DIABETIC KETOACIDOSIS

DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by

hyperglycemia, ketonuria, acidosis, and dehydration.

Pathophysiology and Etiology

• Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat
for fuel.
• Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver.
• Ketone bodies are organic acids that cause metabolic acidosis.
• Increase in the secretion of glucagon, catecholamines, growth hormone, and cortisol, in response to
the hyperglycemia caused by insulin deficiency, accelerates the development of DKA.
• Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium,
sodium, phosphate, and water.
• Caused by inadequate amounts of endogenous or exogenous insulin.
o Frequently occurs due to failure to increase the dose of insulin during periods of stress (eg,
infection, surgery, pregnancy).
o May occur in previously undiagnosed or untreated diabetics.

Clinical Manifestations
Early

• Polydipsia, polyuria
• Fatigue, malaise, drowsiness
• Anorexia, nausea, vomiting
• Abdominal pains, muscle cramps

Later

• Kussmaul respiration (deep respirations)

• Fruity, sweet breath
• Hypotension, weak pulse
• Stupor and coma

Diagnostic Evaluation

• Serum glucose level is usually elevated over 300 mg/dL; may be as high as 1,000 mg/dL.
• Serum and urine ketone bodies are present.
• Serum bicarbonate and pH are decreased due to metabolic acidosis, and partial pressure of carbon
dioxide is decreased as a respiratory compensation mechanism.
• Serum sodium and potassium levels may be low, normal, or high due to fluid shifts and
dehydration, despite total body depletion.
• BUN, creatinine, hemoglobin, and hematocrit are elevated due to dehydration.
• Urine glucose is present in high concentration and specific gravity is increased, reflecting osmotic
diuresis and dehydration.

NURSING ALERT
Severity of DKA cannot be determined by serum glucose levels; acidosis may be prominent with
glucose level of 200 mg/dL or less.
Management

• I.V. fluids to replace losses from osmotic diuresis, vomiting.

• I.V. insulin drip—regular insulin infused only to increase glucose utilization and decrease lipolysis.
• Electrolyte replacement—sodium chloride and phosphate as required, potassium chloride and
bicarbonate based on laboratory results.

Complications

• Premature discontinuation of I.V. insulin can result in prolongation of DKA.

• Too-rapid infusion of I.V. fluids in cases of severe dehydration can cause cerebral edema and death.
• Failure to institute subcutaneous insulin injections before discontinuation of I.V. insulin can result in
extended hyperglycemia.

Nursing Assessment

• Assess skin for dehydration poor turgor, flushing, dry mucous membranes.
 • Observe for cardiac changes reflecting dehydration, metabolic acidosis, and electrolyte imbalance
hypotension; tachycardia; weak pulse; electrocardiographic changes, including elevated P wave,
flattened T wave or inverted, prolonged QT interval.
• Assess respiratory status Kussmaul breathing, acetone breath characteristic of metabolic acidosis.
• Perform GI assessment nausea, vomiting, extreme thirst, abdominal bloating and cramping,
diarrhea.
• Determine GU symptoms—nocturia, polyuria.
• Observe for neurologic signs—crying, restlessness, twitching, tremors, drowsiness, lethargy,
headache, decreased reflexes.
• Interview family or significant other regarding precipitating events to episode of DKA.
o Patient self-care management before hospitalization
o Unusual events that may have precipitated episode (eg, chest pain, trauma, illness)

Nursing Diagnoses

• Deficient Fluid Volume related to hyperglycemia

• Ineffective Therapeutic Regimen Management related to failure to increase insulin during illness

Nursing Interventions
Restoring Fluid and Electrolyte Balance

• Assess BP and heart rate frequently, depending on patient's condition; assess skin turgor and
temperature.
• Monitor intake and output every hour.
• Replace fluids as ordered through peripheral I.V. line.
• Monitor urine specific gravity to assess fluid changes.
• Monitor blood glucose frequently.
• Assess for symptoms of hypokalemia—fatigue, anorexia, nausea, vomiting, muscle weakness,
decreased bowel sounds, paresthesia, arrhythmias, flat T waves, ST-segment depression.
• Administer replacement electrolytes and insulin as ordered. Flush the entire I.V. infusion set with
solution containing insulin and discard the first 50 mL because plastic bags and tubing may absorb
some insulin and the initial solution may contain decreased concentration of insulin.
• Monitor serum glucose, bicarbonate, and pH levels periodically.
• Provide reassurance about improvement of condition and that correction of fluid imbalance will help
reduce discomfort.

