Updates in the Management of Diabetic

Ketoacidosis
Kathryn Evans Kreider, DNP, FNP-BC

ABSTRACT
Diabetic ketoacidosis (DKA) is an emergency for people with diabetes characterized by
hyperglycemia, metabolic acidosis, and ketosis. DKA onset and recurrence can largely
be prevented through patient education. Nurse practitioners are well positioned to
promote patient education, self-management, and individualized patient care. This
article outlines updates in the clinical management of patients with DKA to optimize
care and reduce costs.

Keywords: diabetes, diabetes mellitus, diabetic ketoacidosis, endocrine emergency,

hyperglycemia
Ó 2018 Elsevier Inc. All rights reserved.

D
iabetic ketoacidosis (DKA) is a metabolic
derangement characterized by hyperglyce-
mia, metabolic acidosis, and ketosis.1 DKA
occurs in patients with diabetes who have a lack of
circulating insulin relative to physiologic
requirement, such as in type 2 diabetes mellitus
(T2DM), or absolute depletion, such as in type 1
diabetes mellitus (T1DM),2 in the presence of
increased counterregulatory hormones (cortisol,
growth hormone, epinephrine, and glucagon). The
lack of adequate insulin can occur from medication
noncompliance, infection, or a precipitating
pathologic event, such as a myocardial infarction, that
causes an increased metabolic demand for insulin.
The Centers for Disease Control and Prevention
(CDC) United States Diabetes Surveillance System
recently reported an increase in DKA episodes in the
US between 2009 and 2014, with an average annual
increase of 6.3%.3 DKA can occur at any age but
primarily occurs in those aged younger than 30 years
(36% incidence) and between 30 and 50 years (27%
incidence).2 The highest incidence of DKA is for
those aged between 11 and 15 years.4 In addition,
girls and women and the immigrant population are at
higher risk.
In the past, DKA had a fatality rate of 1% to 5%.
Older adults and individuals who have comorbid risk
factors are in the highest risk category.1 In recent
years, however, the overall mortality of DKA has
declined due to earlier detection and increased
evidence-based management. In fact, the recent
CDC US Diabetes Surveillance System report indi-
cated that the mortality for DKA has decreased
to 0.4%.3
Episodes of DKA typically require an emergency
department visit or hospital admission for the patient
to receive insulin, intravenous (IV) fluids, and elec-
trolyte correction. Hospital encounters can be costly,
with recent reports suggesting that a single hospital
encounter for DKA treatment can cost up to
$17,500,5 with an average length of stay of 3.4 days.
Further, the annual direct and indirect cost of DKA
treatment in the US exceeds $2.3 billion.1
DKA and recurrent DKA are largely preventable
through better outpatient management, patient ed-
ucation, and promoting self-care behaviors.6 Nurse
practitioners (NPs) have an opportunity to educate
patients about the risks of DKA, promote self-
management, and offer patient-centered care. Pre-
sented here is a review the management of DKA and
updates in clinical care.
DIAGNOSIS
The diagnosis of DKA is made based on the meta-
bolic triad of high blood glucose (BG) levels
(generally > 250 mg/dL), acidosis (pH < 7.2), and
the presence of urine or serum ketones (Table).5
Inpatient providers commonly rely on laboratory data

