3/22/2018 PulmCrit - Four DKA Pearls

PulmCrit (EMCrit)
Search the site ...

ABOUT PULMCRIT GENIUS GENERAL HOSPITAL PULMCRIT TOC

You are here: Home / PULMCrit / PulmCrit – Four DKA Pearls

PulmCrit – Four DKA Pearls

May 7, 2014 by Josh Farkas — 10 Comments

Introduction
I have a confession to make: I love treating DKA. It’s satisfying to take a patient from severe
acidosis, electrolytic disarray, and hypovolemia to normal physiology during an ICU shift.
Although it's usually straightforward, there are some pitfalls and a few tricks that may help your
patients improve faster.0
Pearl #1: Avoid normal saline
A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is
worseningof the patient’s acidosis with decreasing bicarbonate levels (example below). This
occurs despite an improvement in the anion gap, and is explained by a hyperchloremic
metabolic acidosis caused by bolusing with NS. This could be a real problem for a patient
whose initial bicarbonate level is extremely low.1 A while ago I made the switch from NS to
lactated ringers (LR) for resuscitation of DKA patients, and have not observed this phenomenon
when using LR.
0

https://emcrit.org/pulmcrit/four-dka-pearls/ 1/12
3/22/2018 PulmCrit - Four DKA Pearls

0
Example of the effect of normal saline resuscitation during the initial phase of DKA
resuscitation. This patient received approximately 3 liters normal saline between
admission labs and the next set of labs as well as an insulin infusion, all textbook
management per American Diabetes Association guidelines. The anion gap decreased
from 33 mEq/L to 30 mEq/L, indicating improvement of ketoacidosis. However, the
bicarbonate decreased from 8 mEq/L to 5 mEq/L due to a hyperchloremic metabolic
acidosis caused by the normal saline. Note the increase in chloride over four hours.
Failure of the potassium to decrease signi cantly despite insulin infusion may re ect
potassium shifting out of the cells in response to the hyperchloremic metabolic acidosis.
0
There is only one randomized controlled trial comparing NS to LR for resuscitation in DKA (Zyl
et al, 2011). These authors found a trend towards faster improvement in pH when using LR
compared to NS (p = 0.076). They also found that patients in the NS group experienced a
decrease in average serum bicarbonate during the rst hour of treatment (from 8.86 to 8.21
mEq/L), whereas patients in the LR group experienced an increase in average serum
bicarbonate during the rst hour of treatment (from 7.71 mEq/L to 8.83 mEq/L). Although the
authors concluded that this was a negative study, the data suggests an advantage of using LR
in correcting the acidosis.
0
There is better data supporting the use of Plasmalyte in DKA. Plasmalyte is a balanced
crystalloid with nearly the same pH effects as LR (more about Plasmalyte here). Rinaldo
Bellomo’s research group in Australia performed a retrospective analysis of patients with DKA
who received predominantly NS or Plasmalyte (Chua et al 2012). Patients who received
plasmalyte had more rapid improvement in their serum bicarbonate. There was no difference
in the strong ion gap (an index of ketoacids, similar to the anion gap), indicating that the higher
bicarbonate in the plasmalyte group was due to avoidance of a NS-induced hyperchloremic
acidosis. Mahler et al 2011 performed a prospective randomized controlled study of NS vs.
Plasmalyte which also showed higher bicarbonate levels and less hyperchloremia in the

https://emcrit.org/pulmcrit/four-dka-pearls/ 2/12
3/22/2018 PulmCrit - Four DKA Pearls

