This document provides information on diabetic ketoacidosis (DKA), including its definition, etiology, pathophysiology, clinical manifestations, diagnostic studies, emergency management, and collaborative management. DKA is caused by a lack of insulin and is characterized by high blood glucose, the presence of ketones in the blood and urine, and acidosis. It can result from type 1 or type 2 diabetes, especially during times of stress or illness. The pathophysiology involves the breakdown of fat for energy which produces acidic ketones. Left untreated, DKA can lead to diabetic coma and death. Treatment focuses on fluid resuscitation, insulin administration, electrolyte replacement, and monitoring.

1. Mrs Dipali Dumbre
Msc. Nursing
Medical Surgical Nursing
SCON

2. Definition
Diabetic ketoacidosis (DKA), also referred to as diabetic
acidosis and diabetic coma, is caused by a profound
deficiency of insulin and is characterized by
hyperglycemia, ketosis, acidosis, and dehydration.

3. Etiology
 Type 1 diabetes
 Type 2 diabetes in conditions of severe illness or stress
when the pancreas cannot meet the extra demand for
insulin.
 Precipitating factors include
Illness and infection
Inadequate insulin dosage
 Undiagnosed type 1 diabetes
 Poor self-management, and neglect.

4. Pathophysiology
 When the circulating supply of insulin is insufficient,
glucose cannot be properly used for energy so that the
body breaks down fat stores as a secondary source of fuel .
 Ketones are acidic by-products of fat metabolism that can
cause serious problems when they become excessive in
the blood.
 Ketosis alters the pH balance, causing metabolic acidosis .

5.  Ketonuria is a process that begins when ketone bodies are
excreted in the urine.
 During this process, electrolytes become depleted as
cations are eliminated along with the anionic ketones in an
attempt to maintain electrical neutrality.
 Insulin deficiency impairs protein synthesis and causes
excessive protein degradation.

6.  Insulin deficiency also stimulates the production of
glucose from amino acids in the liver and leads to further
hyperglycemia.
 Because there is a deficiency of insulin, the additional
glucose cannot be used and the blood glucose level rises
further, adding to the osmotic diuresis.
 Untreated, this leads to severe depletion of sodium,
potassium, chloride, magnesium, and phosphate.
 Vomiting caused by the acidosis results in more fluid and
electrolyte losses.

7.  Eventually, hypovolemia followed by shock.
 Renal failure may eventually occur from hypovolemic
shock.
 This causes the retention of ketones and glucose, and the
acidosis progresses.
 Untreated, the patient becomes comatose as a result of
dehydration, electrolyte imbalance, and acidosis.
 If the condition is not treated, death is inevitable.

8. Clinical Manifestation
 Dehydration such as poor skin turgor,
 Dry mucous membranes,
 Tachycardia,
 Orthostatic hypotension.
 Lethargy and weakness.
 As the patient becomes severely dehydrated, the skin becomes
dry and loose, and the eyeballs become soft and sunken.
 Abdominal pain is another symptom of DKA that may be
accompanied by anorexia and vomiting.

9.  Finally, Kussmaul respirations (rapid, deep breathing
associated with dyspnea) are the body's attempt to reverse
metabolic acidosis through the exhalation of excess carbon
dioxide.
 Acetone is noted on the breath as a sweet, fruity odor.
 Laboratory findings include a blood glucose level above 300
mg/dl .
 arterial blood gas
 pH below 7.30,
 serum bicarbonate level less than 15 mEq/L (15 mmol/L),
 Ketones in the blood and urine.

10. Diagnostic Studies
 History and physical examination
 Blood studies, including immediate blood glucose,
complete blood count,
 Ketones,
 pH, electrolytes,
 Blood urea nitrogen
 Arterial blood gases
 Urinalysis, including specific gravity, pH, glucose, acetone

11. EMERGENCY MANAGEMENT:
 Etiology
Undiagnosed diabetes mellitus
• Inadequate treatment of existing diabetes mellitus
• Insulin not taken as prescribed
• Infection
• Change in diet, insulin, or exercise regimen
 Assessment findings
• Thirst
• Abdominal pain
• Nausea and vomiting
• Gradually increasing restlessness, confusion, lethargy

12. • Flushed, dry skin
• Eyes appear sunken
• Breath odor of ketones
• Rapid, weak pulse
• Labored breathing (Kussmaul respirations)
• Fever
• Urinary frequency
• Serum glucose 300 mg/dl (16.7 mmol/L)
• Glucosuria and ketonuria

13. Collaborative Management
 Administration of intravenous fluids
 Intravenous administration of rapid-acting insulin
 Electrolyte replacement
 Assessment of mental status
 Recording of intake and output
 Central venous pressure monitoring (if indicated)
 Assessment of blood glucose levels
 Assessment of blood and urine for ketones
 ECG monitoring
 Assessment of cardiovascular and respiratory status
 ECG, Electrocardiogram.

14.  Intervention:
Initial
• Ensure patent airway.
• Administer oxygen.
• Establish IV access with large-bore catheter.
• Begin fluid resuscitation with 0.9% NaCl solution 1 L/hr
until BP stabilized and urine output 30-60 ml/hr.
• Begin continuous regular insulin drip 0.1 U/kg/hr.
• Identify history of diabetes, time of last food, and
time/amount of last insulin injection.

15.  Ongoing Monitoring
• Monitor vital signs, level of consciousness, cardiac rhythm,
oxygen saturation, and urine output.
• Assess breath sounds for fluid overload.
• Monitor serum glucose and serum potassium.
• Administer potassium to correct hypokalemia.
• Administer sodium bicarbonate if severe acidosis (pH 7.0).

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