?Stroke/AMI/PE/Sepsis/I don't know.

[jrm818]

So the renal system is in the spotlight now. Also, I take it we're supposed to assume that he's hypercoaguable, which certianly supports a PE hypothesis. My ddx list hasn't changed much, I'm wondering if he's throwing clots all over - into his lungs, kidneys,(can you throw a clot into the arterioles feeding specific toes? That's the only explanation I could come up with for that interesting perfusion issue).

Has his SOB resolved? If the SpO2 is at all reliable (which I doubt), I'd guess not.

I assume they are CT'ing his lungs?

I'm still not quite sure what would be causing his BP issues...with a BP dependent rather heavily on colloid and alpha agents it sounds like he's likely hypovolemic...at least intravascularly. Is he third spacing? Any signs of ascites? If not, it must have gone interstitial, and he has the edema to prove it.

MI looks pretty unlikely at this point.




Also I'm throwing Lupus out there. It's gotta be right once in a while

 

[MrBrown]

Buggered if Brown knows, where is the Consultant when you need him?

 

[Melclin]

Also, I take it we're supposed to assume that he's hypercoaguable, which certianly supports a PE hypothesis.

You're not really supposed to assume anything, Im just relaying as much of the information as I have written down/remember. The PT was normal.

That's the only explanation I could come up with for that interesting perfusion issue.

It did occur to me. LOL. But what is the likelihood of throwing two clots to two different arteries at the same time affecting the same three toes on each foot (the effect was bilateral). My thought was more neuro. The middle three toes are innervated by different spinal nerves to the outside two. So I thought that might have something to do with it. Getting different levels of sympathetic tone for some reason?

Has his SOB resolved? If the SpO2 is at all reliable (which I doubt), I'd guess not.

It has. To be honest it was never severe in the first place (I should have mentioned that) and it was pretty much gone when we got to ED with 8LPM. Blood gas was ordered, I never saw it, but he had been taken off supplemental O2 when we got back.

I assume they are CT'ing his lungs?

Yep PE was highest on the list at that time. There was some commotion from the imaging people about V/Q versus CT and the ED nurses were b**tching about them. The registrar I was talking to, who was most helpful, was quite sure it was a PE. Evidently the consultant wasn't as sure given we weren't in the cath lab.

Any signs of ascites? If not, it must have gone interstitial, and he has the edema to prove it.

No ascites. No remarkable odema other than the very mild kind I mentioned at the start.

Also I'm throwing Lupus out there. It's gotta be right once in a while

Its not lupus. And I measured his neighbour's cat urine for uranium, dead end there too. Maybe paraneoplastic syndrome?

[/QUOTE]

10char

 

[Aidey]

Both hyperkalemia and a PE can cause hypotension. Although his K+ isnt that astronomical, I've seen pts with higher that have a normal BP. He may also be dehydrated and/or have an infection, and it is just a combination of things.

 

[firetender]

Patient Care?

Okay, here's what I see. Here are the OP's comments, in the whole thread about the actual patient as if he were a human being:

*slightly overweight and unkempt man in bed holding a colostomy bag against his stomach. He is alert and oriented and says that he has tingling in both legs and his left arm, and feels nauseated.

*He had gone to the toilet in the AM of this current day (~6am) and it, “felt like he was walking on blistered feet”, at which time his tingling sensation started.

*(a “day or two” before being discharged, they “didn’t give me any drugs or nothing” for the PE).

* Once in the ambulance the patient quite suddenly starts to sweat profusely (You could actually see the drips of sweat forming in seconds from nowhere) and states that he “feels like S**t” and is mildly short of breath (reports SOB after prompting for “any problems with your breathing”).

* The pt is mildly anxious.


LATER ====

Pt is significantly more anxious than he was.
Denies chest pain or discomfort.
Now feels nauseated.

THEN HE ASKS FOR ====

You eventually get access - Meds? fluids?
Transport decisions?
Ddx?