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Table. Diagnosis of Diabetic Ketoacidosis7
Variable Mild
Arterial pH 7.25-7.3
Serum bicarbonate, mEq/L 15-18
Urine ketones Positive (trace or higher)
Serum ketones Positive
Anion gap, mEq/L >10
Mental status Alert
to confirm DKA, whereas outpatient providers rely
on history, presentation, BG levels, and
urine ketones.
Common presenting symptoms include abdom-
inal pain and the classic triad of hyperglycemia
symptoms: polydipsia, polyphagia, and polyuria.
Physical examination findings can include any or all
of tachycardia, hypotension, Kussmaul respirations,
significant dehydration, or a change in mental status.7
It is important to consider differential diagnoses of
metabolic acidosis that may include lactic acidosis or
hyperchloremic acidosis. Differential diagnoses for
ketosis include starvation ketosis (dietary history,
weight trends) or alcoholic ketoacidosis (alcohol
consumption history), hyperemesis, isopropyl
alcohol, or ketotic hypoglycemia.1
Euglycemic DKA (euDKA), which occurs when
the patient presents with acidosis and ketosis but has a
glucose
200 mg/dL, has become an emerging
concern. Causes of euDKA can include recent insulin
administration, decreased caloric intake, substantial
alcohol consumption, chronic liver disease, or rarely,
glycogen storage issues.8 In addition, there have
been increasing reports of euDKA caused by a new
class of drugs for diabetes, sodium glucose
cotransporter 2 (SGLT-2) inhibitors. In May 2015,
the US Food and Drug Administration added a
warning about the risk of DKA with use of these
drugs. One study suggested that the risk of DKA for
patients using SGLT-2 inhibitors was twice as high as
those prescribed a dipeptidyl peptidase IV inhibitor,
after controlling for other risk factors, although the
risk of hospitalization was low.9 The exact cause of
this relationship is unknown, but several theories
include reduced insulin doses when SGLT-2 is
2 The Journal for Nurse Practitioners - JNP
Diabetic Ketoacidosis
Moderate Severe
7- < 7.24 < 7.00
10- <15 <10
Positive Positive
Positive Positive
>12 >12
Alert/drowsy Stupor/coma
initiated, an increase in glucagon, or decreased
excretion of ketone bodies.1 Other related factors
may be mild infection, increased activity, reduced
food intake, or insulin reduction or omission.10 Case
reports of traditional and euDKA occurring while
using SGLT-2 inhibitors has been shown in patients
with T1DM and in those with T2DM.11 Many
patients with euDKA present with nausea and
vomiting but are misdiagnosed due to the lack of
clear glucose elevation.
DIAGNOSTIC WORKUP
Providers in outpatient settings where laboratory re-
sults are not readily available should rely on BG and
ketone values for the initial diagnosis. BG values will
typically be > 250 mg/dL, although up to 10% of
patients in DKA may present with euDKA.9 For this
reason, some experts argue that the cutoff BG value
for diagnosing DKA should be decreased to
200 mg/dL.12
Ketone measurement is an important diagnostic
component and severity classification of DKA for
patients in the outpatient setting. Urine ketones will
test positive, although may be as minimal as “trace”
ketones. Urine dipsticks measure acetoacetate (AcAc)
and acetone but not b-hydroxybutyrate (b-OHB).
Given this, the measurement of AcAc in the urine
tends to underestimate the severity of DKA, because
the ratio of AcAc to b-OHB can be 1:10 during
ketoacidosis.13 Other limitations with urine ketone
testing include lag time in change in urine ketones,
difficulty obtaining urine from dehydrated patients,
and subjective measurements by the patient. Many
experts agree that measurement of blood or capillary
ketones is preferred due to these limitations.9
Volume -, Issue -, -/- 2018
 Some outpatient glucometers, measure b-OHB in
addition to BG levels. Several of these types of moni-
toring systems are available on the market. These
meters measuring capillary ketones have been shown to
have high sensitivity, specificity, positive predictive
value, and negative predictive value in identifying
DKA compared with urine ketone testing.14 Patients
with diabetes who have access to b-OHB meters may
have reduced emergency department visits, time to
recovery from DKA, and the potential for reduced
costs.15 Currently, these systems are not widely used
and are expensive but may be beneficial to consider for
patients who are at risk for DKA.
In the emergency department, initial recom-
mended laboratory tests include a blood gas, elec-
trolytes, complete blood count with differential,
