T

he rescue squad arrives at the emergency

department (ED) with Chad Smith, 72
years old, who was found unconscious
on the basement floor of his home. En
route to the hospital, Mr. Smiths respi-
rations became very shallow. An endotracheal tube
was inserted, and its placement was confirmed by
end-tidal CO
2
detection. Since arriving at the ED,
he has remained comatose and is not assisting the
ventilator. His vital signs are blood pressure, 80/48
mmHg; heart rate, 112 beats per minute; and tem-
perature, 91.8F. He has a sinus tachycardia with-
out ectopy. The glucometer indicates a finger stick
blood sugar (FSBS) reading of panic high.
Mr. Smith is among the 5.9% of people in the
United States with diabetes.
1
A significant percentage
of them will experience diabetic ketoacidosis (DKA),
a state of hyperglycemia, hyperketonemia, and meta-
bolic acidosis.
2,3
DKA typically affects those with type
1 diabetes, although patients with type 2 diabetes
who suffer from hyperglycemic hyperosmolar nonke-
totic syndrome also experience DKA, and with
increasing incidence.
4,5
In January 2002, the
American Diabetic Association (ADA) reported that
there are approximately 100,000 hospitalizations for
DKA annually.
6
Its also the leading cause of death
among children with diabetes, nearly 40% of whom
present with DKA in addition to new-onset diabetes.
7
The ability of emergency nurses to learn and rec-
ognize the signs and symptoms of DKA profoundly
affects outcome and survival rate. In 1980, the age-
adjusted death rate among patients with diabetes
was 30.8 per 100,000 patients, with DKA listed as
the cause of death. By 1996, this number had
dropped to 20.4, a change attributed to streamlined
care and modern treatment modalities.
8
PATHOPHYSIOLOGY
DKA is initiated by trauma or conditions such as
new-onset diabetes or congestive heart failure,
which place the body under stress and increase the
levels of catecholamines, cortisol, growth hor-
mones, and glucagon. Excesses of these hormones
decrease the effectiveness of insulin.
4,9
In the pres-
ence of insulin resistance or deficiency, hyperglycemia
occurs, decreasing the movement of glucose from the
intravascular spaces to the intracellular spaces. With
the cells then starving from lack of glucose, the
body starts metabolizing its own fats and pro-
teins. As fats are broken down, a process called
lipolysis occurs, in which free fatty acids form and
travel to the liver, where they become keto acids
that place the body in a state of hyperketonemia.
10
When the bodys glucose level rises, fluid shifts
from the intracellular to the intravascular spaces.
Subsequently, when the kidneys ability to filter
the hyperglycemic blood is overcome, they begin
spilling the extra glucose into the renal system.
Because of the molecular size of glucose and its
osmotic pressure, fluid follows the glucose
through the renal system and into the bladder,
causing the patient to experience polyuria.
2
This
leads to intracellular as well as generalized dehy-
dration, which, along with the bodys inability to
rid itself entirely of the ketones, leads to metabolic
acidosis.
3,9
During early DKA, the glomerular fil-
tration rate decreases as kidney function becomes
impaired. Coupled with a shift of potassium (K
+
)
from the cells into the extracellular spaces, this
causes elevated K
+
levels. And as DKA progresses,
profound diuresis occurs, causing a drop in serum
K
+
level. Once rehydration is initiated, K
+
begins
Diabetic Ketoacidosis
Rapid identification, treatment, and education can improve
survival rates.
By Gordon Lee Gillespie, BSN, CEN, and Melody Campbell, MSN, CEN, CCRN
ajn@lww.com AJN