THEN THE SUMMARY======

No one else wants to have a shot at an alert and oriented bloke, tachycardic with no blood pressure and some neuro deficits, sweating like a stockbroker?

THEN THE (I don't know what that is) ============

To be honest it was never severe in the first place (I should have mentioned that) and it was pretty much gone when we got to ED

________________________________________

And now, picture five more medics, standing around talking with Melclin, and in a total of 23 posts, here's what any of them have to say about the human being whom they are discussing

VENEFICUS : I am going to have to say there is not enough info yet to make any definitive decisions.

That actually surprised me! Oh, wait a minute, that wasn't about the patient, it was about the "decision" Sorry!

JRM818: With such uncertainty I'd be inclined towards rather conservative supportive treatment until we have some more information

"Supportive" that's kind of a nice, human word

AIDEY: As annoying as this saying is, treat the pt, not the monitor

Everybody is so damned concerned about what's going on, nobody is paying attention to what's happening, except AIDEY, but he treats the issue apologetically as a cliche!

It's not a cliche it's a real patient. To his credit, Melclin asks people, "Hey, what would you actually DO?" But, well, no one bites.

Can't record an SPO2
Monitor registers false beats
BP by palpation (why?)

In the unit, sweats (does it stop and when?)
says feels like S***
and then...
NOTHING

Sorry folks, the scenario looks like swiss cheese; especially when Melclin retracks any urgency to the breathing situation. At that point I said; he's really not helping us here.

Okay, sure it's nice to know why. But here I see a neglected patient because nobody's asking questions having to do with what would be determining urgency; taking measures to stabilize; and moving. Each and every one of those things would be reflected in "How is the patient?"

Even an "I'd treat as if... and roll" would be reassuring.

Does anyone do anything as a medic anymore or is everyone wanting to be MDs??

 

[SanDiegoEmt7]

I think the common supportive measures and general patient care were implied. When a case study is posed, generally it is discussed with the goal of finding a definitive diagnosis and its definitive treatment, so that when similar signs and symptoms are seen in the field it adds a different differential to the toolbox (or a different way of looking at the same differential).

If everyone had said, fluid bolus, O2/ventilations prn, comfort the patient to the ED, and left it at that it wouldn't have been a very interesting discussion. I'm assuming that most people leave out the details of patient care you are discussing because they are a given. If every response had included them, this thread would be twice as bulky and still not contain a definitive answer.

Buuuuuut, Firetender I do love you point of view on this and previous topics, I just think that most people are skipping the givens in search of an answer. (At least I hope so, eeek)

 

[Aidey]

<-------- she!

 

[Melclin]

Okay, here's what I see. Here are the OP's comments, in the whole thread about the actual patient as if he were a human being:
________________________________________

And now, picture five more medics, standing around talking with Melclin, and in a total of 23 posts, here's what any of them have to say about the human being whom they are discussing

That actually surprised me! Oh, wait a minute, that wasn't about the patient, it was about the "decision" Sorry!

"Supportive" that's kind of a nice, human word

Everybody is so damned concerned about what's going on, nobody is paying attention to what's happening, except AIDEY, but he treats the issue apologetically as a cliche!

It's not a cliche it's a real patient. To his credit, Melclin asks people, "Hey, what would you actually DO?" But, well, no one bites.

Can't record an SPO2
Monitor registers false beats
BP by palpation (why?)

In the unit, sweats (does it stop and when?)
says feels like S***
and then...
NOTHING

Sorry folks, the scenario looks like swiss cheese; especially when Melclin retracks any urgency to the breathing situation. At that point I said; he's really not helping us here.

Okay, sure it's nice to know why. But here I see a neglected patient because nobody's asking questions having to do with what would be determining urgency; taking measures to stabilize; and moving. Each and every one of those things would be reflected in "How is the patient?"

Even an "I'd treat as if... and roll" would be reassuring.

Does anyone do anything as a medic anymore or is everyone wanting to be MDs??

