Tag: crazy numbers

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Pseudohyperkalemia

The highest potassium I have ever seen? That would be 15.5 mEq/L.

It’s not real. It was pseudohyperkalemia from leukocytosis. The patient had chronic lymphocytic leukemia with a white count of 300,000. If you are not familiar with this condition, check out these posts on Renal Fellow Network: Westervelt and Nate. Nice full text references here and here (pdf).

The pseudohyperkalemia merit badge

The first time I saw this was when I was senior resident. I was sleeping in the call room my pager buzzed. It was the oncology floor with a potassium of 9. The patient had CML and was in a blast crisis. His leukocyte count around 100,000. I immediately suspected pseudohyperkalemia and ordered a whole blood potassium from the ABG lab. It was normal so I went back to sleep. The next morning I received an angry call from the Hemo-Onc fellow. The patient was coding and he was furious that I only ordered an ABG instead of treating the hyperkalemia.

I don’t know if the patient coded from hyperkalemia, but I wish that I had gotten out of bed and evaluated the patient. I solved the problem the nurses alerted me to, but if I assessed him, maybe I could of averted an arrest.

Regrets…

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Saltiest Sodium. Dumbest Dude.

My work-shop on sodium includes a bit on all the cases of hyponatremia due to fraternity hazing.

I also include the crazy case of Jennifer Strange.

But I had never heard of idiot induced hypernatremia until this case report:

A nineteen year old male drank a quart sized bottle of soy sauce on a bet.

Two hours later he was brought to the ER comatose and seizing. His sodium was 177. They initiated hypotonic fluids and arranged transfer to a tertiary care center. At the tertiary care center the sodium was still higher at 191. The doctors then changed the fluids to D5W at 12,000 mL per hour. They gave 6 liters of D5W in 30 minutes.

After the infusion he opened his eyes and regained spontaneous movement. He was discharged on hospital day four neurologically intact with only some minor abnormalities on the head MRI, all attributed to postictal changes.

How high is a sodium of 191? MedCalc will not even accept it as a possible sodium concentration:

A couple items of note:

  • The infusion of D5W raised his serum glucose from 365 (hyperglycemia causes insulin resistance) to 1,116 mg/dL.
  • The authors do not comment on what access they used to infuse D5W at a liter every five minutes.
  • In addition to the hyperglycemia, the D5W infusion dropped the potassium from 5.1 to 2.5 in 30 minutes! That is kind of terrifying.
  • The authors use the Katz correction for hyperglycemia, (eat it Hillier).
  • The authors do not discuss how they decided on 6 liters of D5W. Full correction down to 140 would by roughly 12 liters, so perhaps they decided on 12 liters in an hour with continuous neurologic assessment and when he began to have spontaneous motor movement after 30 minutes they slowed down.

Some nerdery about the sodium exposure: He drank a quart of soy sauce. A quart is 946 mL. The article states that soy sauce is 17-18% sodium chloride. Here are some meta calculations, in case you are interested:

Read the article, it’s a good read and it has the highest urinary sodium I have ever seen, 270 mmol/L (almost twice as salty as normal saline). They discuss other extreme hypernatremic conditions, and theories on rapid or slow correction.

Slides for Keynote | PDF

Update from Twitter:

@kidney_boy I would guess they used a pressure bag or infuser (e.g. Trauma 1) to get in a L every 5 min
— Seth Trueger (@MDaware) June 10, 2013

@mdaware @kidney_boyA good 14 ga 1.75 inch peripheral IV can do 333 cc/min with a 1 meter pressure head to gravity.
— philroman (@philroman) June 11, 2013

@kidney_boy I’ve seen 216 before. Started at 196, rose more with initial NS administration. Kid with ichthyosis, and bad dehydration.
— Ken Tegtmeyer (@pccm_doc) June 11, 2013

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Salty dog, the highest sodium I ever saw.

A series of sodiums from 176-188 mmol/L

Those are not glucoses. They are Sodiums. And, except for maybe an infant with congenital adrenal hyperplasia when I was a resident, those are the highest sodiums I have ever seen.