September 2002

Supplement 13
Gordon Lee Gillespie is an emergency nurse at Mercy Franciscan
Hospital-Mount Airy, Cincinnati, OH. His mentor, Melody Campbell,
is critical care CNS and trauma coordinator at the Upper Valley
Medical Center, Troy, OH.
shifting back into the cells, causing severe
hypokalemia.
2, 4
IDENTIFICATION
The symptoms of this condition are polyuria, poly-
dipsia, and polyphagia.
4
Because of Mr. Smiths
coma, the nurses were unable to assess him for these
symptoms. During his physical assessment, how-
ever, he demonstrated hypother-
mia, tachycardia, hypotension, and
vomiting, all of which are associ-
ated with DKA. Other symptoms
associated with the condition
include Kussmaul respirations (rapid
and deep respiratory pattern), car-
diac arrhythmia, altered mental sta-
tus, an acetone or fruity breath,
nausea, weakness, weight loss,
blurred vision, flushed face, and leg
cramps.
2,4
Patients presenting with
typical symptoms of DKA, an
altered level of consciousness, or
several of the additional symptoms
should have a FSBS test performed
to rule out hyperglycemia and pos-
sible DKA. Its important to note,
however, that FSBS values can be
erroneously low if the patient is
severely dehydrated or hypoten-
sive.
11
Therefore, serum glucose lev-
els should always be compared
with the initial FSBS value. This is
especially important if FSBS level
will be used to evaluate the effec-
tiveness of subsequent treatment.
Hematocrits below 20% and above
70% may also cause lower FSBS
values.
DIAGNOSIS AND INTERVENTION
When Mr. Smith arrived at the ED, an electrocar-
diogram, chest radiograph, and routine urinalysis
were performed, and FSBS, complete blood count
(CBC), chemistry panel, and serum ketone level
were assessed. These diagnostic tests are typically
used to confirm the presence of DKA and to deter-
mine its severity in patients with signs and symp-
toms. Further diagnostic tests, such as urine,
sputum, wound, and blood cultures, as well as
assessment of arterial blood gas, cardiac enzyme,
amylase, and lipase levels will help identify the
cause of DKA. Also, consider administering preg-
nancy tests to women of childbearing age.
2
Intervention will vary depending on test results.
Patients with DKA usually present with elevated K
+
levels. As rehydration and insulin therapy take effect,
these levels will begin decreasing. If the initial K
+
level is less than 5.5 mEq/L, 20 mEq potassium chlo-
ride should be added to the primary fluid. If the K
+
level is less than 3.3 mEq/L, 40 mEq potassium chlo-
ride should be added.
3
As the acidosis increases, the
pH continues to drop. However, the acidosis isnt
treated until pH drops to less than 7.0. Treating the
acidosis when pH is higher than 7.0
increases the risk of hypokalemia
and cardiac arrhythmia and brings
about a shift in the oxyhemoglo-
bin dissociation curve that causes
decreased tissue oxygenation.
3,4
If
urinalysis, radiographs, or CBC
show signs of infection, start antibi-
otic therapy after cultures have
been obtained. Maintain continu-
ous cardiac monitoring to check for
arrhythmia that may result from
changes in K
+
levels.
MANAGEMENT
Once DKA is identified, manage-
ment of the patient is twofold. The
precipitating stressors must be iden-
tified and treated, as must the
serum glucose level and the addi-
tional significant symptoms.
Precipitating stressors include
infection, trauma, myocardial in-
farction, congestive heart failure,
cerebrovascular accident, gastroin-
testinal bleeding, and new-onset
diabetes. Other stressors include
emotional stress, cocaine use, mis-
management of insulin or of oral
diabetic agents, and concurrent use
of medications such as corti-
costeroids, thiazide diuretics, and phenytoin.
4,10
Mr. Smith was immediately started on a 0.9%
normal saline (NS) IV fluid bolus for hypotension
and hyperglycemia. He was also given 10 units of
regular insulin via intravenous push (IVP).
Patients with DKA typically need 3 to 6 L NS
during the first few hours after onset.
10
The ADA
recommends that 0.9% NS be administered intra-
venously at 15 to 20 mL/kg/hr for 60 to 90 min-
utes.
6
Others have recommended that 0.9% NS be
given intravenously at 15 mL/kg/hr for one hour,
then at 7.5 mL/kg/hr for 2 hours, then at 3.75
mL/kg/hr for the next 24 to 36 hours as long as the
corrected serum sodium isnt elevated.
12
Once the
hypovolemia and hypotension are corrected, the
0.9% NS should be changed to 0.45% NS.
10
14 AJN

September 2002

Supplement http://www.nursingcenter.com
Maintain
continuous
cardiac
monitoring to
check for
arrhythmia that
may result from
changes in K
+
levels.
ajn@lww.com AJN