What do you want mate? Someone to post an extensive list of ways in which we'd rub his tummy and tell him he's special? I went and got a towel and wiped drops of sweat off his brow because it was dripping in his eyes. I spoke to his family because no one else was and his daughter was crying. I helped him empty his colostomy bag. But who gives a toss? So would everyone else. Its just basic humanity. I don't need to post that and nor does anyone else need to suggest it in their posts.

Its a given.

I'm not interested in other peoples versions of their human touch. I'm good with people and I'll get better in time with experience and personal reflection. What I need from the forum is suggestions about this case that would help me to make treatment, triage and transport decisions in the future.

Thanks to this discussion, I've already realized I really should have considered bleeding. I didn't consider electrolytes until I saw the blood work. To big gaffs with early signs I could have noticed that I now know about. I've noticed other little things as well that would help me in future. Which is exactly what I hope for when I post jobs like this.

Sorry folks, the scenario looks like swiss cheese; especially when Melclin retracks any urgency to the breathing situation. At that point I said; he's really not helping us here.

That's because the job was swiss chesse. It was a very dynamic case. It was very complex in terms of the changing nature of his physical assessment. It was also a job that was sandwiched in-between 6 other jobs that day. All told its not that easy to communicate it all.

Also I didn't retract any urgency. It was never there to begin with, I said he was mildly short of breath after being prompted. What I did is recognize that I didn't really provide much detail in my resp assessment.

I do, however, wish more people had weighed in with treatment and transport opinions but I didn't see yours there either firetender.

You already have too much information (my bad, I'm rushing to the end with a thirst for the wisdom of the board), but based on my first post...

Fluids?
Inotropes/Pressors?
Antibiotics?
Oxygen?
Working diagnosis?
Tx decisions?

 

[Aidey]

Working dx of kyperkalemia, possible PE, possible sepsis. Had this been my pt he would have gotten a 12 lead, IV, O2 with EtCO2, Calcium, fluids if the calcium didnt fix the BP, albuterol (part of the hyperK protocol) and follow up treatment depending on what changes happened. No inotropes or pressors, unless for some reason his BP continued to tank after the calcium.

For me, forming a tx plan difficult in a case like this when I don't have the EKG and EtCO2, because those 2 things could confirm or refute my dxs rather quickly.

 

[Melclin]

Working dx of kyperkalemia, possible PE, possible sepsis.

For me, forming a tx plan difficult in a case like this when I don't have the EKG and EtCO2, because those 2 things could confirm or refute my dxs rather quickly.

For my own benefit (not to be argumentative), how would EtCO2 effect your decisions in this case? (Are we talking nasal prong EtCO2? Those things would be awesome to have).

 

[Aidey]

For my own benefit (not to be argumentative), how would EtCO2 effect your decisions in this case? (Are we talking nasal prong EtCO2? Those things would be awesome to have).

It wouldn't necessarily change what I would or wouldn't do, but it helps me figure out if there is more than one thing going on. If I throw the pt on the EtCO2 and its 38 mm/hg with normal waveform my suspicion for PE just dropped a bunch. There isn't a lot I can do for a PE, but if it is something mimicking a PE there may be something I can do. The catch in this case is that it is possible he is in metabolic acidosis from his kidney problems, so even if he doesn't have a PE his CO2 may be low.

It is really just part of drawing a complete picture, and it helps me see how sick the patient is overall. If I started giving this patient medications like calcium and bicarb for the kidney issues I absolutely want to monitor his EtCO2 because that, his EKG and his BP are going to be the 3 places I would see the biggest changes if the medications were having a positive effect.

And yes, they are nasal prong EtCO2 readers. We have EtCO2 cannulas, where we can use them to give O2, or just to monitor their CO2.

 

[jrm818]

Working dx of kyperkalemia, possible PE, possible sepsis. Had this been my pt he would have gotten a 12 lead, IV, O2 with EtCO2, Calcium, fluids if the calcium didnt fix the BP, albuterol (part of the hyperK protocol) and follow up treatment depending on what changes happened. No inotropes or pressors, unless for some reason his BP continued to tank after the calcium.