The primary management concern was the speed of correction. The first Na at 188 was drawn at 4:32 pm. Four hours later it was 177, a change of 11 mEq. Too fast. Here is the salient section from UpToDate:

Rate of correction in chronic hypernatremia — There are no definitive clinical trials, but data in children (particularly infants) suggest that the maximum safe rate at which the serum sodium concentration should be lowered in patients with chronic hypernatremia is 12 meq/L per day. To be safe, we suggest a maximum rate of correction of the serum sodium of 10 meq/L per day in patients who have had hypernatremia for at least 24 hours. The following findings provide support for this conclusion:

  • A retrospective case control study included 97 children with hypernatremia and dehydration; the mean baseline serum sodium was 165 meq/L. The rate of reduction in serum sodium was significantly faster in the children who developed cerebral edema compared with children who had no complications following correction of the hypernatremia (1.0 versus 0.5 meq/L per hour).
  • Similar findings were noted in another report in which the rate of reduction in serum sodium was 1.0 meq/L per hour in the nine infants who developed seizures compared with 0.6 meq/L per hour or less in 31 infants who did not develop seizures.
So Bud Rose, the dean of electrolytes, says 12 mEq per day.
Burton Rose

My patient moves 11 mEq in 4 hours after receiving 500 mL of normal saline. Now what? I was convinced that continuing normal saline would perpetuate the overly rapid correction of the sodium and put the patient at risk of cerebral edema. But since the patient was still in hypovolemic shock, I couldn’t just stop the fluids.

I ordered 3% saline. I ran it at 100 mL/hour and 5 hours later the sodium was back up to 186. I was going in circles. I then changed back to normal saline and over the subsequent 48 hours we corrected the sodium at roughly 0.5 mEq/l/hr. The whole time I was going through this I was wondering is it all necessary? Is rapid correction of hypernatremia as dangerous as Rose said it was? Is half a miliequivalent/L/hr a real evidence based speed limit?

I put this question to a fourth year medical student and he did an excellent job diving into the evidence (or lack there of) on the topic. Here is his analysis:

docx | pdf 
I think he is a little hard on Rose’s guidelines. The student’s analysis criticizes one of 4 references that are provided in UpToDate (though his criticism is appropriate and is the sole reference in Rose’s landmark Clinical Physiology of Acid Bas Disorders) to support of the 0.5 mEq/L/hr speed limit.
The four UpToDate references are:
  1. Rose’s own textbook, Clinical Physiology of Acid Bas Disorders. The page to look at in my 5th edition is 777.
  2. Kahn et al. Controlled fall in natremia and risk of seizures in hypertonic dehydration. Intensive Care Med (1979) vol. 5 (1) pp. 27-31
  3. Fang et al. Fluid management of hypernatraemic dehydration to prevent cerebral oedema: a retrospective case control study of 97 children in China. Journal of Paediatrics and Child Health (2010) vol. 46 (6) pp. 301-3
  4. Blum et al. Safe oral rehydration of hypertonic dehydration. J Pediatr Gastroenterol Nutr (1986) vol. 5 (2) pp. 232-5
I will look at each reference in detail.
The section in Rose’s text is very similar to the UpToDate card. The relevant paragraph is on page 777 in my 5th edition (black cover). The sole reference in this paragraph, is the 1986 Blum article (number 4 from the above list).
iPhone, a surprisingly effective photocopier.
Kahn retrospectively looked at the care of infants. They used half normal saline and gave it at 160 mL/kg/day (6.7 mL/kg/hr). All of the patients were 0-5 months, so maintenance fluids would have been 4 mL/kg/hr.

What book did this great page on maintenance fluids come from?

Nine of the first 47 patients developed seizures that could not be explained by other etiologies (fever, hypocalcemia, hypoglycemia) and so were ascribed to rapid fluid restoration, Group I. They matched these nine to 22 age-matched children who were treated contemporaneously but did not have a seizure, Group II. The investigators then changed the protocol for treating infants with hypernatremia to 120 mL/kg/day and included data on 9 patients under 5 months who were treated this way, Group III.

Here is the primary data on the three groups:

All three groups had similar sodiums but Group I had significantly higher BUNs than Group II, with I +II vs III and I vs III being non-signifigant.

The protocol called for patients in Group I and II to get only 160 mL/kg/day. Both groups significantly exceeded this. Group III hit its fluid goal nearly on the nose. They blamed the excess fluid on oral replacement and volume resuscitation with sodium bicarbonate.