September 2002

Supplement 15
Routine treatment includes administering regular
insulin 0.1 to 0.15 units per kg IVP followed by a
0.1 unit/kg/hr IV infusion.
10
An insulin infusion is pre-
pared by adding regular insulin to 0.9% NS to reach
the desired concentration, usually a 1:1 ratio. The
tubing needs to be primed and an extra 10 to 50
mL of fluid wasted through continuous priming
to accommodate for the insulin being absorbed by
polyvinyl chloride tubing.
2,13
If the glucose level doesnt drop by 50 to 100
mg/dL every hour, the insulin infu-
sion rate should be doubled.
2,3,10
Regardless of the initial FSBS read-
ing, insulin therapy should be
maintained until electrolyte values
have been obtained and K
+
therapy
is initiated (if the K
+
level is lower
than 5.5 mEq/L).
6,12
Once the hourly
blood sugar measurements are less
than 250 mg/dL, the hourly rate of
intravenous insulin should be re-
duced by half. Start an infusion of
5% dextrose and 0.45% NS at 100
to 150 mL/hr to replace the 0.9%
(or 0.45%) NS infusion. The insulin
infusion should continue until at
least two of the following outcomes
occur: the anion gap is less than
14 mEq/L, the venous pH is 7.3
or greater, or the bicarbonate level is
greater than 18 mEq/L.
2,3,10
For
treating acidosis, if the pH is less
than 6.9, the ADA recommends
adding 100 mmol of sodium bicar-
bonate (NaHCO
3
) to 400 mL ster-
ile water and administering the
solution over two hours. If the pH
is 6.9 to 7.0, 50 mmol of NaHCO
3
should be
added to 200 mL sterile water and given over two
hours. Reevaluate the venous pH every two hours.
When the pH reaches 7.0, no further NaHCO
3
need be administered.
NURSING CARE AND ONGOING ASSESSMENT
Nursing care of patients with DKA includes a
thorough nursing assessment as well as patient and
family education.
Primary assessment involves evaluation of air-
way, breathing, and circulation (ABC), as well as
neurologic status. First, assess airway patency. If the
patient is not able to breathe on his own insert an
oral or nasopharyngeal airway.
6
If vomiting occurs,
oral suctioning may be required. If breathing is inef-
fective or the patient is vomiting and comatose, pro-
tect the airway by inserting an endotracheal tube
then confirming its placement with an end-tidal
CO
2
detector, auscultation of breath sounds, and a
portable chest radiograph.
2,6
Assess circulation, ob-
tain vascular access, and start a 0.9% NS infusion.
If the patient is hypotensive, a fluid bolus must be
given.
2
Finally, assess the patients neurologic status:
Is he alert and responsive to verbal or painful stimuli?
Secondary assessment. Undress the patient,
and if theres hypothermia, control temperature
using warmed blankets, overhead heating lamps,
and warmed IV fluids. Insert a
nasogastric tube if the patient is
vomiting, and insert an indwelling
urinary catheter in order to moni-
tor output and obtain urinalysis.
If the patient has been intubated,
place a nasogastric tube to decom-
press the stomach.
4
Initiate cardiac
monitoring to check for arrhyth-
mia, which may result from elec-
trolyte imbalances. Take steps to
make the patient comfortable, such
as by administering antiemetics or
analgesia.
Obtain a thorough history from
the patient and family in order to
identify what may have precipitated
the DKA episode. Perform a head-
to-toe exam to identify abnormali-
ties, establish a baseline assessment,
and help identify root causes and
sequelae of the condition.
The frequency of follow-up
assessments will vary depending on
the baseline assessment and stabil-
ity of the patient. For example, alert
patients may be able to report
symptom changes to nursing staff, whereas those
who are unconscious will require assessment hourly
(or more frequently, if necessary). Reassessment
includes examination of ABC, and assessment of
neurologic status and vital signs.
2,4
EDUCATION
Once the patient is extubated, he will need educa-
tion in diabetes management in order to prevent
recurrence and sequelae. Patients who dont believe
they have diabetes (as reported by family members)
pose a particular challenge to nurses, who will need
to tailor education accordingly.
Management during concurrent illness and daily
FSBS monitoring are of the utmost importance,
even if the disease is well controlled by oral agents.
Signs and symptoms of DKA need to be reviewed
with the patient and family during each ED visit for
Chronic vision
changes may
prevent elderly
patients with
diabetes from
administering
insulin on
their own.
hyperglycemia and whenever diabetes is identified
in the ED.
4
Also, urge patients to get annual
influenza vaccines to prevent sepsis and pneumo-
niacommon stressors that precipitate acute DKA
episodes.
13
Sick-day management. Advise patients to seek
professional medical assistance for uncontrolled
fevers, urinary frequency or discomfort, persistent
cough, or ulcerations. If antibiotics have been pre-
scribed for these illnesses, explain the importance of