serum glucose, creatinine, serum or urine ketones, or
both, and urinalysis.16 Any woman with child-
bearing potential should receive a urine pregnancy
test, and other diagnostic assessments should be done
based on presenting symptoms, such as cardiac
markers, electrocardiogram, urine drug screens, or
blood cultures.7 If the patient requires hospital
admission, a further workup may include tests such as
chest x-ray imaging and an arterial blood gas. An
anion gap (AG) should be calculated to assist in
determining the severity of DKA (see “Metabolic
Acidosis”). Box 1 reviews common precipitants
of DKA.
MANAGEMENT
Multiple studies have suggested that centers that use
an evidence-based care algorithm have improved
outcomes in DKA management. Improvement in
outcomes may include quicker resolution of DKA
and increased adherence to fluid resuscitation and
electrolyte replacement guidelines,17 decreased
hospital admissions and length of stay, and
cost savings.18
FLUID REPLACEMENT
The replacement of fluids is the initial treatment of
DKA and is believed to be the most important initial
aspect of treatment.5 The goal of fluid administration is
to restore circulatory volume, clear ketone bodies, and
correct electrolyte disturbances caused by the fluid
shifts that occur in dehydration. The water deficit is
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Box 1. Common Precipitants of Diabetic
Ketoacidosis9
Common Precipitants of Diabetic Ketoacidosis9
The Five “I’s”
 Infection
 Infarction (myocardial, heart attack)
 Infant (pregnancy)
 Indiscretion (such as street drugs)
 Insulin lack (noncompliance, dose reduction,
inability to afford, pump malfunction)
Other:
 Medications (corticosteroids, sympathomi-
metics, atypical antipsychotics)
 New diagnosis of diabetes
 SGLT-2 inhibitor class of diabetes medications
 Unknown
SGLT-2 ¼ sodium glucose cotransporter 2.
estimated as follows: water deficit ¼ (0.6)(body weight
in kg)  (1 e [corrected sodium/140].5
Adult patients with normal renal function and no
evidence of heart failure should receive a rapid bolus
of 0.9% normal saline, generally 1 to 1.5 liters over
the first hour.5 Once the initial bolus of fluids is
given, the patient should be monitored for signs of
improvement, including BG values and ketones.
Patients who are able to consume liquids should aim
to consume at least 2 to 8 ounces per hour as they are
able. It is important to add dextrose to the saline
solution once BG reaches w200 to 250 mg/dL to
avoid hypoglycemia.5
Cerebral edema is a rare but potentially deadly
complication of DKA that occurs primarily in chil-
dren. Cerebral edema occurs when the insulin and IV
fluids used to treat DKA cause a sudden shift from the
extracellular fluid space to the intracellular fluid
space, rapidly reducing osmolarity. Cerebral edema is
deadly in up to 24% of cases. Risk factors include
younger age, new-onset diabetes, longer duration of
symptoms, severe acidosis, low initial bicarbonate
level, low sodium level, high glucose level at pre-
sentation, and rapid hydration.2 Signs of cerebral
edema that require immediate evaluation include
headache, persistent vomiting, hypertension,
The Journal for Nurse Practitioners - JNP 3
bradycardia, and lethargy, and other
neurologic changes.2
HYPERGLYCEMIA
BG levels are typically > 250 mg/dL unless euDKA is
present. Hyperglycemia is precipitated by an increase
in catecholamines, such as growth hormone, cortisol,
and epinephrine, that are released during periods of
imminent physiologic stress. Catecholamines stimu-
late the liver to produce more glucose, often making
it difficult to reduce BG levels.
The treatment of hyperglycemia should be initiated
after fluid replacement has begun because the initiation
of IV fluids can lower glucose significantly. For many
patients with mild DKA, the administration of IV
fluids is enough to restore metabolic balance and clear
the ketone bodies. Most patients with moderate to
severe DKA require insulin to restore homeostasis.
The current guidelines state that the most effective
method of glucose reduction is IV insulin.16 Most
DKA algorithms recommend an IV bolus of 0.1 U/kg,
followed by a continuous infusion of 0.1 U/kg/h.
There is some evidence suggesting that the initial bolus
does not improve patient outcomes, but this aspect
remains controversial.5 Recommendations for insulin
dosing are found in Box 2.
The cost of IV insulin treatment is significant
because this requires admission to the intensive care
unit in many facilities, substantially increasing the cost
of hospitalization. Multiple studies have suggested

