The patient is an 81 year old man found with altered mental status. He has known diabetes mellitus, hypertension, COPD and CHF, but has not taken any medications for the past year.
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 142 | Cl | 96 | BUN | 99 |
| K | 5.5 | HCO3 | 21 | creat | 2.3 |
| Blood Sugar | 568 |
Alb 3.1
ABG on 4 liters nasal oxygen
| ABG | |
|---|---|
| pH | 7.38 |
| pCO2 | 29 |
| pO2 | 133 |
| HCO3 | 18 |
So please address these questions: 1. What is the acid-base disorder? 2.Provide a differential for the causes of the acid-base disorder? 3. What other information do you need?
{ 13 comments… read them below or add one }
I’ll play, appears to be hyperosmolar coma.
AG metabolic acidosis, metabolic alkalosis, resp alkalosis.
AG acidosis – Unlikely uremia due to Cr of 2.3, need ketones, lactic acid. Cocern of GI bleed with elevated BUN relative to SCr. H/H? Possibly due to hypovolemia.
Met. alkalosis – taking alkali or GI losses/vomiting? Urine chloride and aldosterone level. Possible Barter’s/Gittleman’s.
Compensated metabolic acidosis.
BUN out of proportion to Cr, could be dehydration with preexisting renal failure but in an 81 year old with those lytes I’d worry about a urinary tract obstruction (the picture isn’t classic Type 4 but it has some characteristics and there is some overlap). Certainly needs ketone check -compatible with DKA, age a little unusual. Lactate certainly -impending sepsis or cardiogenic shock possible.
Needs immediate Foley cath to see if urine is passing, possible ultrasound for obstruction depending. GI bleed is a possibility , the volume depletion may be a contributor to the BUN but doesn’t explain the acidosis by itself unless there is preexisting renal failure or shock.
Somewhat hyperosmolar, corrected sodium is over 150 so he needs rehydration with hypotonic solution (normal saline only to raise BP if low) – may account for obtundation but numbers aren’t that impressive for hyperosmolar coma without looking for coincident event.
thanks for including the oxygen supplied- may have widened A-a gradient
I love acid base. So here’s my best eyeballed educated guess.His corrected sodium corrected for glucsose is high–> He’s total body water deficient. Now that we have that established, this becomes apparent.
1) Look at the pH. It’s an acidosis. Look at the CO2. It’s low. So this is an acute and primary metabolic acidosis. But what else is going on?
2) Calculate the gap. It’s at least 25. The delta gap is at least 12. There for there is an anion gap metabolic acidosis, with a delta gap of at least 12.
3) That means the CO2, corrected for the delta gap should be at at 12 or lower. It’s not. It’s actually higher than that. That means there is also an acute primary(or chronic compensated) metabolic alkalosis. I don’t know what his baseline is, only his decompensated state. I suspect that his alkalosis may be more of a chronic compensating mechanism for chronic hypercapnea.
4) The data therefor looks like a gap metabolic acidosis (probably a starvation ketosis + uremia (MUDPILES). I would suspect this is an acute process, driven by the hyperglycemia and likely polyuria which has decompensated into ARF. This also gave him an acute compensating respiratory alkalosis, driven by his respiratory drive It don’t think its’ an RTA because his acidosis is an anion gap acidosis but there could be one hiding underneath. I would fix his prerenal state before I made any conclusions about having an RTA as well.
5) The metabolic alkalosis is probably a volume contraction alkalosis, progressive, in the setting of an underlying compensating metabolic alkalosis . In other words, it’s probably a chronic process, exacerbated by volume contraction. So there may be acute and chronic metabolic alkalosis processes going on. Given his prerenal numbers, that would make sense.
6) He also has a compensating respiratory alkalosis, which makes me thing that the anion gap acidosis is the more acute process than is the metabolic alkalosis. CO2 changes quickly in response to bicarb changes, but not the other way around.
It all hinges on what his stable baseline numbers are. Here’s my hypothesis.
