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DKA

Diabetic Ketoacidosis (DKA) is characterized by insulin deficiency leading to hyperglycemia and ketogenesis, resulting in electrolyte imbalances. Clinical manifestations include polydipsia, polyuria, Kussmaul respiration, and altered mental status, with lab findings showing elevated blood glucose, low pH, and positive serum ketones. Nursing interventions focus on hydration, electrolyte management, and blood glucose control through insulin therapy, while education emphasizes recognizing symptoms and adherence to treatment.

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11 views

DKA

Diabetic Ketoacidosis (DKA) is characterized by insulin deficiency leading to hyperglycemia and ketogenesis, resulting in electrolyte imbalances. Clinical manifestations include polydipsia, polyuria, Kussmaul respiration, and altered mental status, with lab findings showing elevated blood glucose, low pH, and positive serum ketones. Nursing interventions focus on hydration, electrolyte management, and blood glucose control through insulin therapy, while education emphasizes recognizing symptoms and adherence to treatment.

Uploaded by

Abby
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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DKA

Pathophysiology
 Process overview
o Insulin deficiency
 Lack of insulin glucose from entering cells
o Ketogenesis
 Body breaks down fat for energy, producing ketones
 Key changes
o Hyperglycemia
 Liver releases more glucose into the blood
o Electrolyte imbalance
 Loss of sodium, potassium, and phosphate due to dehydration and acidosis

Diabetic Ketoacidosis
 End up with an insulin deficiency
 Polyphagia
o Hunger
 Polyuria
o Ketones in the blood stream
o In order to pass lots of pee

Clinical manifestations

 Signs and symptoms


o Polydipsia, polyuria, dehydration
 Poor skin turgor
 Dry mucous membranes
 Tachycardia
 Orthosatic hypotension
o Kussmaul respiration
 Deep, rapid and laboured
o Fruity breath odor
o Nausea, vomiting, abdominal pain
o Mental status changes (lethargy to coma)

Labs
 Blood glucose
o >14 mmol/L
o Should be 4-6 for non diabetic fasting
 Blood pH
o <7.3
 Serum bicarbonate
o <15 mmol/L
 Serum Ketones
o Positive
 Anion Gap
o Elevated
 Electrolytes
o Sodium
 Low or normal
o Potassium
 Elevated initially, may drop with treatment
o Phosphate
 Depleted

Nursing Assessment
 Vital signs
o Monitor for tachycardia, hypotension, tachypnea
o If K high (or after fluid infusion low) cardiac monitor, watch for peaked T wave
 Fluid status
o Assess for signs of dehydration
 Neurological status
o Monitor for confusion or changes in LOC
o GCS
 Glascow coma scale
o Put safety measures if confused
 Lab monitoring
o Frequent blood glucose
o Electrolytes
o Acid-base status (ABG, VBG)

Nursing Interventions
 Hydration
o Administer IV fluids to correct dehydration and support circulation
o Start with 0.9% NaCl solution, then adjust based on sodium levels
 Large volumes of fluid should solve itself
 Electrolyte management
o Monitor and replace potassium as needed
 Risk of hypokalemia during treatment
o Correct sodium and phosphate if necessary
 Phosphate is not a priority
 Focus on sodium and potassium
 Blood glucose control
o Administer insulin infusion per protocol to gradually lower glucose

Medication Treatment
 Insulin therapy
o Note: Withheld until fluid resuscitation is underway
o Regular IV insulin
 Initial bolus of 0.1 units/kg, followed by 0.1/units/kg/hr infusion
o Titration
 Adjust to decrease blood glucose by 3-5 mmol/L per hour
 By products that are the problem the blood sugar
 When blood glucose levels approach 14mmol/L
o 5% dextrose added to regimen
o Monitor to prevent hypoglycemia
 Electrolyte replacement
o Potassium replacement
o Sodium, chloride, bicarbonate, phosphate, magnesium and nitrogen deficits may
need to be corrected
o Pay attention to sodium
 Typically see
o Potassium
 Begin replacement if potassium is below 5.5 mmol/L
 Insulin will cause the potassium to leak
o Phosphate
 Replace if levels are critically low
o Bicarbonate
 Administer if pH is below 6.9, with careful monitoring
 Never going to ask a question about bicarb
 Uncommon to use bicarb as a therapeutic regimen

Prevention of complications
 Hypoglycemia
o Monitor blood glucose regularly as levels decrease
 Hypokalemia
o Watch potassium levels during insulin therapy
 Cerebral edema
o Especially in younger patients, reduce fluid replacement rate if needed
 Infection control
o As DKA often follow infections, monitor and manage as appropriate

Education
 Signs and symptoms of hyperglycemia and DKA
 Importance of adherence to insulin and glucose monitoring
 Sick day management
o Guidelines for diabetes management during illness
 Follow up
o Ensure understanding of medication and lifestyle changes to prevent recurrence

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