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3. Causes
Underdose or missed dose
of insulin
Illness or infection
Overeating
Stress, surgery
Undiagnosed and untreated type I DM.
4. Pathophysiology
Without insulin, the amount of glucose entering the cells is reduced, and production and
release of glucose by the liver is increased. Both factors lead to hyperglycemia. In an attempt
of the body to get rid of the excess glucose, the kidneys excrete the glucose along with water
and electrolytes. This osmotic diuresis, which is characterized by excessive urination
(polyuria), leads to dehydration and marked electrolytes loss.
Lack of insulin
Increased
breakdown of fats
Decreased utilization
of glucose by
muscles, fat, and liver
Increased production
of glucose by liver.
Hyperglycemia
Increased fatty
acids
Acetone
breath
Poor
appetite
Blurred vision
Weaknes
s
Headach
Increased
ketones
bodies
Polyuria
Dehydration
Increased
thirst
(polydipsia)
Nausea
Vomiting
Abdominal
pain
Acidosis
Increasing
rapidly
respirations
5. Clinical manifestations
Acetone breath (fruity odor)
Anorexia, nausea, vomiting, abdominal pain
Polyuria
Polydipsia
Blurred vision, weakness and headache
Orthostatic hypotension (drop in systolic blood pressure of 20 mm Hg or more on
changing from reclining to standing position)
Frank hypotension with a weak, rapid pulse
Mental status changes
Kussmauls respirations
Normal
Impaired glucose Tolerance (IGT)
Possible Diabetes Mellitus
Two-hour blood sugar test performed two hours after using 75 g glucose dissolved
in water or after a good meal. Oral Glucose Tolerance Test (OGTT) is not
recommended for routine clinical use nor screening purposes.
Blood glucose monitoring
Check for Electrolytes imbalances
7. Medical Management
In addition to treating hyperglycemia, management of DKA is aimed at correcting
dehydration, electrolyte loss, and acidosis.
Rehydration
Treat dehydration with NSS 0.9% or 0.45% rapid IV as prescribed.
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D5NS or 5% dextrose in 0.45% saline when the blood glucose level reaches 250 to 300 mg/dL.
Restoring electrolytes
Administer Potassium replacements
Reversing acidosis
Ketone bodies (acids) accumulates as a
result of fat breakingdown. It is reversed
by insulin. Infuse intravenously at a slow
continuous rate.
8. Pharmacologic management (drug study)
Regular insulin
Potassium replacement (KCl)
Metoclopramide (Plasil)
9. Nursing management and Non-pharmacologic treatments
Monitoring fluid, electrolyte and hydration status
Monitor blood glucose level
Administer fluids, insulin, and other medications
Prevent fluid overload
Monitor intake and output accurately
Vital signs monitoring
ABG results monitoring and reporting to the attending physician
Assess mental status and breath sounds
Check ECG reading and make sure that there are no signs of hyperkalemia (tall and
peaked or tented T waves)
Make sure that laboratory values of potassium are normal or approaching normal.
Make sure that the patient is urinating. (no renal shutdown)
Initiate referrals for home care and outpatient diabetes education to ensure patient
continued recovery.
If you cannot follow your usual meal plan, substitute soft foods six
to eight times per day.
The most important concept to teach patients is not to eliminate insulin doses when
nausea and vomiting occur.
Blood glucose and urine ketones must be frequently assessed.
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