Plasmalyte group. Note that there are other proprietary crystalloids available with a
composition nearly identical to Plasmalyte (i.e. Normosol).
0
Bottom line? Normal saline induces a hyperchloremic acidosis which drops bicarbonate levels
in the initial phase of DKA resuscitation, and is probably not the ideal uid to use. LR,
Plasmalyte, or Normosol are better choices.2
0
Pearl #2: Use bicarbonate to treat hyperchloremic, non-anion-gap
acidosis.
The usual debate about bicarbonate is regarding the initial treatment of the patient when the pH
is extremely low. This has already been debated extensively and I’m not going to go there.
0
DKA patients often develop a non-anion-gap, hyperchloremic metabolic acidosis. This may
occur due to gradual development of DKA with urinary excretion of ketoacid (which then cannot
be converted to bicarbonate) and/or initial resuscitation with NS. In these cases the anion gap
closes but the bicarbonate level remains frustratingly low.
0
Why should we care? Some evidence suggests that hyperchloremic acidosis may cause renal
vasoconstriction and worsen renal function. Many DKA protocols suggest delaying initiation
of subcutaneous insulin until the bicarbonate is above 18 mEq/L, so a hyperchloremic acidosis
may delay transition off the insulin infusion. My bias is that patients feel better and breathe
easier when their bicarbonate is normalized so they don’t need to maintain a compensatory
respiratory alkalosis.
0
Predicted Final Bicarb level = Bicarbonate level + Ketone level
0
Ketone level = Anion gap – 10 = (Na – Cl – Bicarb) – 10
0
Predicted Final Bicarb Level = Na – Cl – 10
0
During a DKA resuscitation, keep an eye on the predicted nal bicarb level as calculated above.
This is an estimate of where the bicarbonate level will end up once the anion gap closes and all
ketoacid is converted to bicarbonate. If the predicted nal bicarb level is signi cantly low (i.e.,
<18 mEq/L), the patient is likely to wind up with a hyperchloremic acidosis at the end of the
resuscitation. In such cases, I think it’s reasonable gradually administer some isotonic
bicarbonate toward the end of the resuscitation.3 Bicarbonate may delay clearance of
https://emcrit.org/pulmcrit/four-dka-pearls/ 3/12
3/22/2018 PulmCrit - Four DKA Pearls

ketoacidosis, so it’s best to do this when the ketoacidosis is nearly resolved. To estimate the
amount of bicarbonate needed, the predicted nal bicarb level may be used to calculate the
bicarbonate de cit. For more discussion of this strategy of pH-guided uid resuscitation, see
the last blog.
0
Gradually infusing some isotonic bicarbonate toward the end of the resuscitation is generally
safe. If the isotonic bicarbonate is constituted in D5W, it may cause a mild increase in the
glucose level. Occasionally this increase in glucose may cause the insulin drip to be titrated up,
which can be bene cial in terms of speeding the resolution of ketoacidosis. However, care
should be taken to avoid hypoglycemia if the insulin drip remains at a high rate. Bicarbonate
may decrease the potassium level due to intracellular shifting, but this generally isn’t an issue as
potassium is already being monitored and aggressively repleted.
0
To be painfully clear, I’m not advocating for the use of bicarbonate to treat ketoacidosis, but
rather to treat non-anion-gap, hyperchloremic acidosis if this is signi cant. The bene ts of
treating a hyperchloremic acidosis are debatable. If you want the patient to have a normal
anion gap and normal bicarbonate level at the end of your shift, the above approach is
effective.
Pearl #3: Avoid intubation if possible.
When approaching a critically ill patient, securing the airway is often an initial consideration.
However, in DKA this is fraught with hazard and often destabilizes the patient. With the
exception of a patient who has truly developed respiratory muscle fatigue (and lost the ability to
generate a compensatory respiratory alkalosis), intubation will typically worsen the patient.
0
First, the act of intubation is dangerous. Sick DKA patients typically have extremely low
bicarbonate levels, for which they are compensating with a respiratory alkalosis (for example,
consider a patient with bicarbonate of 2 mEq/L, PaCO215 mm, and pH 6.75). If there is
di culty intubating this patient and the PaCO2 rises to, say, 60mm then the pH will fall to 6.15.
Approaches to mitigate this risk include attempting to mask-ventilate the patient in the peri-
intubation period or awake intubation. It should be noted that DKA patients may develop
gastroparesis and are at risk for aspiration. In summary, even if the patient has an
anatomically normal airway, the physiology of DKA makes this a dangerous procedure.
0
Second, if the patient was generating a reasonable compensatory alkalosis then the PaCO2 is
usually higher on the ventilator than prior to intubation. The ET tube adds resistance to the
respiratory circuit. If the patient is passive on the ventilator, the ventilator only provides active
https://emcrit.org/pulmcrit/four-dka-pearls/ 4/12
3/22/2018 PulmCrit - Four DKA Pearls