The net result was a wide spread in the rate of correction of sodium:

  • The kids that seized: 1.02 mEq/L/hr
  • The kids that did not seize but were on the same treatment protocol: 0.62 mEq/L/hr
  • The kids on the conservative protocol, also without seizures: 0.35 mEq/L/hr

Fang looked at 97 children with hypernatremia. Mean sodium was 164.5. Mean age 13 months. He performed a case-control study with the cases being patients who developed cerebral edema. Manifestations included seizures, eyelid edema, papilledema in all the patients and bulging fontanel in 36 and pupillary abnormalities in 9 cases.

The data shows cerebral edema was more common with bolus therapy, especially when the bolus was faster, higher sodiums were associated with cerebral edema but much of that disappeared in multivariate analysis as higher sodiums were also associated with increased rate of correction and ind increased bolus rates. Using ROC the investigators found a rate of fluid administration of 6.8 ml/kg/hr was safest. And the average decrease in serum sodium in the cerebral edema group was 1 mEq/L/hr and 0.5 mEq/L/hr without cerebral edema.

The final reference is Blum’s study of oral rehydration, this is the reference my med student was upset with. As he outlined, this was a study of oral rehydration rather than a study of rates of treatment. The cohort was composed of eighteen infants, 6 months or younger admitted with hypernatremia (Na > 150) and treated with oral fluid resuscitation. They compared the hypernatremia outcomes to a second cohort of 26 infants who received IV rehydration for hypernatremia. Average sodium for both groups was 160.

In both groups the reduction of sodium was slow (0.3 mEq/L/hr) and no patient developed seizures.

In Burton Rose’s Clinical Physiology of Acid-Base and Electrolyte Disorders this observational study with no seizures is the sole reference behind the recommendation for a slow restoration of normal sodium. Weak sauce. Of note Androgue’s review of hypernatremia in the NEJM from 2000 references the same Blum and Khan articles to support its recommendation of slow treatment.

So in the end, the recommendation for slow normalization of sodium is based on a handful of studies in infants with no randomized or even prospective studies. What is unbelievable to me is no one references a study that reviews the functional/neurological outcomes of patients with the highest sodiums admitted to a large hospital based on the speed of correction. Seems like an easy study and in its absence we are left to trust in the physiology of babies.

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Crazy numbers: the lowest hemoglobin I have ever seen

When I was a resident I saw a really low hemoglobin. I don’t remember what the number was but I remember the circumstances. I was working the ER at Riley Children’s hospital and EMS pulled up with a infant who was short of breath. The family had been feeding him cows milk instead of formula and as a result he had severe iron deficiency anemia. Great case and after a few transfusions and some parental education, everyone lived happily ever after.

Last week I saw another lowest hemoglobin. Since I wasn’t blogging when I was a resident I don’t know if this hemoglobin is lower than that poor kid but here it is:

Hemoglobin of 3.6 g/dL. The hematocrit is still a double digit number, but still that’s a really low hemoglobin.

This is a dialysis patient who started having some vomiting that looked a little “dark” but didn’t really bother him. A day or so later he developed some dark colored diarrhea. Still didn’t bother him. Then he found himself short of breath, like he missed a treatment and got volume overloaded. This kept getting worse so he finally decided to get in his car and drive to the ER. The admitting hemoglobin was 3.7 followed by a repeat by I’m sure a disbelieving ER doc.

Diagnosis duodenal ulcer and after a half dozen transfusions and a prescription for BID omeprazole he was discharged home to lived happily ever after.

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Hyperkalemia or not

A patient came to the hospital with a swollen arm. The ED suspected a DVT and ordered a doppler ultrasound which confirmed their suspicion. The admission labs included a chem-7 which revealed a potassium of 7. Her creatinine was 1 and she wasn’t taking an ACEi, ARB, aldactone, ketoconazole, or potassium supplements. The ER was surprised and repeated the study and checked an EKG:

Narrow QRS and unimpressive T-waves

The EKG gave no hint of hyperkalemia, though EKG changes are not a sensitive marker for hyperkalemia. The ED gave insulin, glucose and Kayexalate for the lab finding of hyperkalemia. We were consulted to determine the cause of the hyperkalemia. The patient’s past medical history was significant for primary thrombocytosis and during the hospital stay her platelet count rose to over a million.

dats a lot o’platelets

We presumed that his hyperkalemia was actually pseudohyperkalemia due to the high platelet count. Platelets release potassium when they clot and the risk of pseudohyperkalemia rises as the platelet count approaches a million.