NURSING ALERT
Electrolyte levels may not reflect the total body deficit of potassium (primarily) and sodium (to a
lesser extent) due to compartment shifts and fluid volume loss. Replacement is necessary despite normal
to high values.
DRUG ALERT
Interruption in insulin administration may result in reaccumulation of ketone bodies and worsening
acidosis. Glucose will normalize before acidosis resolves so I.V. insulin is continued until bicarbonate
levels normalize and subcutaneous insulin takes effect and the patient starts eating.
Preventing Further Episodes of DKA

• Review with patients precipitating events and causes of DKA

• Assist patient in identifying warning signs and symptoms of DKA.

• Instruct patient in sick-day guidelines (see page 928).

Patient Education and Health Maintenance

• Make sure that patient and caretakers can demonstrate drawing up and administering insulin in the
proper dose, blood glucose monitoring, and urine ketone testing.
• Make sure that patient and caretakers know whom to notify in the event of hyperglycemia, stressful
situation, or symptoms of DKA.

Evaluation: Expected Outcomes

• BP and heart rate stable; glucose and bicarbonate levels improving

• Verbalizes sick-day guidelines correctly
DIABETIC KETOACIDOSIS
DKA is caused by an absence or markedly
inadequate amount of
insulin. This deficit in available insulin results
in disorders in the
metabolism of carbohydrate, protein, and
fat. The three main
clinical features of DKA are:
• Hyperglycemia
• Dehydration and electrolyte loss
• Acidosis
Pathophysiology
Without insulin, the amount of glucose
entering the cells is reduced
and the liver increases glucose production.
Both factors
lead to hyperglycemia. In an attempt to rid
the body of the excess
glucose, the kidneys excrete the glucose
along with water and
electrolytes (eg, sodium and potassium). This
osmotic diuresis,
which is characterized by excessive urination
(polyuria), leads to
dehydration and marked electrolyte loss.
Patients with severe
DKA may lose up to 6.5 liters of water and up
to 400 to 500 mEq
each of sodium, potassium, and chloride over
a 24-hour period.
Another effect of insulin deficiency or deficit
is the breakdown
of fat (lipolysis) into free fatty acids and
glycerol. The free fatty
acids are converted into ketone bodies by
the liver. In DKA there
is excessive production of ketone bodies
because of the lack of insulin
that would normally prevent this from
occurring. Ketone
bodies are acids; their accumulation in the
circulation leads to
metabolic acidosis.
Three main causes of DKA are decreased or
missed dose of insulin,
illness or infection, and undiagnosed and
untreated diabetes
(DKA may be the initial manifestation of
diabetes). An
insulin deficit may result from an insufficient
dosage of insulin
prescribed or from insufficient insulin being
administered by the
patient. Errors in insulin dosage may be
made by patients who
are ill and who assume that if they are eating
less or if they are
vomiting, they must decrease their insulin
doses. (Because illness,
especially infections, may cause increased
blood glucose levels, patients
do not need to decrease their insulin doses
to compensate
for decreased food intake when ill and may
even need to increase
the insulin dose.)
Other potential causes of decreased insulin
include patient
error in drawing up or injecting insulin
(especially in patients
with visual impairments), intentional skipping
of insulin doses
(especially in adolescents with diabetes who
are having difficulty
coping with diabetes or other aspects of their
lives), or equipment
problems (eg, occlusion of insulin pump
tubing).
Illness and infections are associated with
insulin resistance. In
response to physical (and emotional)
stressors, there is an increase
in the level of “stress” hormones—glucagon,
epinephrine, norepinephrine,
cortisol, and growth hormone. These
hormones
promote glucose production by the liver and
interfere with glucose
utilization by muscle and fat tissue,
counteracting the effect
of insulin. If insulin levels are not increased
during times of illness
and infection, hyperglycemia may progress
to DKA (Quinn,
2001c).
Clinical Manifestations
The signs and symptoms of DKA are listed in
Figure 41-8. The
hyperglycemia of DKA leads to polyuria and
polydipsia (increased
thirst). In addition, patients may experience
blurred vision,
weakness, and headache. Patients with
marked intravascular
volume depletion may have orthostatic
hypotension (drop in systolic
blood pressure of 20 mm Hg or more on
standing). Volume
depletion may also lead to frank hypotension
with a weak, rapid
pulse.
The ketosis and acidosis of DKA lead to GI
symptoms such as
anorexia, nausea, vomiting, and abdominal
pain. The abdominal
pain and physical findings on examination
can be so severe that
they resemble an acute abdominal disorder
that requires surgery.
Patients may have acetone breath (a fruity