For me, forming a tx plan difficult in a case like this when I don't have the EKG and EtCO2, because those 2 things could confirm or refute my dxs rather quickly.

Learning point for me: Would you be at all concerned about the possibility of heart failure not related to the hyper-K state? When I was thinking about supporting BP chemically I was worried about increasing the demand on what may be an already failing heart (and so I didn't really propose any specific treatment, thus part of firetenders objection I suppose). I'd have the same concerns about albuterol, although it's not being given for quite the same reason. The pressors the hospital gave don't seem to have killed this pt., so I suppose that's part of the answer, but I'm interested in the decision calculus that goes into the decision from your perspective.

You're not really supposed to assume anything, Im just relaying as much of the information as I have written down/remember. The PT was normal.

So why was the blood "clotting quickly"? I don't know any other reasons that would happen, but that's likely just ignorance on my part.

It did occur to me. LOL. But what is the likelihood of throwing two clots to two different arteries at the same time affecting the same three toes on each foot (the effect was bilateral). My thought was more neuro.

It was a bit of an outlandish guess. I bet you could have written a paper about it if it had turned out to be right.

The middle three toes are innervated by different spinal nerves to the outside two. So I thought that might have something to do with it. Getting different levels of sympathetic tone for some reason?

I'd never seen the innervation described like that. I flipped back through some old notes, and they have the toes all in the same dermatome. Dermatomes are sensory of course, but I can't find a good description of the sympathetic innervation of the toes, and if anything I'd expect the distribution to be more overlapping than the sensory distribution - not well segregated enough to see differences between toes. That said, if you could point me in the direction of some better information, I'd be appreciative.

This does actually make me think a bit more about a neuro pathology. I thought about a spinal cord/nerve root issue when you first described the extent of the pale cold skin, but again since the distribution wasn't really dermatomal, I decidyed that the issue was more likely that the more distal structures were poorly perfused.

I don't know that I would consider this really plausible, but I can imagine a scenario where [nerve root compression, partial SCI, degeneraiton of some sort] would cause in effect a partial sympathectomy - which could cause the tachycardia and hypotension corrected with alpha agents and fluid, could cause the pale skin due to reflex vasoconstriction wherever sympathetic innervation persists, sweating due to reflex sympathetic overdrive wherever innervation persists (was he sweating all over or just his pink bits?),

A bit too hypothetical to have anything to do with the care of this patient at the moment, so apologies to firetender for that mental diversion...

It has. To be honest it was never severe in the first place (I should have mentioned that) and it was pretty much gone when we got to ED with 8LPM. Blood gas was ordered, I never saw it, but he had been taken off supplemental O2 when we got back.

That leas me to believe that the ABG didn't show much of an oxygenation issue. That might knock PE down the list a tad?

I'll play along with the decisions:

Fluids?

yes, but I have the benefit of seeing the ED treatment now so the decision is easier.

Inotropes/Pressors?

Initially I said no, now I say yes, again thanks to seeing the ED response

Antibiotics?

Not yet

Oxygen?

yes, for presumptive PE with an unreliable SpO2, discontinue if the ABG shows he's oxygenated appropriately.

Working diagnosis?

working dx of renal failure with PE until PE is ruled out, but I'm starting to feel like we're going to find that PE isn't the primary issue.

ddx:
PE, renal, neuro , infection isn't off the list yet, bleed, cardiac failure (due to...)

Its not lupus. And I measured his neighbour's cat urine for uranium, dead end there too. Maybe paraneoplastic syndrome?

I'll buy a beer for anyone who guesses paraneoplastic and is right...but this is your scenario, so I'm not sure you can cash in this time....

 

[Veneficus]

As vene correctly deduced (I though it would take a little longer :wacko: ), peaked T-waves would cause this and yes it was due to hyper-K.

I see that at least once a day, it is why i take a manual pulse, which also helps during heart tones.

