Off Label

The guy is probably there because of some well intentioned charitable gesture someone is making. Is there really a concern he'll make it to something more than routine IFT's if even that? I'd just consider graciously tolerating him part of my training. Take the high road and just complete the course work and go. 

Radiographic interpretation is an advanced practice/physician level skill that requires credentialing and a formal privileging process.  Out of scope for pre-hospital use. 

Aux États-Unis, le niveau de sophistication médicale de l'ambulance ne peut pas prendre
 en charge de telles entités de diagnostic avancées. De nombreuses fois, nous ne pouvion
s pas traiter ce que nous avons trouvé avec ces appareils de toute façon.

Without the order, I guess you don't treat the pain. I wouldn't give an order for pain with what you've given here...what was the report to the doc? 

What are we supposed to get from an abstract? I couldn't read the whole study so all I can say is that the authors are saying that mask ventilation isn't inferior to intubation. Unless someone has passed the pay wall for this journal, no one else can make any coherent statement either. "Not inferior" is being used as a  a statistical term here and does not have the same significance as a conversational "just as good".

Abstracts are useless, really.

On 1/29/2017 at 6:11 PM, paramatt_ said:

it is reasonably common to have poor airway control on seizing patient's, especially those with trismus, even if its just short term...anyone have any good airway management techniques in such situations?

Paralysis.

2 hours ago, 1EMT-P said:

We should be able to provide these patients with additional resources so they can improve their health.

What additional resources would have helped here? 

On 1/17/2018 at 1:35 PM, Just Plain Ruff said:

sadly, 3 days after admission he passed due to sepsis from the infected foot

I'd say he died from complications of obesity. 

23 minutes ago, paramedicmike said:

That doesn't change the veracity of his statements within this thread or elsewhere in these forums. 

That medics know just enough to look stupid? That's as rude as calling someone you don't know a moron. That he died of a debilitating and painful disease is a real tragedy, but if he was the upstanding guy he apparently was, he'd own that. 

As quiet as this site is, it's better than nuthin'

I wondered why that took so long to be challenged too.

On 11/6/2017 at 5:45 PM, BushyFromOz said:

Epi has alpha and beta effects, however, the beta blocker prevents vasodilation, also, Epi has to be administered at higher concentrations to have Alpha receptor activation. At these higher doses, without Beta-1 stimulation, the vasoconstriction from the Epi could result in uncontrolled BP increase and worsening pulmonary edema.

I'm not following this either. Seems to be some confusion about what epi does and alpha and beta stimulation/antagonism. There would be no danger at all of causing uncontrolled hypertension in this scenario without a completely unreasonable dose or accidental bolus. As these cases go, a modest dose (about .03-.04) in a patient with a failing LV on beta blockers will frequently not even get the HR over 100, if that. 

Glad you're OK and doing well.

Don't forget a little salt and pepper and some butter.....oh, and some napkins

Facebook? Over at Nurseanesthesia.org, it was the same thing. Now it's an echo chamber for people wanting to see how competitive they are for anesthesia training.

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.

2 hours ago, Just Plain Ruff said:

I don't think there are really any set medical conditions that cause crush injuries or syndrome.

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.

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!

10 hours ago, Kenny0471 said:

 

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.

 

 

Do you know what all of this means?

Reversing carfentanil and reversing fentanyl is the difference between pushing a car and pushing a shopping cart.

17 hours ago, Arctickat said:

 

Why would CPAP be contraindicated? I know it increases intrathoracic pressures and reduced preload, but in this particular case, that could be a good thing. Sounds to me like he's in shock as a result of acute hypoxemia secondary to the CHF. The Digoxin will prevent any compensatory tachycardia. CPAP would have been my goto as I did an IV NS bolus and prepped a Norepi infusion in the event that CPAP was not sufficient in reducing respiratory workload and improving the hypoxia.

Curious as to choosing NE instead of an inotrope like epi or even dopamine. Is there a specific element here that you like NE for?

9 hours ago, 1EMT-P said:

This patient proved to be a challenge, because of the fact that he had CHF and Pulmonary Edema. Normally we would have used CPAP along with Nitroglycerin, but given his low blood pressure those weren't viable options so I consulted with a Physician. The Physician ordered a 250 ML fluid bolus of 0.9% Sodium Chloride, following the fluid bolus then BP was 80/60, the Physician then ordered an additional 250 ML fluid bolus which brought the BP to 92/64 followed by 40 MG's of Lasix IV given slowly.

Counter intuitive, giving volume in that situation. Then take it off with Lasix. Perhaps just a stop gap measure to get the coronary perfusion pressure up.

O2 for SaO2 > 92, epi for MAP > 70 mmHg (start with .03/kg/min) while en route.  Determining DNR is a good idea, verbal is OK just to tell the receiving hospital what the patient said in the event he becomes unresponsive. A pretty hard buy to not resuscitate then and there based on what the guy says in his living room or back of the ambulance unless someone produces a document or corroborator.

Based on hx/ PE, I'd say his LV was pooping out (as opposed to his RV 2/2 PHTN). If he pulls through, someone could suggest palliative care?

On ‎5‎/‎27‎/‎2017 at 7:34 PM, Spock said:

I can think of any number of drugs to give this patient and none of them include NTG or ASA.  ERDoc is certainly correct in that this is rate related and with the a SBP of 110, the patient leans toward stable rather than unstable although that may not be the case for very long.  Diltiazem is the drug of choice here followed by beta blockers, amiodarone, and perhaps verapamil.  My service carries diltiazem and amiodarone but not beta blockers or verapamil.  I wish we carried a beta blocker such as esmolol, lopressor, or labatelol.  

The last patient I had go into AFIB with RVR was under general anesthetic and already in a lateral position for a video assisted thoracoscopy.  When prepping the patient, I had placed the defib pads on him because he was sicker than crap.  Just before incision, the rate took off into the stratosphere and the BP as measured by my arterial line dropped like a rock.  The last numbers I saw was a rate of 180 and a SBP of 50.  I sync cardioverted with 200j and knocked him into sinus rhythm.  The surgeon was quite happy and we finished the case after cleaning the infection out of his chest.  He had a rocky ICU course but survived.  The risk of cardioversion is dropping a clot into the brain and stroking out but there really was no choice here.  

May the Tube be with you

Spock  

Sound like the Afib here was 2/2 the type of surgery and problem the patient was having. I'm going to guess he didn't have a CHADS score that would suggest risk of a LA thrombus. I'd say you were pretty safe in DCCV'ing this guy (not that it sounded like you had  much of a choice.) Good call on the pads. I can't say I'd have thought to do that.

Not trying to be contrary here, but sincerely curious...is there really an established need and demonstrated utility to tactical paramedics in the day and age of very close access to trauma centers via ground and air? What ultimately saves trauma patients is delivery to a surgeon. Why isn't it enough to evacuate patients to waiting medics/flight crews outside of the line of fire? How long can meaningful care be given by tactical teams on scene?

I get that there may be shelter in place situations, or barricaded/trapped patients, but I'm wondering if that happens a lot to where having a medic on the team makes a difference.

Also, do these teams carry WB or blood products?

Thanks