odor), which occurs
with elevated ketone levels. In addition,
hyperventilation (with very deep, but not
labored, respirations) may occur. These
Kussmaul
respirations represent the body’s attempt to
decrease the acidosis,
counteracting the effect of the ketone
buildup. In addition,
mental status changes in DKA vary widely
from patient to patient.
Patients may be alert, lethargic, or
comatose, most likely
depending on the plasma osmolarity
(concentration of osmotically
active particles).
Assessment and Diagnostic Findings
Blood glucose levels may vary from 300 to
800 mg/dL (16.6 to
44.4 mmol/L). Some patients have lower
glucose values, and others
have values of 1,000 mg/dL (55.5 mmol/L) or
more (usually
depending on the degree of dehydration).
The severity of DKA
is not necessarily related to the blood
glucose level. Some patients
may have severe acidosis with modestly
elevated blood glucose
levels, whereas others may have no
evidence of DKA despite
blood glucose levels of 400 to 500 mg/dL
(22.2 to 27.7 mmol/L)
(Quinn, 2001c).
Evidence of ketoacidosis is reflected in low
serum bicarbonate
(0 to 15 mEq/L) and low pH (6.8 to 7.3)
values. A low PCO2
level (10 to 30 mm Hg) reflects respiratory
compensation
(Kussmaul respirations) for the metabolic
acidosis. Accumulation
of ketone bodies (which precipitates the
acidosis) is reflected
in blood and urine ketone measurements.
Sodium and potassium levels may be low,
normal, or high,
depending on the amount of water loss
(dehydration). Despite
the plasma concentration, there has been a
marked total body depletion
of these (and other) electrolytes. Ultimately,
these electrolytes
will need to be replaced.
Elevated levels of creatinine, blood urea
nitrogen (BUN), hemoglobin,
and hematocrit may also be seen with
dehydration.
After rehydration, continued elevation in the
serum creatinine
and BUN levels will be present in the patient
with underlying
renal insufficiency.
Prevention
For prevention of DKA related to illness,
patients must be
taught “sick day” rules for managing their
diabetes when ill
(Chart 41-9). The most important issue to
teach patients is not
to eliminate insulin doses when nausea and
vomiting occur.
Rather, they should take their usual insulin
dose (or previously
prescribed special “sick day” doses) and
then attempt to consume
frequent small portions of carbohydrates
(including foods
usually avoided, such as juices, regular
sodas, and gelatin).
Drinking fluids every hour is important to
prevent dehydration.
Blood glucose and urine ketones must be
assessed every 3 to
4 hours.
If the patient cannot take fluids without
vomiting, or if elevated
glucose or ketone levels persist, the
physician must be contacted.
Patients are taught to have available foods
for use on sick
days. In addition, a supply of urine test strips
(for ketone testing)
and blood glucose test strips should be
available. Patients must
know how to contact their physician 24 hours
a day.
Diabetes self-management skills (including
insulin administration
and blood glucose testing) should be
assessed to ensure
that an error in insulin administration or
blood glucose testing
did not occur. Psychological counseling is
recommended for patients
and family members if an intentional
alteration in insulin
dosing was the cause of the DKA.
Medical Management
In addition to treating hyperglycemia,
management of DKA is
aimed at correcting dehydration, electrolyte
loss, and acidosis
(Quinn, 2001c).
REHYDRATION
In dehydrated patients, rehydration is
important for maintaining
tissue perfusion. In addition, fluid
replacement enhances the excretion
of excessive glucose by the kidneys. Patients
may need up
to 6 to 10 liters of IV fluid to replace fluid
losses caused by
polyuria, hyperventilation, diarrhea, and
vomiting.
Initially, 0.9% sodium chloride (normal
saline) solution is administered
at a rapid rate, usually 0.5 to 1 L per hour for
2 to
3 hours. Half-strength normal saline (0.45%)
solution (also known
as hypotonic saline solution) may be used for
patients with hypertension
or hypernatremia or those at risk for heart
failure. After
the first few hours, half-normal saline
solution is the fluid of
choice for continued rehydration, if the blood
pressure is stable
and the sodium level is not low. Moderate to
high rates of
infusion (200 to 500 mL per hour) may
continue for several
more hours. When the blood glucose level
reaches 300 mg/dL
(16.6 mmol/L) or less, the IV fluid may be
changed to dextrose
5% in water (D5W) to prevent a precipitous
decline in the blood
glucose level (ADA, Hyperglycemic Crisis in
Patients with Diabetes
Mellitus, 2003).
Monitoring fluid volume status involves
frequent measurements
of vital signs (including monitoring for
orthostatic changes
in blood pressure and heart rate), lung
assessment, and monitoring
intake and output. Initial urine output will lag
behind IV
fluid intake as dehydration is corrected.