You remember this classic NEJM article from 1962. 

We then sent the patients blood to the ABG lab in a heparinized syringe rather than a red top and the potassium normalized. Platelets release potassium when they are activated. By measuring the potassium in whole blood rather than serum, the contribution of platelet activation is prevented. The ABG results are the electrolytes to the far left in the screen-grab below (click to enlarge).

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Highest TTKG with hypokalemia

Patient with a lifelong history of hypokalemia. He came to me for a second opinion, his previous nephrologist had been nudging up his potassium dose on every visit and the patient was now on 70 mEq of KCl daily and was getting uncomfortable with endlessly increasing doses of potassium.

At the time I saw him these were his labs (he had decreased his potassium supplementation to 20 mEq/day):

  • Blood
    • sodium: 128
    • glucose: 90
    • potassium: 2.8
    • Creatinine: 0.9
    • BUN: 11
    • Magnesium: 1.8
    • Calculated osmolality: 265
  • Urine 
    • sodium: 135
    • potassium: >100
    • Osmolality: 637
Trans-tubular potassium gradient: 14.9. That’s crazy high for a patient with hypokalemia, one should expect it to be less than 2 for hypokalemia of extra-renal origin, and only 7 or 8 for hypokalemia from hyperaldosteronism. Halperin et al. were not able to get the TTKG that high even when they took normokalemic patients and doped them with fludrocortisone and 50 mEq of oral potassium. 
And that 14.9 is assuming the urine potassium is 100, our lab doesn’t do serial dilutions so who knows what the actual potassium is? 120? 140?
I’m still waiting for the renin and aldo but I smell some Bartter’s
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That’s not a gap, its the Grand Canyon!

When I talk about toxic alcohols causing anion gap metabolic acidosis I emphasize that these patients have large anion gaps. When you see an anion gap of 16 or 20 think uremia and lactic acid, not methanol. The cases I have seen have almost all had gaps greater than 25 and typically they run in the 30s.

But I have never heard of or seen a gap as big the one that came into the ICU this week-end:

To summarize the data from above. A patient was admitted with an anion gap of 65 that went up to 70 in the next 6.5 hours. I can visualize the ER doc reading the first chemistries, freaking out and re-ordering them, assuming that if the anion gap is greater than the chloride it must be a lab error, hence the repeat labs at 150 minutes after the first set.

Think about that, the anion gap was larger than the chloride concentration.

What kind of alien infestation causes numbers like that?

So when working up a large anion gap one tries to explain the anion gap. The lactic acid was only 34.5 mmol/L. So this patient has the highest lactic acid ever, yet it only covers half the gap. She also had serum ketones that remained positive at a 1:8 dilution and a creatinine of 14.

So is that it? Lactic acidosis, ketosis and uremia for an anion gap of 70? I sent off a D-lactic acid and a 5-oxoproline level, cause what the hell, when’s the next time I’m going to see an anion gap of 70. A toxic alcohol screen was sent.

To compete the picture the ABG was: 6.95/13.4/187 with a measured bicarb of 3. With numbers this crazy a trip to the Henderson-Hasselbalch formula is probably not a bad idea:

MedCalc has a sweet HH calculator

So 6.97 is pretty close to the 6.95 measured, so no lab error at least in the ABG. Running Winter’s formula (1.5 x HCO3) + 8 ±2 gives a predicted pCO2 of 13, so no respiratory component to the metabolic acidosis.

The next step is to look for toxic alcohols while waiting for the assay to come back from toxicology lab at Children’s Hospital of Michigan. The osmolal gap calculation should be greater than 10 in the presence of methanol, isopropyl alcohol or ethylene glycol. The measured osmolality was 327.

MedCalc also has a sweet osmolar gap calculator

So no significant osmolal gap rules out a toxic alcohol. This was confirmed by the toxicology screens that eventually came back. Given the anuric renal failure, profound intractable acidosis and unknown anions still unaccounted for we initiated CVVHD. You can see the effect that had on her bicarbonate and creatinine.

The patient has since recovered and we have learned that she was on metformin so we are toying with metformin induced lactic acidosis as the etiology. Any other thoughts?
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Lowest sodium I have ever seen

I’m not sure if it is really the lowest sodium but it definately was among the lowest.

I received a call regarding a consult for a patient with a sodium of 105.