inhalation with passive exhalation (compared to the patient prior to intubation who was actively
inhaling and exhaling). In practice it is generally impossible to achieve the same level of
respiratory alkalosis on the ventilator that a strong non-intubated patient can generate.
0
For a patient with mental status alteration due to the DKA, it may be best to avoid intubation as
long as the patient is protecting their airway (noting that traditional criteria to evaluate airway
protection such as absence of a gag re ex or GCS scoring are not supported by evidence).4 If
mental status changes are due to DKA, improvement often occurs rapidly. Ultimately this is a
clinical decision which must be made at the bedside by an experienced physician. If there is
doubt, close observation and serial evaluation may be helpful.
0
Pearl #4: Continue long-acting basal insulin throughout the DKA
resuscitation.
Many DKA patients already have an established home medication regimen involving basal long-
acting insulin (i.e., insulin glargine or insulin detemir). The traditional approach to managing
DKA has been to holdthe long-acting insulin until the patient has recovered and subsequently to
overlap this with the insulin infusion for a few hours. Recent British guidelines suggest
continuingthe patient’s long-acting insulin throughout treatment of DKA. For example, if the
patient has been noncompliant, a full daily dose of long-acting insulin could be given
immediately upon admission to the hospital. Administration of long-acting insulin doesn’t
obviate the need for an insulin infusion, which should be administered as usual.
0
Continuing the long-acting insulin has three advantages. First, it protects against the classic
error of shutting off the insulin infusion due to hypoglycemia, with subsequent worsening of the
ketoacidosis. If the insulin infusion gets turned off in a patient who has received their long-
acting insulin, the patient will still have some basal insulin on board and their ketoacidosis
probably won’t worsen. Second, it speeds transition from the insulin infusion to subcutaneous
insulin: there is no longer a need to extend the infusion in order to overlap with the
subcutaneous insulin. Finally, it reduces rebound hyperglycemia when the insulin infusion is
stopped.
Conclusions
Current DKA protocols using normal saline and delayed initiation of long-acting insulin are
proven to work well. With the possible exception of patients whose admission bicarbonate
level is extremely low (who may be harmed by the initial drop in bicarbonate due to bolusing
NS), the choice of uid is unlikely to have any long-lasting effects. However, newer approaches

https://emcrit.org/pulmcrit/four-dka-pearls/ 5/12
3/22/2018 PulmCrit - Four DKA Pearls

employing balanced crystalloids and continuation of long-acting insulin are likely to make
patients improve more rapidly, reducing the time spent on insulin infusions and cutting
healthcare costs.5
0
Notes:

(1) I have seen a few patients who presented with bicarbonate levels in the 7-8 mEq/L range, were bolused with normal saline, and subsequently had undetectably low

bicarbonate levels on serum chemistry (the assay just reads “<5 mEq/L”). These patients ultimately did ne, but they scared me. I wonder if there are very occasional

patients who present with profound acidosis and are pushed off the edge of the acid-base cliff by normal saline.

Another group of patients with DKA who could be signi cantly harmed by normal saline resuscitation are patients presenting with life-threatening hyperkalemia. The

inorganic metabolic acidosis induced by normal saline will tend to shift potassium out of cells, hindering efforts to reduce the potassium.

(2) Addendum 1/26/15: A prior version of this blog included the statement that Plasmalyte has a SID of 49 and is therefore gently alkalinizing, possibly making it the ideal

uid selection for DKA. I have subsequently realized that this is a myth (discussed here) – the sodium gluconate in Plasmalyte is incompletely metabolized and therefore

Plasmalyte is not nearly as alkalinizing as predicted. Plasmalyte may be very slightly more alkalinizing than LR, but it is questionable whether this difference is clinically

signiHOME EMCRIT-RACC
cant. I have subsequently revised this blog postPULMCRIT EMNERD
accordingly. Please accept ISEPSIS
my apologies. Plasmalyte ABOUT
remains a good selection of uidCONTACT
for resuscitation of DKA.

(3) Isotonic bicarbonate is typically obtained by adding 150 mEq of bicarbonate (usually 150 ml of 8.4% bicarbonate) to a liter of D5W or sterile water. In the US,

bicarbonate typically comes in ampules of 50ml volume of 8.4% bicarbonate, so isotonic bicarbonate is constituted by adding three such ampules per liter.

(4) With regards to the gag re ex, I agree with the Ron Wall’s Manual of Emergency Airway Management and MackWay-Jones et al 1999 that it is not useful. Recent

evidence (i.e. Duncan R et al 2009) has dispelled the dogma that a GCS of 8 or less mandates intubation in poisoned patients. Given that DKA patients and intoxicated

patients both suffer from short-term toxic/metabolic encephalopathy, this nding likely applies to DKA patients as well.