Box 2. Overview of Diabetic Ketoacidosis Management5,16

Intravenous fluids
1,000e2,000 mL 0.9% NaCl over 1e2 h.
Continue 0.9% NaCl or switch to 0.45% NaCl at 250e500 mL/h depending on serum sodium.
When BG level ¼ 200-250 mg/dL, change to 5% dextrose in 0.45% NaCl.
Insulin
Regular human insulin intravenous bolus of 0.1 U/kg (optional), followed by continuous insulin infusion at
0.1 U/kg/h.
When BG
250 mg/dL, reduce insulin rate to 0.05 U/kg/h; thereafter, adjust rate to maintain glucose level
at w200 mg/dL.
Subcutaneous rapid-acting insulin might be an alternative to intravenous insulin in patients with
mild-to-moderate DKA.
Potassium
 Serum potassium (K+) level > 5.0 mEq/L (no supplement required; monitor every 2 hours)
 K+ level 3.3e5 mEq/L (add 20-40 mEq potassium chloride to replacement fluid)
 K+ level <3.3 mEq/L (hold insulin; give 20-30 mEq/h until > 3.3)
 Goal K+ level 4-5 mEq/L
 Oral potassium may be considered depending on patient status
Bicarbonate
Not routinely recommended. If pH < 6.9 consider 50 mmol/L in 500 mL of 0.45% normal saline over 1 hour
until pH increases to  7.0
Transition to subcutaneous insulin
Continue insulin infusion until resolution of ketoacidosis. To prevent recurrence of ketoacidosis or rebound
hyperglycemia, continue intravenous insulin for 2e4 h after subcutaneous insulin (basal) is given.
For patients treated with insulin before admission, restart previous insulin regimen and adjust doses as
needed. For patients with newly diagnosed diabetes mellitus, start total daily insulin dose at 0.6 U/kg/d.
Consider multidose insulin given as basal and prandial regimen.

