1. Describe the pathophysiologic changes in DKA.

a. Why do blood glucose levels increase?

DKA is caused when the body has little or no insulin to use. The blood glucose level keeps
rising to dangerous levels. This is called hyperglycemia. DKA most often starts from
infection. Hormonal changes lead to increased liver and renal glucose production and
decreased glucose use in peripheral tissues. Increased production of counterregulary
hormones leads to the production of ketoacids and resultant ketonemia and metabolic
acidosis. DKA most commonly occurs in a person with type 1 diabetes. The lack of insulin
leads to mobilization of fatty acids from adipose tissue because of the unsuppressed adipose
cell lipase activity that breaks down triglycerides into fatty acids and glycerol.

b. What are commonly seen blood glucose levels?

The definitive diagnosis of DKA consists of blood glucose levels >250 mg/d, but is usually
much higher.

c. What fluid and electrolyte disturbances commonly occur?

Typical overall electrolyte loss includes 200-500 mEq/L of potassium, 300-700 mEq/L of
sodium, and 350-500 mEq/L of chloride. The combined effects of serum hyperosmolarity,
dehydration, and acidosis result in increased osmolarity in brain cells that clinically
manifests as an alteration in the level of consciousness.

d. What causes the fluid and electrolyte disturbances?

Hyperglycemia leads to osmotic diuresis, dehydration, and a critical loss of electrolytes.
Hyperosmolality of extracellular fluids from hyperglycemia leads to a shift of water and
potassium from the intracellular to the extracellular compartment. Extracellular sodium
concentration frequently is low or normal despite enteric water losses because of the
intracellular-extracellular fluid shift. Serum potassium levels may be normal or elevated,
despite total potassium depletion resulting from protracted polyuria and vomiting.
Metabolic acidosis is caused by the excess ketoacids that require buffering by bicarbonate
ions; this leads to a marked decrease in serum bicarbonate levels.

e. What acid-base disturbances are commonly seen?

Serum pH <7.35.

f. Why do the acid-base disturbances occur?

When the accumulated ketones exceed the body's capacity of extracting them, they
overflow into urine (ie, ketonuria). If the situation is not treated promptly, more
accumulation of organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosis),
with a drop in pH and bicarbonate 1 serum levels. Respiratory compensation of this acidotic
condition results in rapid shallow breathing (Kussmaul respirations).
2. Describe the medical management of a patient in DKA.
a. How is the fluid status monitored in the acute stage of DKA?
The dehydrated patient’s lips and mouth may be dry and the tongue furrowed. Temperature
may be elevated. In patients with poor renal function and excess fluid volume, assess for
edema around the eyes and in the limbs, increasing abdominal girth, increasing blood
pressure and pulse volume, jugular venous distention, and orthostatic hypotension. Edema
occurs with excess interstitial fluid and often is not apparent until interstitial volume
increases by 2 to 3 L. Daily weights are good indicators of fluid status because 1 kg of body
weight equals 1 L of fluid. Check the clinical indicators of fluid imbalance. Fluid overload can
cause hypertension. Jugular venous pressure increases with volume overload. Orthostatic
hypotension may indicate volume depletion. In severe volume depletion, the jugular venous
pulsation may not be visible even with the patient lying flat.

b. How is hypovolemia corrected? How rapidly is fluid volume replaced? Why?

The first goal of fluid therapy is to restore volume and maintain perfusion to the brain,
heart, and kidneys. Infuse 1 L of isotonic saline over 30 to 60 minutes. Usually, a second liter
is given in the next hour. The second goal of fluid therapy, replacing total body fluid losses,
is achieved more slowly, usually 0.45% saline. When blood glucose levels reach 250 mg/dL
give 5% dextrose in 0.45% saline. This solution prevents hypoglycemia and cerebral edema,
which can occur when serum osmolarity declines too rapidly. During the first 24 hours of
treatment, the patient needs enough fluids to replace the actual volume deficit and ongoing
losses. This may be as much as 6 to 10 L. Watch for signs of fluid replacement by monitoring
blood pressure and urinary intake and output.

c. How are blood glucose levels monitored? How often?

Hourly blood glucose measurements using a blood glucose meter. If a patient exhibits
clinical symptoms of hyperglycemia that do not reflect the bedside blood glucose
measurement, a lab glucose measurement is obtained. For the patient receiving a
continuous IV insulin infusion, bedside blood glucose is measured hourly for first 8 hours
after initiation, then at least every 2 hours thereafter.

d. How are elevated blood glucose levels corrected?

The outcome of insulin therapy is to lower serum glucose by about 75 to 150 mg/dL/hr.
Unless the episode of DKA is mild, regular insulin by continuous IV infusion is the treatment
of choice. Effective blood insulin levels are reached quickly when an IV bolus dose is given at
the start of the infusion. An initial IV bolus dose of 0.1 unit/kg is followed by an IV drip of 0.1
unit/kg/hr. Continuous insulin infusion is used because of the 4-minute half-life of IV insulin.
Subcutaneous insulin is started when the patient can take oral fluids and ketosis has
stopped.
 e. How quickly is blood glucose corrected? Why?
Slowly lower blood glucose to prevent hypokalemia.