(5) Honestly I don’t really care much about health care costs, I’m more interested in getting patients better faster. However, it’s hard to change our ways in the healthcare

system, especially when it comes to protocols which have been around for a long time. Perhaps if administrators and insurance companies realize that new approaches

would save them money, this may spur change. I would bet that a DKA protocol using only Normosol/Plasmalyte for volume resuscitation (with use of D10W infusions to

provide dextrose and complete avoidance of normal saline) as well as initiation of long-acting insulin immediately on admission would reduce hospital and ICU length of

stay, reducing costs.

About Latest Posts

Josh Farkas Social Me

Josh is the creator of PulmCrit.org. He is an assistant professor of Pulmonary

and Critical Care Medicine at the University of Vermont (Burlington Vermont, USA).

Share this:

 Facebook 27  Twitter  Reddit  Google  Pinterest 2  Email  Print

https://emcrit.org/pulmcrit/four-dka-pearls/ 6/12
3/22/2018 PulmCrit - Four DKA Pearls

Filed Under: PULMCrit

Tagged With: DKA

Subscribe Now
If you enjoyed this post, you will almost certainly enjoy our others. Subscribe to our email list to keep informed on
all of the Resuscitation and Critical Care goodness.

email address

SUBSCRIBE

This Post was by the EMCrit Crew, published 4 years ago. We never spam; we hate spammers! Spammers
probably work for the Joint Commission.

Comment Here

10 Comments on "PulmCrit – Four DKA Pearls"

b i link b-quote u ul ol li code spoiler

Comment Here - Speak Your Mind - Also leave your name, a liations, and any con icts you may
have.

 newest  oldest  most voted

Philippe Rola  

Great post as usual Josh!

Guest

https://emcrit.org/pulmcrit/four-dka-pearls/ 7/12
3/22/2018 PulmCrit - Four DKA Pearls

George, think about bicarb as an innocent bystander. ALl it does is maintain electroneutrality. The actual
"ingredient" is the sodium, without chloride. We have a lot of H20, a lot of CO2 and carbonic anhydrase.
We have an endless supply of "bicarb." The addition of Na without Cl (a very high SID!) is what corrects
the hyperchloremic acidosis. Look up Peter Stewart and John Kellum's work on this. Google will lead you
to Kellum's site which breaks Stewart's work down. In my opinion, infusions are only needed when you
abused NS in the rst place (SID zero solution).

cheers!

 2  Reply  2 years ago

Joan  

Great article! I love my "DKAer's" also! Nothing more satisfying than xing a messed-up pt all in one shift!
Guest
Look forward to seeing what else you have to offer! Thanks!

 1  Reply  3 years ago

Anonymous  

"The usual debate about bicarbonate is regarding the initial treatment of the patient when the pH is
Guest
extremely low. This has already been debated extensively and I’m not going to go there".

Can you give me a reference or article on this statement? Trying to grasp Bicarbonate infusions and
when they are helpful/non-helpful. My understanding is that bicarbonate works by converting to CO2 in
the liver and your body needs to blow of the additional CO2 –> therefore not as helpful unless patient is
able to breath at a faster rate. Please help me out a bit on this.

Thanks.

George

 1  Reply  3 years ago

Josh Farkas  

Thank you! Glad the blog was helpful.

Guest

 0  Reply  3 years ago

https://emcrit.org/pulmcrit/four-dka-pearls/ 8/12
3/22/2018 PulmCrit - Four DKA Pearls

Matt Anderson  

Sodium bicarb will increase extracellular pH while increasing intracellular pH–likely doesn't matter if you
give bicarbonate or not. Never has been shown to be helpful in human studies (ie animal studies show
Guest
bene t) — it does decrease inotropy and vasoconstriction but I haven't found anything in 'humans' that
showed it to decrease pressors, change EF, etc. Moreover, acidosis is likely bene cial in sick patients. I
get that <6.8 can be a reason to worry but it shouldn't be b/c of the pH it should be b/c you need to
reverse the cause of the low pH. sick –> low pH (not vice versa). I would argue that bicarbonate in DKA
with hyperCl (that is otherwise HD stable—and most likely uneven if they are not )is likely wasteful and I
haven't seen any literature to support more RRT in patients with hyperCl. Pearl 2 to me is a case of
Euboxia. Again, pH is a marker of illness, not the cause of illness — we overTx this 'marker' (as we do
lactate) far too much. I do like the idea of adding a long acting insulin to my initial DKA mgmt. I'm
actually go to start doing this from now on.… Read more »

 0  Reply  2 years ago

Dean Burns  

Does the above blog post apply to children too?

