion met when the crush has occurred.

So far I have found this topic very interesting. In Australia up until recently the ANZCOR actually advised against removal of crush objects, however have moved away from this and recommended where safe to do so that they are removed.

Thanks again for your feedback.

On ‎7‎/‎30‎/‎2017 at 11:01 AM, Spock said:

Crush injuries are well documented in the literature.  They are usually caused by trauma but can be from medical conditions such as the diabetic patient that passes out and lays on the floor for days before being found.  Glucose levels are through the roof and the patient is in DKA.  We saw a lot of crush injuries in Haiti after the 2010 earthquake and amputated many limbs.  Biggest concern for crush injuries is the sudden release of toxins when the offending structure is removed from the patient.  They become acidotic and will crash as fast as you can say boo.  Have the bicarb and calcium ready along with plenty of fluid.  The PA Department of Health has a decent crush injury protocol but I am biased because I wrote it.  Most of my references were from the Israeli military since they have more experience than most.  Actually, the first SAR teams to arrive in Haiti were from Mexico, Israel, and Turkey.  

Compartment syndrome, renal failure, and gangrene are some of the more dire results of crush injuries.  

If this helps to lead you on the correct path for writing a paper then I hope it helps.  There are many good search engines for medical conditions and you should avail yourself of all except Wikipedia which can be written by any knuckle head.  

Spock

May the tube be with you.

 

Hi Spock,

Thank you for this, you are right in so far as the DKA from a diabetic patient, in fact this was a case scenario in my workbook. I found researching it interesting.

What I was further trying to understand is not so much the "cut and dry" of crush injuries causing toxic releases but more the other side of the equation where a medical condition may promote a crush injuries (DKA diabetic who is immobilized).

Hi Everyone,

I am having a little trouble seeking an answer to this question.

what type of medical conditions could result in a crush injury or crush syndrome.

Would this be something along the lines of Diabetes?

Thank you for your input.

Thank you guys appreciate the information.

11 minutes ago, Off Label said:

Kenny,

I just ask because I don't understand what cytochrome oxidase at cytochrome A3 is let alone cytochrome A3. I was asking because I was curious as to the back round you were bringing to your training.

Good news for me is that I don't need to know that stuff to treat cyanide poisoning!

Ha You are right, why do we need to know what cytochrome oxidase is, at a cellular level. We are there to treat it. But that is the question they wish to have an answer for.  But to answer your question, Cytochrome oxidase is just part of the cellular reaction that cyanide has, the most important thing that we need to know at an EMT or above level is the shift in the oxyhaemoglobin dissociation curve and how our treatment can rectify this injury.

The enzyme cytochrome c oxidase or Complex IV is a large transmembrane protein complex found in bacteria and the mitochondrion of eukaryotes. I believe that your cyanide poison kits that are present in some states in the Americas actually acts on this enzyme to promote a positive shift in the curve, however I have no researched this a lot.

But hey I am just a training, I like this forum so far, very helpful people. I am sure I will have other questions. Thanks again all.

2 hours ago, chbare said:

Good day. You are a bit off but the general reasoning in the the right direction. I will post a video that I filmed some years ago while I was in graduate school. It covers this topic, but I'd ask that you review the concepts of ferrous versus ferric Iron and ultimately, the concept of oxidation state. The Iron in Cytochrome c oxidase is in a similar configuration as haemoglobin but the enzyme dynamics dictate a narrative that is counter to the typical "blood poisoning" that sometimes surrounds a discussion of Cyanide Toxicity. 

I must warn you that I was grossly overweight and profoundly depressed when I made the video, so it's not super high fidelity, but the information is relevant nonetheless. 

 

Hi There,

I don't judge people, no need to clarify. I appreciate any and all feedback required.

Thank you very much for your time mate.

10 hours ago, Just Plain Ruff said:

So Brother, what got you to work on this?  Personal enrichment or a requirement for a course?  

The best cyanide video I ever remember was a world war 2 video where the platoon used cyanide to kill a enemy regiment while they were sleeping.  I cannot remember what movie it was from but the enemy regiment was a african regiment.  

Maybe the Wild Geese or something like that.  

Hi,

I am currently studying paramedics within Australia.

Could you find me the video? That would be appreciated, although I have actually watched a few videos regarding this.

Thanks!

4 hours ago, Off Label said:

Do you know what all of this means?

Hi Off Label,

In a perfect world I would say that I understand 85% of this, yes.

I found the major cause of cyanide poisoning is the ability for the cellular damaged causes by the attachment to hemoglobin.

Do you care to elaborate on this? I am very much happy for any kind of constructive feedback

Hi Everyone,

I have been working on the pathophysiology of Cyanide poisoning I believe that I have captured this correctly, but would love a second a opinion..

Pathophysiology: Cyanide exposure can be a result of inhalation, ingestion or absorption. Once this has entered the body it is rapidly spread to the organs of the body. Inside the cells of the body the cyanide binds to ubiquitous metalloenzymes, rendering them inactive for use. The primary reason toxicity causes by cyanide poisoning is a result of the inactivation of cytochrome oxidase at cytochrome A3.

Intracellular, cyanide attaches itself to ubiquitous metalloenzymes, rendering them inactive. The toxicity results from inactivation of cytochrome oxidase and further uncouples mitochondrial oxidative phosphorylation and inhibiting cellular respiration even in the presence of excessive oxygen saturation during treatment. Because of this cellular respiration shifts from aerobic to anaerobic, causing a rise is lactic acid. Because of this process the brain and heart which are at the highest risk due to the additional oxygenation required for normal homeostatic purposes.

One type of treatment (Antidote) of cyanide positioning can be to convert (oxidize) ferrous ions in hemoglobin to ferric ions. This forms methemoglobin, which is hemoglobin with ferrous ion in the oxidized state. Cyanide which has a greater attraction to these ferric states of the cells. Because of this the cyanide is released from the cytochrome oxidase and combines with the newly created methemoglobin.  This process allows cytochrome oxidase to results its function in cellular respiration.

Methemoglobin cannot transport oxygen, so without counter measures this will result in further tissue damage and necrosis. So this all forms part of a 3 phase treatment plan that is aimed at restoring the hemoglobin to its original state. Through the administration of amyl nitrate, sodium nitrate the conversion of ferrous hemoglobin to methemoglobin to capture the cyanide molecules, Further to this administration of hydroxocobalamin with or without sodium thiosulfate allows the detoxification to be completed and cellular respiration recommence.

Please feel free to provide constructive feedback