Diabetic ketoacidosis Flashcards
How does ketosis occur
- Insulin deficiency = decreased cellular uptake of glucose.
- lipolysis produces acetylCoa
- AcetylCoa cannot enter krebs cycle with pyruvate so builds up
- This is converted into 3 ketone bodies (acetone, acetoacetate and B-hydroxybuterate)
- Ketones are strong acids = metabolic acidosis
What causes the dehydration and electrolyte imbalances in DKA?
- in ketoacidosis, osmotic dieuresis as a result of hyperglycaemia continues but polydipsia does not = hypovolaemia and dehydration.
- Acidosis and decreased insulin cause K+ to move out of the cells into the ECF, where it is lost by dieuresis
- anorexia and vomiting worsen hypokalaemia
- Magnesium and phosphourous are lost in urine
How is DKA diagnosed
- History of diabetes mellitus, ketoaemia on ketometer and a metabolic acidosis.
- If hx of DM unknown compatable clinical signs in history eg PUPD weight loss and polyphagia with an elevated BG and glucosuria
What is the limitation of using dipsticks to detect ketosis
- They detect acetoacetate but b-hydoxybuterate is the primary ketone formed, so only weak positive in some cases.
- dipstick is more reliable on plasma than urine but handheld ketometer preffered
how can the anion gap help diagnose ketosis?
- high anion gap (addition of acid)
- if no known toxin ingestion and a normal lactate is supportive evidence for the presence of ketosis
What is non hyperglycaemic diabetic ketoacidosis
- known diabetic patients treated with SGLT2 inhibitors
- These control BG independantly of insulin so can still get ketosis despite normal glucose.
- can still be very ill with significant acidosis
What are common additional albratory findings? (other than hyperglycaemia, ketosis, acidosis and hypokalaemia)
- compensatory respiratory alkalosis
- non regenerative anaemia
- left shifted neutophils
- ALP elevations
- heinz bodies (cat)
- AST and ALT elevations (mainly cat)
- hypophosphataemia
- Hypomagnesia
- Aztotaemia
What is the significance of comorbidities in DKA
- 70% of dogs and 80% cats with DKA will have co-morbidities
- Thought that they lead to the production of counter regulatory hormones (glucagon, cortisol, GH, catecholamies) which reduces glycaemic control, tipping into DKA
What are the most common comorbitities which precipitate DKA
- UTI
- hyperadrenocortism
- Pancreatitis
- Neoplasia
- treatment with steroids
what is the challenge of urine sediment exam in DKA?
pyuria can be mild or absent (hyperglycaemia surpresses immune function) so lack of an active sediment does not rule out DKA.
- urine culture should be performed in all
What further investigations are needed in patients presenting with DKA
- urine culture
- adrenal axis testing (delayed by several weeks if suspicious)
- Screen for pancreatitis with imaging and CPLi FPLi
- Thoracic and abdo imaging to screen for neo and other disease
Why is insulin thereapy not started immediately?
- hypovolaemia is made worse as glucose moves from ECF to ICF drawing water with it
- hypokalaemia needs to be corrected before starting insulin
What is pseudohyponatraemia in DKA?
Hyperglycaemia pulls water from the intracellular to extracellular space, diluting the sodium.
- correct sodium for glucose: every 3.5mmol/l Gluc decreases sodium by 1mmol/l
- divide glucose by 3.5 then add to sodium to correct it
Why are maintanence fluid rates higher in DKA?
due to ongoing osmotic dieuresis
- likely 5ml/kg/hr
- need constant reassessment of the cardiovascular system to correct deficits and avoid overload
What may cause initial potassium measurement to be normal in DKA?
- Decreased GFR due to hypovolaemia decreases K+ excretion
- Acidosis cause K+ to shift out of cells in exchange for an H+
- still need to supplement it as will rapidly drop when insulin starts
When should insulin therapy be initiated
When any hypovolaemia is corrected and the K+ is normalised (patient is normally perfused)
What is the purpose of insulin administration in DKA?
- eliminating ketone body production and increasing metabolism of the ketones present.
- Will cause glucose to drop before it has the desired effect on ketones - therefore the need for glucose supplementation
Briefly describe the IM insulin protocol
- 0.2IU/kg regular insulin initially given IM followed by 0.1IU/kg hourly thereafter with hourly glucose monitoring.
- If dropped by >4mmol/l then decrease dose to 0.05IU/kg.
- If dropped by <2mmol/l increase dose to 0.2IU/kg
- endpoints and dextrose supplementation as per IV
Briefly describe the IV insulin protocol
add 2.2IU/kg to a 250ml bag of saline and run 50ml through the line. Administer as per table with BG check every 2 hours
Are there any alternatives to soluable insulin protocols
still the standard of care
Study in cats use a combination of s/c and IM glargine administration and had good results
When managing DKA how quickly so you want the glucose to reduce?
rapid changes >4mmol/l/hr are not desirable as they can have neuro effects as a result of changing osmolarity
What considerations need to be made for ongoing fluid therapy
- initial bolus therapy to correct hypovolamia
- ongoing rate needs to correct any dehydration, provide maintanence and ongoing losses.
- need to count the total amount from all fluid bags
- regular reassessment to avoid overload
How many/ what fluid bags would you need if doing the variable rate insulin protocol?
- Insulin CRI, with the rate set as per the table.
- Dextrose CRI, concentration as per the table
- Hartmans with additives, eg metoclopramide, K+, to be run at a fixed rate
- Plain hartmans, the rate can be adjusted based on the others so that the overall volume meets the patients requirements
When can regular insulin therapy be discontinued?
When acidaemia is resolved, the ketouria/ketonaemia reduced and the patient is eating or tolerating regular tube feeding well.
How do you decide the dose of subcutaneous insulin?
- immediately after DKA achieving tight glycaemic control is not possible and glucose curves are meaningless.
- Give an appropriate dose for the patients weight and recheck glucose only to make sure there is no hypoglycaemia
- recheck and consider dose adjustment a week later
Hypomagnesia is a relatively rare complication of insulin therapy. What might you notice and how would you supplement it?
- Hypomagnesia can cause the hypokalaemia to be refractory to treatment.
0 supplement at 0.5 - 1mmol/kg/day and recheck every 24hr
What adverse effects can be caused by hypophosphataemia and how is it supplemented
- neuro signs (mainky dogs and haemolysis (mainly cats)
- supplement with potassium phosphate at 0.03 - 0.12mmol/kg/her.
- NB cannot mix with calcium containing fluids (saline only) and contains potassium so may need to adjust your rates
Is Bicarbonate indicated in acidosis as a result of DKA?
- rare, the acidaemia is from ketosis (addition of acid) rather than loss of bicarb. usually IVFT and insulin will resolve
- bicarb has know adverse effects and can worsen hypokalaemia.
- only give if acidaemia is refractory to therapy and causing cardiotoxicity
Is a central line indicated? when should you place one?
- useful as on lots of infusions, multiple ports, less phlebitis, less likely to get tangled.
- Placed under sedation when the patient is euvolaemic (easier)
Would antibiotics be useful?
Can consider empiric use of co-amoxyclav awaiting culture due to the prevelance of UTI and the limitations of urine sediment. discontinue if culture negative
What do you need to consider for GI support in DKA
- gastric hyperacidity, decreased motility and nausea are common.
- maropitant and metoclopramide are commonly indicated
- Omeprazole is indicated if there is evidence of mucosal ulceration.
- if >48hr anorexia consider feeding tube to promote intestinal healing and faster transition onto s/c insulin
