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.
 PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS

The signs and symptoms of DKA are listed in Figure. The hyperglycemia of DKA leads to
polyuria and polydipsia (increased thirst). In addition, patients may experience blurred
vision,weakness, and headache. Patients with marked intravascularvolume 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
pulseThe 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 (withvery deep, but not labored, respirations) may
occur. These Kussmaul respirations represent the bodys 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).
 PHYSICAL FINDINGS

ASSESSMENT AND DIAGNOSTIC FINDINGS

The timely diagnosis of DKA is crucial and allows for prompt initiation of therapy. DKA is
characterized by hyperglycemia, ketosis, and metabolic acidosis (increased anion gap)
along with a number of secondary metabolic derangements. Occasionally, the serum
glucose is only minimally elevated. Serum bicarbonate is frequently <10 mmol/L, and
arterial pH ranges between 6.8 and 7.3, depending on the severity of the acidosis.
Despite a total-body potassium deficit, the serum potassium at presentation may be
mildly elevated, secondary to the acidosis. Total-body stores of sodium, chloride,

phosphorous, and magnesium are also reduced in DKA but are not accurately reflected
by their levels in the serum because of dehydration and hyperglycemia. Elevated blood
urea nitrogen (BUN) and serum creatinine levels reflect intravascular volume depletion.
Interference from acetoacetate may falsely elevate the serum creatinine measurement.
Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are commonly found as
well. Hyperamylasemia may suggest a diagnosis of pancreatitis, especially when
accompanied by abdominal pain. However, in DKA the amylase is usually of salivary
origin and thus is not diagnostic of pancreatitis. Serum lipase should be obtained if
pancreatitis is suspected. The measured serum sodium is reduced as a consequence of
the hyperglycemia [1.6-mmol/L (1.6 meq) reduction in serum sodium for each 5.6-
mmol/L (100 mg/dL) rise in the serum glucose]. A normal serum sodium in the setting of
DKA indicates a more profound water deficit. In conventional units, the calculated
serum osmolality [2 (serum sodium + serum potassium) + plasma glucose (mg/dL)/18
+ BUN/2.8] is mildly to moderately elevated, though to a lesser degree than that found
in HHS.

In DKA, the ketone body, -hydroxybutyrate, is synthesized at a threefold greater rate

than acetoacetate; however, acetoacetate is preferentially detected by a commonly used
ketosis detection reagent (nitroprusside). Serum ketones are present at significant levels
(usually positive at serum dilution of 1:8). The nitroprusside tablet, or stick, is often
used to detect urine ketones; certain medications such as captopril or penicillamine may
cause false-positive reactions. Serum or plasma assays for -hydroxybutyrate more
accurately reflect the true ketone body level. The metabolic derangements of DKA exist
along a spectrum, beginning with mild acidosis with moderate hyperglycemia evolving
into more severe findings. The degree of acidosis and hyperglycemia do not necessarily
correlate closely since a variety of factors determine the level of hyperglycemia (oral
intake, urinary glucose loss). Ketonemia is a consistent finding in DKA and distinguishes
it from simple hyperglycemia. The differential diagnosis of DKA includes starvation
ketosis, alcoholic ketoacidosis (bicarbonate usually >15 meq/L), and other increased
anion gap acidosis.

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).

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.

Criteria (The American Diabetes Association )

Diabetic ketoacidosis is distinguished from other diabetic emergencies by the presence

of large amounts of ketones in blood and urine, and marked metabolic acidosis.
Hyperosmolar hyperglycemic state (HHS, sometimes labeled "hyperosmolar non-ketotic
state" or HONK) is much more common in type 2 diabetes and features increased plasma
osmolarity (above 320 mosm/kg) due to profound dehydration and concentration of the
blood; mild acidosis and ketonemia may occur in this state, but not to the extent
observed in DKA. There is a degree of overlap between DKA and HHS, as in DKA the
osmolarity may also be increased.Ketoacidosis is not always the result of diabetes. It
may also result from alcohol excess and from starvation; in both states the glucose level
is normal or low. Metabolic acidosis may occur in people with diabetes for other reasons,
such as poisoning with ethylene glycol or paraldehyde.

The American Diabetes Association categorizes DKA in adults into one of three stages of
severity

MANAGEMENT

collaboration therapy carry out for management of DKA

For prevention of DKA related to illness, patients must be taught sick day rules for
managing their diabetes when ill. 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

FLUID MANAGEMENT

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
.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

Potassium

Despite total-body potassium depletion, mild to moderate hyperkalemia is not

uncommon in patients with hyperglycemic crises. Insulin therapy, correction of acidosis,
and volume expansion decrease serum potassium concentration. To prevent
hypokalemia, potassium replacement is initiated after serum levels fall below 5.5 mEq/l,
assuming the presence of adequate urine output. Generally, 2030 mEq potassium (2/3
KCl and 1/3 KPO4) in each liter of infusion fluid is sufficient to maintain a serum
potassium concentration within the normal range of 45 mEq/l. Rarely, DKA patients may
present with significant hypokalemia. In such cases, potassium replacement should begin
with fluid therapy, and insulin treatment should be delayed until potassium
concentration is restored to >3.3 mEq/l to avoid arrhythmias or cardiac arrest and
respiratory muscle weakness.