Plasma expanders may be
necessary to correct severe hypotension that
does not respond to
IV fluid treatment. Monitoring for signs of
fluid overload is especially
important for older patients, those with renal
impairment,
or those at risk for heart failure.
RESTORING ELECTROLYTES
The major electrolyte of concern during
treatment of DKA is
potassium. Although the initial plasma
concentration of potassium
may be low, normal, or even high, there is a
major loss of
potassium from body stores and an
intracellular to extracellular
shift of potassium. Further, the serum level
of potassium drops
during the course of treatment of DKA as
potassium re-enters the
cells; therefore, it must be monitored
frequently. Some of the factors
related to treating DKA that reduce the
serum potassium
concentration include:
• Rehydration, which leads to increased
plasma volume and
subsequent decreases in the concentration
of serum potassium.
Rehydration also leads to increased urinary
excretion
of potassium.
• Insulin administration, which enhances the
movement of
potassium from the extracellular fluid into
the cells.
Cautious but timely potassium replacement
is vital to avoid
dysrhythmias that may occur with
hypokalemia. Up to 40 mEq
per hour may be needed for several hours.
Because extracellular
potassium levels drop during DKA treatment,
potassium must be
infused even if the plasma potassium level is
normal.
Frequent (every 2 to 4 hours initially)
electrocardiograms and
laboratory measurements of potassium are
necessary during the
first 8 hours of treatment. Potassium
replacement is withheld
only if hyperkalemia is present or if the
patient is not urinating.
REVERSING ACIDOSIS
Ketone bodies (acids) accumulate as a result
of fat breakdown.
The acidosis that occurs in DKA is reversed
with insulin, which
inhibits fat breakdown, thereby stopping acid
buildup. Insulin
is usually infused intravenously at a slow,
continuous rate (eg,
5 units per hour). Hourly blood glucose
values must be measured.
IV fluid solutions with higher concentrations
of glucose,
such as normal saline (NS) solution (eg,
D5NS or D50.45NS),
are administered when blood glucose levels
reach 250 to 300 mg/dL
(13.8 to 16.6 mmol/L) to avoid too rapid a
drop in the blood
glucose level.
Various IV mixtures of regular insulin may be
used. The nurse
must convert hourly rates of insulin infusion
(frequently prescribed
as “units per hour”) to IV drip rates. For
example, if
100 units of regular insulin are mixed in 500
mL 0.9% NS,
then 1 unit of insulin equals 5 mL. Thus, an
initial insulin infusion
rate of 5 units per hour would equal 25 mL
per hour. The insulin
is often infused separately from the
rehydration solutions to allow
frequent changes in the rate and content of
rehydration solutions.
Insulin must be infused continuously until
subcutaneous
administration of insulin resumes. Any
interruption in adminis- tration may result in
the reaccumulation of ketone bodies and
worsening acidosis. Even if blood glucose
levels are dropping to
normal, the insulin drip must not be stopped;
rather, the rate or
concentration of the dextrose infusion should
be increased. Blood
glucose levels are usually corrected before
the acidosis is corrected.
Thus, IV insulin may be continued for 12 to
24 hours until the
serum bicarbonate level improves (to at least
15 to 18 mEq/L)
and until the patient can eat. In general,
bicarbonate infusion to
correct severe acidosis is avoided during
treatment of DKA because
it precipitates further, sudden (and
potentially fatal) decreases
in serum potassium levels. Continuous
insulin infusion is
usually sufficient for reversing DKA.
Nursing Management
Nursing care of the patient with DKA focuses
on monitoring
fluid and electrolyte status as well as blood
glucose levels; administering
fluids, insulin, and other medications; and
preventing
other complications such as fluid overload.
Urine output is monitored
to ensure adequate renal function before
potassium is administered
to prevent hyperkalemia. The
electrocardiogram is
monitored for dysrhythmias indicating
abnormal potassium levels.
Vital signs, arterial blood gases, and other
clinical findings are
recorded on a flow sheet. The nurse
documents the patient’s laboratory
values and the frequent changes in fluids
and medications
that are prescribed and monitors the
patient’s responses. As DKA
resolves and the potassium replacement rate
is decreased, the
nurse makes sure that:
• There are no signs of hyperkalemia on the
electrocardiogram
(tall, peaked [or tented] T waves).
• The laboratory values of potassium are
normal or low.
• The patient is urinating (ie, no renal
shutdown).
As the patient recovers, the nurse reassesses
the factors that
may have led to DKA and teaches the patient
and family about
strategies to prevent its recurrence (Quinn,
2001c). If indicated, the nurse initiates a
referral for home care to ensure the patient’s
continued recovery.