So,

O/A at the ED

NIBP: 98/50
Manual Pulse: 120
ECG: SR, T-waves peaked in V2, V3 & II
SpO2: varying between 65 and 90 with an utterly dodgy pleth waveform, on 8LPM by simple face mask.
GCS:15

Nurse notes that his blood is clotting extremely quickly when she draws for labs.

Nothing like a WAG clotting time.

The middle three toes on each foot are now extremely pale, while the other two are relatively well perfused. The pt has stopped sweating.

before or after treatment?

Before would be really bad. After not as bad.

His face and chest are far more pale than when he presented.

because he is busy trying to die.

-4L normal saline
-1L of gelofusine
-1mg of metaraminol

Art line BP is averaging around 80/40 and seems dependant on the manual rapid infusion of gelofusine by a trusty ICU registrar who is accompanying the array of various important looking doctors now bustling about.

Blood work:

Na+: 132mmol/L, K+: 6.7mmol/L, Ca+: 2.31 mmol/L, Albumin: 43 g/L, Lipase: 13.5, Ck: 47ng/dl, Troponin T: 0.01ng/dl?, Creatinine: 158 micromol/L Urea: 10.2 mmol/L, Haemoglobin: 16.5mg/dl, Glucose: 9 mmol/L, C-reactive protein: 4.9mg/L.

While his K is not at 7 yet, I might be seriously thinking about some emergent dialysis.

We really really need to know what his coag values are. To determine if he is in or at risk for DIC in addition to the local clotting.

(Some of the units of measurement might be wrong, the lab results came without units which would be fine if it wasn't for the frustrating differences in the use of various units of measurement between the US and Aus).

Well you guys are upside down

With Glucose + Insulin is ordered.

Tight regulation of hormonal control is a normal ICU event. The insulin shold help lower his K+ also.

A further 500mls of gelofusine is hung. BP, 5 minutely during the infusion of the third 500mls: 110/43, 110/49, 120/51. Pulse is consistently 110-120.

because he is losing protein, possibly from liver complications and/or a nephrotic syndrome.

1L has been removed from his colostomy.

Not surprising.

He is ready to go off to CT. What are you thinking now?

He is CTD.

This dude has some major issues. Let's make a summary.

Recent surgery.

Most likely an adenocarcinoma. Hopefully only invasive and not metastatic. If it was the likely locations of spread and destruction are: lymph, liver, lung, and bone.

FE deficiency is a high likelyhood.

If his liver is involved it cold account for a lack of albumin, but I think his greatest loss is from his Kidney.

Clotting can be caused from a myriad of things, no way to pinpoint.

If there is bone spread anemia is almost a promise. Furhter increasing his hypoxic problems.

Let's not even get into paraneoplastic syndromes.

He already had a PE, so he is at risk of basically infarct everywhere.

Kidney complications from surgery and likely acute kidney failure, is going to really be a problem in managing his hemodynamics.

Urine protein would help.

If he has some sort of post surgical infection, there could be not only DIC but all kinds of organ damage, particularly to the Heart and adrenals would complicate the matter in a large way.

If he is lucky, clotting is restricted to the pulmonary system and his toes. If not, he probably already has several micro infarcts. If he is really unlucky, in his coronaries, kidney, and adrenals as well.

For treatment, this is going to be one tough customer. But let's look at just prehospital:

Fluids?

yes for sure, NS, LR, and colloid if you have it.
This has to be weighed against overloading the heart's ability to pump and putting him into cardiogenic shock, but I would start with at least 1L or isotonic and 250 of colloid if available. At hospital some Plasma and RBCs. Stay away from Platelets.

Inotropes/Pressors?

If he stopped sweating prior to treatment or his HR decreased, Yes, if not I would hold off.

Antibiotics?

Couldn't hurt, but I don't see it making a difference.He has a reasonable suspicion to be septic, so some vanc would be good prophylactically.

Oxygen?

If you must, but he probably would only get about 4L of cannula from me. His o2 carrying ability is likely diminished from things o2 will not really make a huge difference with.

Working diagnosis?

Renal and clotting complications from surgery.

Tx decisions?

The hospital that did his surgery or a really great surgical intensivist for transport. Prehospital treatment already discussed.

