Diabetic Ketoacidosis Flashcards
Which cells of the pancreas would dysfunction occur for DKA?
The beta cells, resulting in an absolute or relative deficiency of insulin.
What does insulin deficiency promote?
- Lipolysis
- Proteolysis
- Ketogenesis
What happens to fatty acids released form the adipose tissue with a lack of insulin?
- The fatty acids are converted to coenzyme acyl-CoA => acetyl CoA => acetoacetic acid and B-hydroxybutyric
- Acetoacetic acid, acetone and B-hydroxybutyric acid are ketone bodies. *They are insulin antagonist which will contribute to worsening hyperglycaemia and ketonemia.
- This will provoke acidosis, fluid depletion and hypotension.
What are the electrolyte abnormalities found in DKA patients?
Sodium, potassium, phosphorus and magnesium are lost excessively due to osmotic renal secretion.
Why is DKA bad?
- Increase in glucose in urine causes osmotic diuresis (Na + K) leading to polyuria, polydipsia and dehydration
- Absence of insulin causes:
-release of free fatty acids from adipose tissue (lipolysis)
-creates acetoacetate + B-hydroxybutyrate (ketone bodies)
-proteolysis
-ketogenesis - Electrolytes imbalances
-Na
-K
-Phosphorous
-Mg
(lost through renal and then electrolytes move from intracellular space into the vascular space = total body deficit) - Often there is a concurrent disease
-pneumonia
-pancreatitis
-hyperadrenocorticism (Cushing’s) - CBC
-mild polycythemia
-leukocytosis due to infection - Biochemistry
-liver enzyme abdnormalities (ALT and Alk Phos)
-elevated pancreatic enzyme (Amylase and Lipase)
What do you need to add to convert B-hydroxybutyric acid to acetoacetic acid in urine and why?
Hydrogen peroxide. To be able to detect the presence of this ketone body on a urine strip.
What is the treatment plan for DKA patients?
IVF and insulin.
Main fluid of choice is 0.9%NaCl due to Na depletion.
Once Na is >140mmol/L - change to isotonic buffered solution.
Lactate isn’t a good choice due to lactate metabolism in the liver competing with ketone metabolism.
Insulin supplementation causes a shift of serum K+ back into intracellular spaces = rapid drop in serum K. Hence KCL supplementation is required.
Same thing for Phosphate!
What is the treatment goal for DKA?
Slowly lower BG by 50-100 mg/dL/hr to a BG of 200-250 after 8 - 10 hours and clearance of ketones
What are the two techniques for insulin administration in a DKA patient?
- IM
-loading dose of 0.2U/kg
Then
-0.1U/kg/hr
-when BG <250mg/dL
Then
-Insulin q4-6 IM @ 0.1-0.4 U/kg
-IV supplementation of 2.5-5% dextrose to maintain BG @ 150-300 mg/dL until patient is eating and no more ketones - IV CRI
- 2u/kg (K9) and 1.1u/kg (felines) in 250ml bag of 0.9%NaCl
- run 1st 50ml through the IV line as plastic absorb insulin
- rate of 10ml/hr
- supplement with dextrose as above
- Remember to treat all concurrent diseases
- Ketones takes about 3 days to clear and Hyperglycaemia takes about 12 hours.
What is the pathophysiology of DKA?
The beta cells of the pancreas are affected
- results in absolute or relative deficiency of insulin
- causing lipolysis, proteolysis and ketogenesis
- increased in ketones, and H+ and low HCO3 resulting in severe metabolic acidosis
Often there is concurrent disease processes
- pancreatitis
- infection
Ketones and glucose spill into urine causing osmotic diuresis
-ketones drags Na and K into urine causing dehydration
In a normal body during starvation, the body uses free fatty acids and convert that into ketones and use that as energy source. However, because a diabetic has decreased insulin production, gluconeogenesis increases and so does ketogenesis. Ketones can’t be used as an energy source due to lack of insulin and that’s where imbalances occur.
What are the physical examination findings of a DKA patient?
- Dehydration
- Weakness
- Depression
- Tacypnea
- Vomiting
- Acetone smelling breath
- Kussmaul respiration (Slow breathe to blow off build up of CO2)
- Acute abdo + abdo distension
- Hepatomegaly
- cats: diabetic neuropathy
What does dehydration cause in a DKA patient?
- Contraction of intravascular fluid space
- Pre-renal azotemia
- Decreased GFR
- Decreased glucose and hydrogen ion secretion
- Which results in increase glucose and ketones in vascular space
How do you diagnose DKA?
- Clinical signs and persistent fasting hyperglycemia, glucosuria, ketonaemia and ketonuria
- acid/base and CBC
- biochemistry (amylase and lipase)
- T4 in cats
- urinalysis with culture
- ECG
What are the clinical abnormalities found in DKA patients?
- CBC
- mild polycythemia (from dehydration)
- leukocytosis (infection or inflammation)
- Biochemistry
- liver abnormalities
- ALT and Alk Phos increased
- BUN /creatinine increased
- low USG
- hyperlipidemia
- no insulin = no lipoprotein lipase = lipemia
- high amylase and lipase (pancreatic enzymes)
- Exocrine pancreatic insufficiency (EPI)
- from chronic pancreatitis
- trypsin-like immunoreactivity (TLI) low
- urinalysis
- glucosuria
- ketonuria
- proteinuria
- bacteriuria
Treatment of DKA
- ~36-48 hours to reach normal
- the slower the better
- insulin and fluids
- IV lines and extension set ups to be replaced q48hours
- monitor urine output (minimum of 1-2ml/kg/hr)