3. What electrolytes are monitored in the acute stage of DKA? Why? Na, K Hyper/Hypokalemia
a. How are electrolyte imbalances corrected? How rapidly is this accomplished? Why?
Hypokalemia prevention requires replacement of 20 to 30 mEq K in each liter of IV fluid to
keep serum K between 4 and 5 mEq/L. If serum K is < 3.3 mEq/L, insulin should be withheld
and K given at 40 mEq/h until serum K is ≥ 3.3 mEq/L; if serum K is > 5 mEq/L, K
supplementation can be withheld. Use of electrolyte replacement solutions based on lab
findings.

b. How are acid-base disturbances monitored? How often?

Arterial blood gas measurement is usually performed to demonstrate the acidosis; this
requires taking a blood sample from an artery. Subsequent measurements (to ensure
treatment is effective), may be taken from a normal blood test taken from a vein, as there is
little difference between the arterial and the venous pH. The serum CO2 test is performed to
determine metabolic acid-base abnormalities. Every one hour.

c. How are acid-base disturbances corrected? How quickly is this accomplished? Why?
The administration of sodium bicarbonate solution to rapidly improve the acid levels in the
blood is controversial. There is little evidence that it improves outcomes beyond standard
therapy, and indeed some evidence that while it may improve the acidity of the blood, it
may actually worsen acidity inside the body's cells and increase the risk of certain
complications. Its use is therefore discouraged, although some guidelines recommend it for
extreme acidosis (pH<6.9), and smaller amounts for severe acidosis (pH 6.9–7.0)

4. Describe the nursing management of a patient in DKA.

a. How is fluid status assessed?
Daily weights are good indicators of fluid status. Check the clinical indicators of fluid
imbalance. Assess vitals. Assess urine concentration. Assess mucous membrane and skin
turgor. Assess for edema around eyes and in the limbs, increasing abdominal girth,
increasing blood pressure and pulse volume.

b. What are the complications of fluid replacement and how are they prevented?
Fluid overload can cause hypertension, especially in patients with kidney failure. It can also
cause pulmonary edema and edema in extremities. Monitor for fluid imbalance.
c. How are blood glucose levels assessed? How often?
Hourly blood glucose measurements using a blood glucose meter. If a patient exhibits
clinical symptoms of hyperglycemia that do not reflect the bedside blood glucose
measurement, a lab glucose measurement is obtained. For the patient receiving a
continuous IV insulin infusion, bedside blood glucose is measured hourly for first 8 hours
after initiation, then at least every 2 hours thereafter. Urinalysis.

d. What are the complications of lowering blood glucose levels and how are they prevented?
Hypoglycemia can be avoided by assessing therapy effectiveness with hourly blood glucose
measurements.

e. How are electrolyte disturbances assessed? How often?

Every one hour. Anion gap. Vital signs.

f. What are the complications of electrolyte replacement and how are they prevented?
Hyperkalemia. High potassium levels greater than 5.0 mEq/L should be reported. 7.0 mEq/L
or higher can cause cardiac arrest. Monitor ECG for QRS spread and peaked T waves, a sign
of hyperkalemia. Assess renal function. Check specific gravity of urine to assess for
hypernatremia. Observe for edema and overhydration resulting from an elevated serum
sodium level. Keep accurate intake and output record.

g. How are acid-base disturbances assessed? How often?

Arterial blood gases are usually ordered to assess disturbances of acid-base balance. Anion
gap measures cations (sodium and potassium) and anions (chloride and bicarbonate).

h. What are the complications of acid-base correction and how are they prevented?
If a bicarbonate excess is present, then metabolic alkalosis results. Respiratory alkalosis to
compensate.

i. Define anion gap, serum osmolality and venous CO2.

Anion gap is the difference between the electrolytes, measured cations (sodium and
potassium), and measured anions (chloride and bicarbonate to determine the unmeasured
cations and anions in the serum. The formula used is: Anion gap = (sodium + potassium) –
(chloride + bicarbonate). An elevated anion gap greater than 17 mEq/l indicates metabolic
acidosis, a decreased anion gap less than 10 mEq/l indicates metabolic alkalosis.
A serum osmolality test measures the amount of chemicals dissolved in the liquid part
(serum) of the blood. Chemicals that affect serum osmolality include sodium, chloride,
bicarbonate, proteins, and sugar (glucose). A serum osmolality test is done on a blood
sample taken from a vein. Serum osmolality is measured to check the balance between the
 water and the chemicals dissolved in blood and Find out if severe dehydration or
overhydration is present.
Venous CO2 is the amount of carbon dioxide in the blood. The serum CO2 test is performed
to determine metabolic acid-base abnormalities.

j. How are serial anion gaps, serum osmolalities and venous CO2 results used?
The serum CO2 test is performed to determine metabolic acid-base abnormalities. Anion
gap indicates metabolic acidosis/alkalosis. Serum osmolalities indicates dehydration or
overhydration.