Baseline: CO2 High; HCO3 HIGH. Chronic respiratory acidosis with compensating metabolic alkalosis
Subacute changes: polyuria–> worsening metabolic contraction, now with an acute primary metabolic acidosis instead of just a compensating one. CO2 may rise in response as well. This may make him more confused and drink less.
Acute changes:—> Decompensated ARF–> He’s been thrown over the edge. Now he’s really dry and uremic and with starvation ketones. This gives him an anion gap metabolic acidosis (acute) which drives down his CO2 as a compensatory respiratory alkalosis.
Treatment: Normal saline. The most important medication in the internists arsenal.
I agree with J: Metabolic gap acidosis with underlying met alkalosis and respiratory alkalosis.
Couple of points:
1. corrected Na ~148 –> this gentlemen is very likely hyperosmolar and BUN/Cr ratio elevation, while could be complicated by a GI bleed, likely c/w profound vol contraction + dehydration. This patient is deceiving very sick and has a % mortality up to 50%. He should be cared for in the unit and given his need for up to 12 L of IVF he may need to be intubated if his heart failure is significant.
2. I have a difficult time trusting FiO2 estimates with NC >2L, and this makes calculating the Aa gradient less precise, regardless in this case it is increased (50-100), suggesting lung pathology or profound HF (tough to get pulm edema in such a dry state). History of COPD could explain the metabolic alkalosis from chronic renal compensation. I don’t know if I can explain the respiratory alkalosis (increased central stimulation possible ASA ingestion)
Happy Hospitalist:
Your acid-base interpretation is elegant, but like so many it depends on the patient’s previous status.
I would take objection with one thing. Normal saline is not always the internists best friend and may not be here
In al likelihood the patient is volume contracted, i.e. intravascular sodium low – perhaps acute from GI bleed, perhaps chronic from diabetic coma. He has lost sodium from his body. We don’t know at what rate
The patient is definitely dehydrated- free water low- serum sodium and osmolality high – more likely acute given mental status.
The patient needs sodium – we can not tell from the info given how fast- need vitals, previous history.
But assuming his vitals are stable, no acute GI bleed or other acute fluid loss, his major risk is the osmolality. Only enough normal saline to stabilize his vitals acutely, generally a liter or two at most assuming no acute ongoing loss, should be given. He still needs more sodium but -
At that point his fluids should be half normal saline (with or without potassium depending on the etiology of the problem- the borderline potassium may mask a body deficit if kidneys are OK)
To replace him with only normal saline will not provide him with adequate free water and in my experience has the potential to actually aggravate the dehydration, cause the sodium to rise -with attendant CNS and intracellular problems.
A common error by house officers, in part because we are not precise with our language, is making the distinction between dehydration and volume depletion.
Dehyrdation- low intravascular free water. Volume depletion- low intravascular volume (essentially sodium ion, but not serum sodium) – in this case we need more information to know how much fluid how quickly but there is no question the patient needs free water preferably in the form of half normal saline
Correction on my treatment. If he’s hypotensive, give normal saline. Other wise, free water, the second most important treatment, would be indicated first, replacing 1/2 his total body water deficit in the first 24 hours.
Also, this kind of thing wouldn’t make it into my ICU unless the vital signs were unstable.
Cory. I disagree he is low on sodium. He is low on free water. Assuming he is still able to concentrate his urine (low urine sodium) his bodies sodium stores will be exactly what the should be. His free water, now that’s another story. By the way, nice catch on my error. I also caught it this morning while re reading my response. I’m surprised read it
I also disagree with your definition of dehydration. I think it encompasses low total body free water, not intravascular. If some one had stable bp and HR they can have normal intravascular volume even if their total body water is decreased and having a serum sodium of 170
And I don’t think he needs sodium. He needs water. And I don’t think he us intravasculr sodium depleted. If he can concentrate his urine, his sodium is perfect
Hospitalist:
I hope Dr. Centor doesn’t mind- it isn’t everyday we can get into a good discussion of this.
Let’s hash this out.
I do not know what that guy’s total body sodium is- they don’t tell us whether he has edema/ascites or not and we don’t know his vitals.