Bicarbonate

Bicarbonate use in DKA remains controversial. At a pH >7.0, reestablishing insulin

activity blocks lipolysis and resolves ketoacidosis without any added bicarbonate.
Prospective randomized studies have failed to show either beneficial or deleterious
changes in morbidity or mortality with bicarbonate therapy in DKA patients with pH
between 6.9 and 7.1 (29). No prospective randomized studies concerning the use of
bicarbonate in DKA with pH values <6.9 have been reported. Given that severe acidosis
may lead to a myriad of adverse vascular effects, it seems prudent that for adult patients
with a pH <6.9, 100 mmol sodium bicarbonate be added to 400 ml sterile water and
given at a rate of 200 ml/h. In patients with a pH of 6.97.0, 50 mmol sodium
bicarbonate is diluted in 200 ml sterile water and infused at a rate of 200 ml/h. No
bicarbonate is necessary if pH is >7.0.

Insulin, as well as bicarbonate therapy, lowers serum potassium; therefore, potassium

supplementation should be maintained in intravenous fluid as described above and
carefully monitored. (See Fig. 1 for guidelines.) Thereafter, venous pH should be
assessed every 2 h until the pH rises to 7.0, and treatment should be repeated every 2 h
if necessary. (See Kitabchi et al. [11] for a complete description of studies done to date
on the use of bicarbonate in DKA.)

In the pediatric patient, there are no randomized studies in patients with pH <6.9. If the
pH remains <7.0 after the initial hour of hydration, it seems prudent to administer 12
mEq/kg sodium bicarbonate over the course of 1 h. This sodium bicarbonate can be
added to NaCl, with any required potassium, to produce a solution that does not exceed
155 mEq/l sodium. No bicarbonate therapy is required if pH is 7.0 (30,31).

Phosphate

Despite whole-body phosphate deficits in DKA that average 1.0 mmol/kg body wt,
serum phosphate is often normal or increased at presentation. Phosphate concentration
decreases with insulin therapy. Prospective randomized studies have failed to show any
beneficial effect of phosphate replacement on the clinical outcome in DKA (32), and
overzealous phosphate therapy can cause severe hypocalcemia with no evidence of
tetany (17,32). However, to avoid cardiac and skeletal muscle weakness and respiratory
depression due to hypophosphatemia, careful phosphate replacement may sometimes
be indicated in patients with cardiac dysfunction, anemia, or respiratory depression and
in those with serum phosphate concentration <1.0 mg/dl. When needed, 2030 mEq/l
potassium phosphate can be added to replacement fluids. No studies are available on
the use of phosphate in the treatment of HHS.

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-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 Diagnosis for Diabetic Ketoacidosis
1. FLUID VOLUME DEFICIT RELATED TO: OSMOTIC DIURESIS DUE TO
HYPERGLYCEMIA, EXCESSIVE DISCHARGE: DIARRHEA, VOMITING; RESTRICTION
INTAKE DUE TO NAUSEA, MENTAL MESS.
Nursing intervention
Monitor vital signs, note any changes in
orthostatic blood pressure.
Monitor your breathing pattern as the
Kussmaul breathing or breathing that smell
ketones.
Monitor the frequency and quality of
breathing, use of accessory muscles
breathing, periods of apnea and cyanosis
Monitor temperature, skin color, or moisture.
Assess peripheral pulses, capillary refill, skin
turgor, and mucous membranes.
Monitor input and output.
Measure weight every day.
2. MBALANCED NUTRITION: LESS THAN BODY REQUIREMENTS RELATED TO:
INSUFFICIENCY OF INSULIN, DECREASED ORAL INPUT, HIPERMETABOLISME
STATUS
Nursing diagnosis
Determine the patient's diet and eating
patterns and compared with food that can be
spent by the patient.
Rational
Hypovolemia manifested by hypotension and
tachycardia. Estimate the severity of
hypovolemia as systolic blood pressure 10
mmHg fall from a lying position to a sitting or
standing.
Need to remove the carbonic acid produced
by respiratory alkalosis respiratoris
compensation to the state of ketoacidosis.
Acetone breath odor caused asetoasetat acid
solution and should be dropped when ketosis
corrected.
Hyperglycemia and acidosis causes normal
breathing pattern and frequency. However,
increased work of breathing, and rapid
shallow breathing and cyanosis is indicative
of respiratory fatigue or loss of capacity
through compensation in acidosis. '
Fever, chills, and diaphoresis are common in
the infection process, fever with rash, dry is a
sign of dehydration.
An indicator of the level of dehydration or
adequate circulating volume.
Estimating the need for fluid replacement,
renal function, and the effectiveness of a
given therapy.
Provides the best assessment of the fluid
status of ongoing and further in giving
replacement fluids.
Rational
Rationale: Identify deficiencies and deviations
from the therapeutic needs.
Weigh weight per day or as indicated
Identification of preferred food / desired include
the needs of ethnic / cultural.
Involve patients in planning the family meal as
indicated.
Give regular insulin treatment as indicated.
Assessing an adequate food intake (including
absorption and utilization).
If the patient's food preferences can be
included in meal planning, this cooperation can
be pursued after discharge.
Increase the sense of involvement; provide
information on the family to understand the
patient's nutrition.
insulin has a rapid onset and quickly and
therefore can help move glucose into cells.