The patient is a 60 year old caucasian woman who had been started on chlorthalidone 3 days prior to admission. Her physician had been wrestling with hypertension and changed her from 25 mg of hydrochorothiazide to 50 mg of chlorthalidone. (The internist was keeping up with her American Journal of Hypertension. Though 50 mg is a whole lotta chlorthalidone.)

Both figures are from Ernst Et al. Hypertension 2006

After one or two days of the new diuretic the patient started vomiting and developed diarrhea. The only thing she was able to keep down was water. When she came to the ER she hadn’t eaten anything solid for two days.

She was admitted with hypovolemic hyponatremia. She was given a bolus of 500 mL of normal saline in the ER and the sodium went up to 108. Additionally her potassium was 2.7 and her magnesium and phosphorous were low. She was started on potassium chloride and sodium phosphate prior to being transferred to the ICU. When I called the nurse I was told the intensivist  planned on starting her on 3% saline.
I was immediately worried about overcorrecting her sodium and developing osmotic demyelination syndrome from 3% saline and aggressive correction of her potassium. Tom Berl had come and spoken to our fellow and had put the fear of potassium in me by discussing a case that was triggered by potassium repletion. From the case report:

This patient was at risk of overcorrection because she had two of the most common clinical settings in which such overcorrection occurs: thiazide use and hypovolemia.

Patients with hypovolemic hyponatremia send conflicting signals to the hypothalamus regarding ADH release. The volume deficiency stimulates ADH (if the body volume deficient, let’s not lose any water via the kidneys) and low osmolality surpresses ADH (the body is too diluted so let’s lose some water to bring the concentration up). In the case of this conflict, volume rules. As I tell my medical students,

Remember the ABC’s, Airway, breathing and circulation. O for osmoregulation is way down in the alphabet.

The problem of rapid correction occurs when you correct the volume deficiency and all of the sudden the hypothalamus asks itself, why am I releasing any ADH with an osmolality of 260?

Then the kidney starts producing urine that you could probably bottle and sell as organically filtered water. Electrolyte free water clearance begins to approach the urine output and the sodium also starts to climb and climb fast.

To protect this patient I told the nurse to decrease the normal saline to 100 mL per hour and to call me if the urine output goes over 200 per hour. We also started checking the sodium every six hours and I ordered urine osmolality, sodium and potassium.

Her sodium started to rise slowly, the urine output increased but never resembled Niagra. After two days her sodium was in the 120s her urine still appeared volume depleted and volume status began to look wet. She developed wheezes and she had a few rales. We had to abandon the normal saline. We started tolvaptan. She received 30 mg once and then 15 mg the next day after she had a brisk response. After that her urine electrolytes resembled SIADH.

Once the sodium crossed 130 I stopped the tolvaptan, restricted her free water, and added a gram of sodium chloride twice a day. Her sodium stabilized around 130.

Around this time I sent a renin aldo ratio. I usually order these before I start a patient on aldactone, because after you start it you need to wash them out for weeks prior to checking for primary hyperaldosteronism. Our patient had difficult to treat hypertension and hypokalemia on admission, so I checked it. I just found out that it came back positive. The high aldosterone was after we had corrected her volume deficiency. I think it is primary, and this may explain why she had persistently low urine sodiums despite successful volume resuscitation.

We looked for a cause of the SIADH, but couldn’t find anything. No narcotics, no pulmonary disease, no malignancy, normal TSH and cortisol, no anti-depressants. She had a normal non-contrast head CT scan on admission. I even ordered a contrasted CT scan of the chest to make sure she didn’t have a cancer in there. Nothing. Idiopathic SIADH hiding behind, at least initially, volume depletion and in the background of primary hyperaldosteronism. Strange case.

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No Dr. Topf, no EKG changes

On Monday night I was called by one of our fellows regarding a patient in the ED with a potassium of 8.5. They had already given insulin, glucose and kayexalate and the follow-up potassium was 8.1. This is not much improvemnt and less than you typically see. The patient was in acute renal failure with a creatinine of 3 and was anuric.

I asked if the patient had any EKG changes and according to the ER doc the patient had just a touch o’QRS widening. What do you think?

Peaked symmetric T’s

Link for more on EKG changes in hyperkalemia

That night his CPK was 5,000. The next day it rose to 341,680.

Now dat’s a spicy meatball!

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