But I am going to assume, because he is hyperosmolar with an elevated BUN, his intravascular sodium is low – he has lost sodium in his urine through osmotic diuresis and/or is bleeding. In the absence of edema and ascites, his total body sodium will be low. That is volume depletion. He may have a normal blood pressure if it happened over time – he has borrowed from his interstitial and intracellular spaces and his sympathetic nervous system may be kicking in. He almost certainly needs some sodium, how much – can’t say without more info.
But most people with that degree of hyperglycemia and elevation of BUN over that time are down sodium overall, unless he is third spacing. He has probably lost lots of sodium in his urine as a result of his hyperglycemia.
Many people with DKA present with normal blood pressure and minimal or no elevation of pulse- they are clearly down total body sodium and need lots of intravascular repletion – they have simply borrowed from their other compartments over time. His ability to concentrate is simply a response, not an indicator. Blood pressure is an inexact measure,especially with chronic loss.
now dehydration- I am going to disagree here too. Serum sodium is a measure of intravascular free water – nothing more, nothing less. When it is high, intravascular free water is low. When it is normal intravascular free water is normal, when it is low, intravascular free water is high. None of those tell you anything about total body sodium or total body water, but it is hard to imagine a person with low intravascular free water (high serum sodium) who has an excess of total body water – they will equilibrate quickly.
I know of no way to measure total body free water- but as I said before when intravascular free water is low (serum sodium high) total body free water will reflect that- that is dehydration. I don’t believe you can clinically define dehydration differently. A high serum sodium is dehydration. The person may or may not be volume depleted, most people would be. The common situation of someone in the desert who loses sodium and water and presents with a sodium of 170 will be both, they have lost water in excess of salt but they are down both. If they haven’t been in the sun too long, their BP may not be low but if that sodium is 170 they are dehydrated. If their BP is down they have lost lots of sodium.
The only common situation where I can think of where you will be volume overloaded with a sodium of 170 is if someone gives you too much sodium bicarb (say post arrest) or too much 3% saline. That person may be volume overloaded -total body sodium high, but dehydrated, intravascular free water low. Treat with diuretics and free water. I guess its possible in DI if the person is volume overloaded for whatever reason.
Again my definition -dehydration – high serum sodium/osmolality -measured laboratorily
volume depletion – loss of sodium acutely (hemmorhage), chronically (diuresis, skin, GI) -measured clinically.
I can;t wait to see what this story is.
Your ballgame -have at me -this is fun.
First of all, let me apologize for all the typos and mistypes in my previous posts. It’s hard getting it all in and proof read on an iPhone. I’m on a regular computer right now.
It’s an interesting discussion all around. I was always taught that dehydration should be reserved for a patient with total body water deficit. I don’t believe that one can compartmentalize the discussion between serum sodium on one end and intracellular sodium on the other because on a microscopic, capillary and cellular level, sodium gradients between the cell and the capillary work as one unit. You don’t have your blood vessel system and then your cell system and they don’t both work independently. If one gets out of wack, the other responds. They work together to maintain homeostasis.
I still don’t think we have enough information to say he is total body sodium low, or even volume depleted, even if he does have an osmotic diuresis. I think you’re seeing he’s total body sodium low because he’s peeing it all out. I’m saying since we don’t know his starting point, and we don’t have enough information to say what his current state is, he very well may be total body sodium high, low, or just right.
We do know he is free water depleted because his serum sodium is high. We don’t know that his total body volume (which is salt and water) is low. He may have started out with high sodium stores with decompensated CHF and his hyperglycuria may have made him pee out a bunch of salt, bringing his total body salt stores back to normal, while his free water may still be down. We don’t know where he came from.