Firetender:

I see the point you are getting at, but I really wasn't inclined to try and type out a bedside manner. It is very important to be calm and kind to this guy and his family. His discharge may well be to the ECU.

I think one of the most important questions are:

Can medicine help this patient? (some may be surprised that while we can most expertly build Frankenstein's monster out of just about anyone, that doesn't equate to helping.) There comes a point when palliative care is the best we can do.

What is the endgame of that treatment?
(home? with deficits? SNF? ICU to the end? See where we are in a few days?)

These are not really decisions for medics in the field though.

As of this reply, I don't think we can answer those questions. More data is needed. Part of that data is asking the pt what he wants.

 

[Veneficus]

Learning point for me: Would you be at all concerned about the possibility of heart failure not related to the hyper-K state? When I was thinking about supporting BP chemically I was worried about increasing the demand on what may be an already failing heart (and so I didn't really propose any specific treatment, thus part of firetenders objection I suppose). I'd have the same concerns about albuterol, although it's not being given for quite the same reason. The pressors the hospital gave don't seem to have killed this pt., so I suppose that's part of the answer, but I'm interested in the decision calculus that goes into the decision from your perspective.....

No, if the guy found a surgeon and anesthesiologist who would put him under and cut him open, he couldn't have heart failre that badly, and would have been extensively screened prior to surgery.

When I was thinking about supporting BP chemically I was worried about increasing the demand on what may be an already failing heart (and so I didn't really propose any specific treatment, thus part of firetenders objection I suppose).

I would also tread cautiously here, but I detailed it in my response.

I'd have the same concerns about albuterol, although it's not being given for quite the same reason.

Not something I'd be concerned about. The problem is just like in trauma, and there very well could be a bleed somewhere still. (though with the hyper coag state I doubt it, because in a massive bleed I would expect hypocoag)

It is a simple case of prefil and hypotension. However, if it has progressed to progressive shock state, it could have damaged the myocardium, but at that point it is damned if you do and damned if you don't.

I am not eager to chemically treat the hyper K+ because he is still neuro intact. In my opinion what he needs is renal support not back of the truck chemistry.

He made it this far, unless there is a change in mental status, he can wait a bit longer.

The pressors the hospital gave don't seem to have killed this pt., so I suppose that's part of the answer, but I'm interested in the decision calculus that goes into the decision from your perspective.

If the fluid and colloid don't bring up the pressure to reasonably perfuse heart, brain, and kidneys, treatment must be escalated.

In the back of the truck I would escalate a step at a time, however, if he stopped sweating prior to at least 500ml of fluid, I would be concerned he no longer had the catecholamine reserve to continue compensation. (for a variety of reasons) That can be managed by most EMS systems using pressors.

 

[jrm818]

Veneficus, as always I learn a lot from your perspectives, but I'm left with a few questions this time, if you don't mind.

before or after treatment?

Before would be really bad. After not as bad.

What is the thinking here? You mention clots in the extremities in your post, is that it?

We really really need to know what his coag values are. To determine if he is in or at risk for DIC in addition to the local clotting.

This has always confused me a bit. Are you looking at INR, PT, or PTT for DIC determination?

For treatment, this is going to be one tough customer. But let's look at just prehospital:

Couldn't hurt, but I don't see it making a difference.He has a reasonable suspicion to be septic, so some vanc would be good prophylactically.

I've been keeping this on my list, but I'm not sure I can articulate why. What s/s specifically point to a septic etiology? What would make or break this diagnosis?

 

[Veneficus]

What is the thinking here? You mention clots in the extremities in your post, is that it?

He has a host of conditions that could cause microvascular clotting, I want to know how extensive it is to determine if some of the clotting is from chronic predisposition or if it is systemic acute clotting.

If he stops sweating prior to treatment, he could be out of catecholamine.

This has always confused me a bit. Are you looking at INR, PT, or PTT for DIC determination?

Yes, I want to know all there is about his blood.

All the coags and all the hematology.