BG ¼ blood glucose; DKA ¼ diabetic ketoacidosis.

4 The Journal for Nurse Practitioners - JNP Volume -, Issue -, -/- 2018
that rapid-acting subcutaneous (SQ) insulin, such as
lispro or aspart, given every 1 to 2 hours, can be
effective in the management of mild DKA.1 SQ
insulin can also be administered in lower levels of
care, which can assist in the cost reduction of the
hospitalization. In fact, using insulin analogs may
reduce hospitalization costs by up to 30%.1
An earlier study evaluating SQ vs IV regular in-
sulin used 0.3 U/kg SQ rapid-acting insulin as a
loading dose, followed by 0.1 U/kg/h until the BG
was < 250 mg/dL. The dose was then reduced to
0.05 U/kg/h until the DKA resolved. Compared
with IV insulin, there was no difference in length of
stay or total amount of insulin needed.19 Other more
recent studies have supported these findings,
including no difference in rates of hypoglycemia
when using SQ insulin compared with IV
insulin.20,21 Recommended doses of rapid-acting SQ
insulin analogs are between 0.075 and 0.1 U/kg/h.
This is similar to the recommended dose of IV insulin
that is initiated in the hospital setting. Alternately, 0.1
to 0.2 U/kg can be administered every 2 to
3 hours.22
For patients in DKA, the goal BG at the time of
treatment is 150 to 200 mg/dL.16
METABOLIC ACIDOSIS
In the case of DKA, metabolic acidosis occurs when
hyperglycemia precipitates an increase in free fatty
acid breakdown, which produce ketone bodies when
metabolized. These ketone bodies cause a decrease in
the alkali reserve causing ketoacidosis. Metabolic
acidosis can be determined by calculating the AG, the
difference between serum cations and anions.1 A
normal AG level is < 9 mEq/L. Patients who present
in DKA typically have an AG > 10 mEq/L.16
Patients who present with symptomatic metabolic
acidosis (Kussmaul respirations, confusion, lethargy)
should be managed as high-acuity patients.
The calculation of AG is (serum cations [sodium]
e anions [chloride þ bicarbonate]).1
ELECTROLYTE MONITORING
Hyponatremia and hyperkalemia are the primary
electrolyte abnormalities that occur in DKA. Hypo-
natremia is caused when the acidosis precipitates a
shift of potassium out of the intracellular space,
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causing an influx of sodium into the cell and extra-
cellular depletion of sodium. The opposite occurs
with potassium: Acidosis causes extracellular shifts of
potassium, creating high serum potassium levels but
relative cellular depletion. In otherwise healthy pa-
tients, hyponatremia and hyperkalemia are both
generally resolved with fluid replacement. Patients in
DKA may occasionally present with hypokalemia,
particularly if they are taking diuretics or were
vomiting. In the case of hypokalemia upon presen-
tation, fluids and potassium replacement should be
given before starting insulin because the insulin
administration may cause a further drop in potassium
levels.1 Patients with severe hypokalemia require
cardiac monitoring.
Resolution of DKA occurs when BG is < 200
mg/dL and 2 of the following have occurred: a serum
bicarbonate level  15 mEq/L, a venous pH > 7.3,
and a calculated AG
12 mEq/L.16 Box 2 contains a
summary of recommendations regarding the
treatment of DKA in adult patients. Comprehensive
algorithms detailing the comprehensive management
of DKA have been published elsewhere.1,2
TREATING THE UNDERLYING PRECIPITANT
Successful identification of precipitating factors is
paramount to effective DKA management. Common
triggers include medication noncompliance, infec-
tion, myocardial infarction, pancreatitis, alcohol
abuse, cerebrovascular accident, trauma, hyperthy-
roidism, or new diagnosis of T1DM.7 Any stress or
inflammatory response in the body could trigger the
production of ketones, resulting in DKA. Patients
should be thoroughly evaluated for underlying causes
based on history, presentation, physical examination,
and laboratory findings. Patients with new-onset
diabetes represent w20% of those presenting with
DKA.5 Newly diagnosed patients will require a
comprehensive care plan, including
diabetes education.
PREVENTION
DKA commonly reoccurs in the same cohort of
patients, and poor adherence to treatment is the
number one precipitant of DKA in the US.5
Discussing medication regimens, feasibility, cost, and
patient satisfaction is imperative to encouraging
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medication compliance and diabetes self-care. Many
patients who present with DKA have added health
concerns, including eating disorders, social issues, or
psychiatric concerns. In addition, some authors have
suggested that patients with insulin-dependent dia-
betes (T1DM or T2DM) do not have adequate “sick
day” education to facilitate appropriate monitoring
and insulin administration during times of illness.23
Studies suggest that patients who have structured
education about DKA prevention can significantly
reduce DKA-related hospitalizations.24
Patients with insulin pumps need adequate edu-
cation about how to manage and troubleshoot their
pump. Education should include how to adjust basal
rates, carbohydrate ratios, and other relevant settings
(target blood glucose, sensitivity, etc). Patients with
insulin pumps also need an “off-pump plan” that
includes a prescription for a basal insulin in case of
pump failure or malfunction. All patients who use
insulin pumps are recommended to establish care
with a provider with advanced diabetes management
training. Comprehensive recommendations regarding
education of patients using insulin pumps are pub-
lished elsewhere.25
As a result of the rise in prevalence of DKA
associated with SGLT-2 inhibitors, it is recom-
mended that SGLT-2 inhibitors be discontinued
during times of increased risk for DKA such as acute
illness, surgery, infection, dehydration, or excessive
alcohol intake.26 SGLT-2 inhibitors are currently not
approved for use in patients with T1DM, although
there are ongoing trials to evaluate the efficacy and
safety in this population.11
SICK DAY MANAGEMENT
Patients with diabetes should be adequately counseled
on how to manage BG levels during periods of illness.
Insulin-dependent patients should have urine ketone
sticks or a b-OHB monitor at home to allow them to
monitor ketones every 2 to 4 hours when sick or when
BG remains elevated. Patients should be instructed to
call their health care provider at the first detection of
ketones. Mild DKA caught early can occasionally be
treated by patients at home (in consultation with a
medical provider) with increased oral fluid intake and
administration of correction insulin. Published rec-
ommendations and algorithms that educate patients on
6 The Journal for Nurse Practitioners - JNP
home management of hyperglycemia and the detec-
tion of DKA are available.16,27
RELEVANCE FOR NPs
NPs are educated to provide holistic care, considering
physical, emotional, and psychosocial needs of the
patient. Given that evidence suggests that DKA onset
and recurrence may be largely related to education
deficits and psychosocial considerations, NPs are well
prepared to assess and intervene for high-risk patients.
Nurse practitioners should assess patients with
diabetes for
 need for educational coaching,
 self-management skill level,
 self-efficacy,
 emotional status, and
 social support.28
Patients with diabetes should also regularly be
evaluated for diabetes distress, depression, or other
mental health concerns.28 Multiple validated tools are
available to evaluate patients for diabetes distress29
and depression.30 Consider referring patients with
complex psychological needs to a mental health
specialist.28
The incidence of DKA has increased in recent
years.3 Although mortality levels have decreased,
DKA remains a medical emergency that must be
managed with precision and timeliness. Providers
who understand the pathophysiology of DKA along
with critical management principles can more readily
provide evidence-based care to patients who present
with DKA. NPs are in an excellent position to
educate patients about diabetes and sick day rules and
to implement individualized patient care plans that
emphasize self-management and early detection
of illness.
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Kathryn Evans Kreider, DNP, FNP-BC, is from the Division
of Endocrinology, Metabolism & Nutrition, Duke University
Medical Center, and is an assistant professor at Duke University
School of Nursing, Durham, NC. She is available at kathryn.
evans@duke.edu In compliance with national ethical guidelines,
the author reports no relationships with business or industry that
would pose a conflict of interest.
1555-4155/18/$ see front matter
© 2018 Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.nurpra.2018.06.013
The Journal for Nurse Practitioners - JNP 7