using the entire prescription, even after symptoms
have improved or subsided. This will ensure that
these illnesses are appropriately treated and will
reduce the incidence of resistant bacterial strains.
Encourage patients to continue their insulin therapy
and medications even when theyre experiencing
nausea and vomiting from other illnesses.
13
To pre-
vent DKA and dehydration, instruct patients to
drink liquids containing carbohydrates (such as
sodas, juices, and gelatins) and salt (such as bouil-
lon).
3,9,13
If patients cant keep these fluids down, or
if nausea and vomiting persist for more than a day,
they will need to consult a health care professional.
When patients with diabetes become ill with a
cold or flu, they should check their urine for ketones
with each voidor at least dailyusing urine ketone
strips from the pharmacy.
13
Patients also should
increase the frequency of FSBS monitoring to
make sure the levels remain under 200 mg/dL. If
readings exceed 200 mg/dL, they should contact
the health care professional.
9
Encourage them to
get extra rest.
13
Finally, remind patients to tell
family members or friends when they become ill,
and to ask family members to check on them
every four hours to make sure the condition has-
nt worsened.
3,13
Consultations. If patients dont adhere to their
medical regimen, its important to identify the rea-
sons why. Patients often deny having a chronic ill-
ness, and therefore dont follow medical advice or
take their medications. Those who struggle to cope
with diabetes may benefit from a psychiatric con-
sultation, which may help them accept the condi-
tion. A spiritual guide or a chaplain can also be
helpful, especially when theres a threat of death,
severe illness, or life-changing complication.
If patients arent following the prescribed regi-
men because they cant afford the cost of medica-
tions or diabetes monitoring equipment, arrange a
social service consultation as soon as possible. A
social worker may be able to help patients to
either obtain these supplies or apply for Medicare
or Medicaid insurance. Provide literature describ-
ing community services.
Furthermore, a registered dietitian can rein-
force the importance of proper diet planning and
self-management of diabetes. Patients may also
benefit from advice on how to accommodate
dietary modifications when grocery shopping or
dining out.
Chronic vision changes may prevent elderly
patients with diabetes from administering insulin on
their own. A registered diabetes educator can help
them choose alternative methods of measuring and
administering insulin, such as teaching friends and
family members to administer the insulin for them,
using a magnifying glass when drawing the insulin,
or using an insulin pen.
Diabetes affects a significant percentage of the
population, and DKA is one of the most serious
health problems resulting from it. Rapid identifica-
tion is essential in order to improve patient out-
comes and overall quality of life. Once the stressors
have been identified, they must be treated. To pre-
vent further occurrence of DKA, educate patients
and their families so they can manage sick days
more effectively and know when to seek medical
assistance.
REFERENCES
1. National Center for Chronic Disease Prevention and Health
Promotion. National diabetes fact sheet: national estimates
and general information on diabetes in the United States.
Revised ed. Atlanta (GA): Department of Health and Human
Services; 1998. http://www.cdc.gov/diabetes/pubs/facts98.htm.
2. Miller J. Management of diabetic ketoacidosis. J Emerg
Nurs 1999;25(6):514-9.
3. Kitabchi AE, Wall BM. Management of diabetic ketoacido-
sis. Am Fam Physician 1999;60(2):455-64.
4. Quinn L. Diabetes emergencies in the patient with type 2
diabetes. Nurs Clin North Am 2001;36(2):341-60, viii.
5. Westphal SA. The occurrence of diabetic ketoacidosis in
non-insulin-dependent diabetes and newly diagnosed diabetic
adults. Am J Med 1996;101(1):19-24.
6. American Diabetes Association. Clinical practice recommen-
dations 2002. Diabetes Care 2002;25 Suppl 1:S1-147.
7. Emergency Nurses Association. Medical emergencies. In:
ENPC provider manual. 2nd ed. Park Ridge (IL): The
Association; 1999. p. 273-301.
8. National Center for Chronic Disease Prevention and Health
Promotion. Diabetic ketoacidosis. In: Diabetes surveillance,
1999. Atlanta (GA): Centers for Disease Control and
Prevention; 1999.
http://www.cdc.gov/diabetes/statistics/survl99/Chap7/
contents.htm.
9. Freeland BS. Diabetic ketoacidosis. Am J Nurs
1998;98(8):52.
10. Jabbour SA, Miller JL. Uncontrolled diabetes mellitus. Clin
Lab Med 2001;21(1):99-110.
11. Atkin SH, et al. Fingerstick glucose determination in shock.
Ann Intern Med 1991;114(12):1020-4.
12. Konick-McMahan J. Riding out a diabetic emergency.
Nursing 1999;29(9):34-40.
13. Grinslade S, Buck EA. Diabetic ketoacidosis: implications for
the medical-surgical nurse. Medsurg Nurs 1999;8(1):37-45.
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