Guest
The paeds DKA literature still seems to be clinging to NS, with its isotonicity being cited as important.
Should we be using LR/Plasmalyte instead of NS in kids with DKA?

 0  Reply  2 years ago

Josh Farkas  

Sorry, but this blog does not apply to pediatrics. I know nothing about pediatrics. This is a blog about
Guest
controversies in adult critical care. From what I hear pediatric DKA is much more complicated than adult
DKA and I would have a low threshold to consult a pediatric endocrinologist, sorry I can't be of further
help.

 0  Reply  2 years ago

Matt Anderson  

Houshyar. Effectiveness of Insulin Glargine on Recovery of Patients with Diabetic Ketoacidosis: A

Guest
Randomized Controlled Trial. J Clin Diagn Res 2015;9(5):OC01–OC05

Anecdotal, I have used this on a few patients since reading the above and your blog — great results.!

https://emcrit.org/pulmcrit/four-dka-pearls/ 9/12
3/22/2018 PulmCrit - Four DKA Pearls

 0  Reply  2 years ago

Divyesh Patel  

Thanks for the review. Agree with LR as uid replacement, starting long acting insulin immediately on
Guest
presentation in ED. Some other tricks that I use work well. I also start a D5 0.45% with KCL at 40 mEq/L
infusion at 150 ml/hr. This is maintenance infusion and it serves 2 purposes: replaces K and prevents
hypoglycemia because RNs on the oor forget to turn insulin infusion off and start D5 at a later time
period. In doing it right away, less to do later. In addition to insulin infusion, I also start a sliding scale
insulin right away along with infusion. Once the glucose drops to < 250 I simply turn off the infusion and
continue SSI. This allow for a smoother transition to SSI. I do not wait of the gap to close because once
the infusion is turned off, I am simply managing the rest of the DKA with SSI and already present long
acting insulin. Much easier and everything is automatic from the beginning.

 0  Reply  2 years ago

Cbrons  

“There is only one randomized controlled trial comparing NS to LR for resuscitation in DKA (Zyl et al,
Guest
2011). These authors found a trend towards faster improvement in pH when using LR compared to NS
(p = 0.076). ” ^^ The study cited concludes: The median time to reach a pH of 7.32 for the 0.9% sodium
chloride solution group was 683min (95% CI 378–988) (IQR: 435–1095 min) and for Ringer’s lactate
solution 540min (95% CI 184–896, P= 0.251) The unadjusted time to lower blood glucose to 14mmol/l
was signi cantly longer in the Ringer’s lactate solution group (410 min, IQR: 240–540) than the 0.9%
sodium chloride solu- tion group (300 min, IQR: 235–420, P= 0.044). No difference could be
demonstrated between the Ringer’s lactate and 0.9% sodium chloride solution groups in the time to
resolution of DKA (based on the ADA criteria) (unadjusted:P=0.934, adjusted:P=0.758) But: Conclusion:
This study failed to indicate bene t from using Ringer’s lactate solution compared to 0.9% sodium
chloride solution regarding time to normalization of pH in patients with DKA. The time to reach a blood
glucose level of 14 mmol/l took signi cantly longer with the Ringer’s lactate solution. ^^^ So the authors
concluded that because LR… Read more »

 0  Reply  9 months ago

FOLLOW EMCRIT EVERYWHERE

Click for More Subscribe Options

https://emcrit.org/pulmcrit/four-dka-pearls/ 10/12
3/22/2018 PulmCrit - Four DKA Pearls

OTHER STUFF

Have a great idea for the next podcast? Share

it here!

Tough Questions. Maybe you have an

answer!

When you're done listening to the podcast,

check out these great sites.

WHO WE ARE LIKE US ON FACEBOOK

We are the EMCrit Project, a team of independent medical
bloggers and podcasters joined together by our common
love of cutting-edge care, iconoclastic ramblings, and
FOAM.

https://emcrit.org/pulmcrit/four-dka-pearls/ 11/12
3/22/2018 PulmCrit - Four DKA Pearls

EMCrit
26,397 likes

Liked Share

You and 1 other friend likes this

SUBSCRIBE BY EMAIL

email address

SUBSCRIBE

EMCrit is a trademark of Metasin LLC. Copyright 2009-. This site represents our opinions only. See here for full disclaimer and here for credits and attribution.

https://emcrit.org/pulmcrit/four-dka-pearls/ 12/12