Total body sodium is defined by his volume status, since water follows sodium. A normal person’s thirst reflex causes them to drink if their serum sodium gets to high. That’s a sign of total body water deficiency. It says nothing about the status of the bodies total salt stores. He could still be total body salt high or low. We don’t know. We do know he’s total body water deficient. A high sodium level in your serum will drive water out of your cells to try and dilute your serum, which is the essence of being dehydrated on a cellular level. It’s as if you stepped into a Ronco food dehydrator. As you lose free water and your serum sodium rises, the intracellular water leaves as well into your blood vessels. If you don’t have enough oncotic pressure, that free water ends up in third spaces. You are total body water deficient. I don’t think it has anything to do with your total body sodium stores.
When nursing home grandpa comes in with the O sign and his serum sodium is 170, he’s not low on salt. He’s low on free water. If he could talk, he wouldn’t ask for a glass of salt water, but rather free water, whether his dehydration was due to a glucose diuresis or not. I suppose the mechanism that got him there is important. If he isn’t drinking free water, he is water deficient, not salt deficient. Water and salt homeostasis are independently maintained by different mechanisms.
Changes sodium concentration generally reflect disturbed water homeostasis, where as alterations in sodium content ( I assume they mean total body sodium stores) are manifest as extra cellular fluid volume contraction or expansion, and imply abnormal sodium balance. At least that’s what Harrison’s says ( you forced me to look it up after 7 years of sitting on my table)
In other words a high serum sodium concentration indicates a free water deficit. Where as if your body is total body sodium high or low, you can have a normal serum sodium, just too much or too little water in your body.
The amount of volume in your blood vessels, I think, has more to do with the oncotic pressure of albumin and other proteins. But it should not be differentiated here for the sake of discussion on dehydration. There are three compartments at work here. 1) Intravascular 2) extra cellular 3) Intracellular. I’m wondering if we are talking past each other when describing extracellular volume vs intravascular status. One obviously is a subset of the other.
As opposed to dehydration, volume depletion is a true state of salt and water. One can be dehydrated without being salt depleted. I’m saying the guy is dehydrated, but we don’t have enough information to say that he’s volume depleted because we don’t know where he started. I understand your argument that he could be total body salt depleted from his osmotic diureses. I just don’t know what his baseline is.
We do have evidence that he’s water deficient, because his serum sodium says he is. I think that’s all we can say with the information we have. In the absence of hypovolemia findings, I would treat with free water only, and avoid giving him more salt, which I’m not convinced he needs.
Man, my brain is tired
I’d like to weigh in on Cory’s discussion about volume status and sodium.
I agree with Cory’s definition of dehydration (loss of free water represented by high serum sodium).
I’m less satisfied with his definition of volume depletion/contraction. While it is useful to define volume overload states (cirrhosis, nephrotic syndrome, heart failure) as increased total body sodium (hyperaldosterone states); I think it is less useful to define volume contracted states by total body sodium depletion. Primarily because salt retention is one of the driving forces of volume overload and can be targeted for treatment (aldosterone antagonists, diuretics, diet); however in volume depletion salt is not the primary problem, volume is. You would not treat a volume contracted patient with salt tablets or hypertonic saline, and I think it a mistake to think of NS infusion as repleting depleted salt stores. Sodium chloride is just a good osmotic agent to keep the fluid intravascular. Because sodium is the primary osmotic agent in blood, total body stores should be low in volume contraction and if you try to treat volume depletion with sodium free products like FFP or albumin over time you’ll have trouble keeping the fluid intravascular, so sodium does play a role in volume depletion treatment — it’s just not the goal or target of therapy.
In the presented patient, I would start with NS boluses for presumed volume contraction then transition to 1/2 NS +/- D5 depending on the BS response to insulin. I’d follow BMPs q2 hrs initially until glucose, sodium, & potassium are stable with IVFs. I’d also monitor sats closely and confirm with ABG as aggressive IVF could turn into pulmonary edema in severe HF patients. I’d likely start 1/2NS fairly quickly pending the results of the corrected sodium on the bmps to keep it less than 150.
Done, done, and done – let’s see what Dr. Centor has cooked up for us tomorrow.
Salicylate poisoning and sepsis can give you this triple disorder (AG acidosis, met alkalosis, acute resp alkalosis). Check salicylate level. Dialysis if the level is up–the altered mentation can be due to neuroglycopenia.