Everything gives you a piece of the puzzle, in this case it is indicated, and at the very least a base to look for potential changes in all aspects of infection, oxygen carrying capability, pro and anti coag factors.

I've been keeping this on my list, but I'm not sure I can articulate why. What s/s specifically point to a septic etiology? What would make or break this diagnosis?

This is not a "what if this guy is the 1 in a million weird presentation?" He has a host of realistic risk factors like:

Potential DIC, potential renal and/or cardiac failure from bacteria, hypotension, potential internal leakage from colostomy, possibly inadvertant fistula created in surgery.

Nothing really concrete, but the possible benefit of helping outweighs the potential risks in this case.

 

[Aidey]

I am not eager to chemically treat the hyper K+ because he is still neuro intact. In my opinion what he needs is renal support not back of the truck chemistry.

He made it this far, unless there is a change in mental status, he can wait a bit longer.

So are neuro deficits your "flag" for chemically treating the hyper K+? Our protocol (and our med director) both have hypotension as the tipping point symptom for treatment.

 

[Veneficus]

So are neuro deficits your "flag" for chemically treating the hyper K+? Our protocol (and our med director) both have hypotension as the tipping point symptom for treatment.

Neuro deficit is a sign of hypoperfusion. I like to treat the patient based on presentation. In the case of electrolyte balance, unless the patient is grossly unstable, in my mind discretion is the better part of valor.

If you look at the vitals throughout, at no point are there any listed that demonstrate severe hypotension. I know some protocols like to make 100systolic the magic number, sometimes 90 systolic, but systolic BP does not correlate with CVP and that makes using systolic bp as a sign of perfusion iffy at best. MAP or if you want to be quick and dirty, pulse pressure, will give you a better measurement. But even the kidneys can survive around 80 or less for a brief period.

Also in order to determine lack of cardiac contractility over hypovolemia, you would need an ultrasound. If you start treating hypovolemia and it is not working it is easier to then go to Calcium than it is the reverse.

Perhaps seeing the QRS amplitude might make the case more compelling, but in absence of that, trying to balance labs without actual results on a patient compensating well is not what I would do in such a short transport. If the protocol demanded it, I would call med control and make a case for not doing it.

Aside from sympathetic response and a mild tachycardia, I can't say this patient disturbs me enough to warrent trying to acutely reverse K+ based on an EKG.

From the lab perspective after getting to the ED, his albumin deficit coupled with his K+ would make me more inclined to fix him with an emergent dialysis which would serve him better in the long run while attempting to find out what caused the renal failure and if it is reversible.

At the very least, figure this guy is going to the ICU and when he gets there, he is going to be put on glucose/insulin control, and the insulin is going to drop his K as well. At that point he is going to have his PH evaluated as well.

Do you think this patient is unstable enough to crash in the next 1/2 hour to hour?

I think it fair to say if you suspected that, more aggressive measures would be indicated. But it is a judgement call, not a right or wrong as I see it.

 

[Aidey]

I'm off to work, so I can't reply in full right now, but with his possible clotting issues is he even a candidate for emergent dialysis? I'm pretty sure they have to get that sorted out first since clotting causes so many complications with treatment. I suppose they could hold off on the heparin, and instead use saline and just adjust the treatment to remove the extra fluid. In his case he needs the dialysis more for cleaning than fluid removal at this point, so he isn't as high a risk for fluid overload as some people would be. .

 

[Veneficus]

I'm off to work, so I can't reply in full right now, but with his possible clotting issues is he even a candidate for emergent dialysis? I'm pretty sure they have to get that sorted out first since clotting causes so many complications with treatment. I suppose they could hold off on the heparin, and instead use saline and just adjust the treatment to remove the extra fluid. In his case he needs the dialysis more for cleaning than fluid removal at this point, so he isn't as high a risk for fluid overload as some people would be. .

I don't think he needs fluid removed, I think he needs renal support for managing the components of his blood.

The best way to fix clotting (especially DIC) is to find out what is causing it and get right to the point.