3. RISK FOR INFECTION (SEPSIS) RELATED TO: INCREASED LEVELS OF GLUCOSE,

DECREASED LEUKOCYTE FUNCTION, CHANGES IN THE CIRCULATION.

Nursing intervention Rational

Observed signs of infection and inflammation.
Improve efforts to prevention by good hand
washing for all people in contact with patients
including the patients themselves.
Maintain aseptic technique in invasive
procedures.
Give your skin with regular care and earnest.
changes to the position, effective coughing and
encourage deep breathing.
: Patients may be entered with an infection that
usually has sparked a state of ketoacidosis or
may have nosocomial infections
Prevents cross infection.
high glucose levels in blood would be the best
medium for the growth of germs.
the peripheral circulation may be disturbed
that puts patients at increased risk of damage
to the skin / skin irritation and infection.
memventilasi Assist in all areas and mobilize
pulmonary secretions.

RISK FOR SENSORY-PERCEPTUAL ALTERATIONS RELATED TO: KETIDKSEIMBANGAN

GLUCOSE / INSULIN AND / OR ELECTROLYTES.

Provides a baseline from which to compare abnormal

Monitor vital signs and mental status.
findings, e.g., fever may affect mentation.

Address patient by name; reorient as needed to place,

Decreases confusion and helps maintain contact with
person, and time. Give short explanations, speaking
reality.
slowly and enunciating clearly.

Schedule nursing time to provide for uninterrupted rest Promotes restful sleep, reduces fatigue, and may
periods. improve cognition.

Keep patients routine as consistent as possible.

Helps keep patient in touch with reality and maintain
Encourage participation in activities of daily living
orientation to the environment.
(ADLs) as able.
 Protect patient from injury (avoid/limit use of restraints Disoriented patient is prone to injury, especially at night,
as able) when level of consciousness is impaired. and precautions need to be taken as indicated. Seizure
Place bed in low position. Pad bed rails and provide precautions need to be taken as appropriate to prevent
soft airway if patient is prone to seizures. physical injury, aspiration.

Retinal edema/detachment, hemorrhage, presence of

cataracts or temporary paralysis of extraocular muscles
Evaluate visual acuity as indicated.
may impair vision, requiring corrective therapy and/or
supportive care.

Investigate reports of hyperesthesia, pain, or sensory Peripheral neuropathies may result in severe
loss in the feet/legs. Look for ulcers, reddened areas, discomfort, lack of/distortion of tactile sensation,
pressure points, loss of pedal pulses. potentiating risk of dermal injury and impaired balance.

Provide bed cradle. Keep hands/feet warm, avoiding

Reduces discomfort and potential for dermal injury.
exposure to cool drafts/hot water or use of heating pad.

Promotes patient safety, especially when sense of

Assist with ambulation/position changes.
balance is affected.

Imbalances can impair mentation. Note: If fluid is

Monitor laboratory values, e.g., blood glucose, serum replaced too quickly, excess water may enter brain cells
osmolality, Hb/Hct, BUN/Cr. and cause alteration in the level of consciousness (water
intoxication).

FATIGUE RELATED TO: DECREASED METABOLIC ENERGY PRODUCTION, INSUFFICIENCY

OF INSULIN, INCREASING ENERGY DEMAND.

Nursing intervention Rational

Monitor BP, pulse, respiratory rate before/after
activity.
Increase patient participation in ADLs as
tolerated.
Alternate activity with periods of
rest/uninterrupted sleep
Discuss with patient the need for activity. Plan
schedule with patient and identify activities
that lead to fatigue
Indicates physiological levels of tolerance.
Increases confidence level/self-esteem and
tolerance level.
Prevents excessive fatigue.
Education may provide motivation to increase
activity level even though patient may feel too
weak initially.

References

Sudarths & Brunner text book of medical and surgical nursing

12th edition PG1180- 1183
Chintamani lewiss medical surgical nursing PG no 1264-1268.
Jameson larry harisons endocrinology pg 278-280
 https://en.wikipedia.org/wiki/Diabetic_ketoacidosis
http://www.diapedia.org/

RAJKUMARI AMRIT KAUR COLLEGE

OFNURSING
NEW DELHI

DIABETIC KETOACIDOSIS

SUBMITTED TO SUBMITTED
BY
DR (MRS.) H. GOYAL MR. YASH RAMAWAT
SENIOR FACULTY M.Sc.NSG
FINAL YEAR
RAKCON RAKCON