DKA

Question 1

What are the ketone bodies?

Answer 1

β-hydroxybutyrate, acetoacetate, and acetone

Question 2

What are the complications of the use of ketone bodies as an energy source?

Answer 2

Ketone bodies stimulate the chemoreceptor trigger zone in the medulla oblongata, leading to anorexia and vomiting. Ketosis also contributes to the osmotic diuresis that is present in clinical diabetes mellitus. These clinical signs all contribute to a propensity to dehydration, volume depletion, hypokalemia (and total body potassium deficits), and acidosis

Question 3

What is the normal cause of death in a cat with DKA that does not survive?

Answer 3

develop renal failure because severe dehydration coupled with sodium loss results in renal hypoperfusion. Dehydration and electrolyte derangements can also cause hyperviscosity, thromboembolism and severe metabolic acidosis

Question 4

How does a hyperosmolar hyperglycaemia present?

Answer 4

depression, dehydration, hypovolemia, and hypokalemia

Question 5

What is hyperosmolar hyperglycaemia?

Answer 5

On a spectrum with DKA
Although hyperosmolar hyperglycemia is a rare clinical presentation in cats, it is worth considering this entity in any cat that is severely depressed or moribund, because the prognosis is near-hopeless,

Question 6

Why is detection of ketones alone not enough to diagnose DKA@

Answer 6

Other conditions can cause ketosis, most notably hepatic lipidosis

Question 7

How do you diagnose hyperosmolar hyperglycaemia?

Answer 7

blood glucose concentrations are greater than 30 mmol/L , plasma osmolarity is greater than 350 mOsm/L, and the cat is moribund or comatose.

osmometers are not commonly used in veterinary clinics, estimates of plasma osmolarity are more usually calculated based on the concentrations of sodium, potassium, and glucose

Question 8

What is the first step in the treatment of DKA?

Answer 8

restore fluid and electrolyte abnormalities and to stop the uncontrolled breakdown of triglycerides to reverse the ketoacidosis. Correction of electrolyte and fluid deficits, and thereby acidosis, is initiated first, followed by reversal of ketone formation with insulin therapy.

Question 9

What are the main electroylytes that need to be corrected?

Answer 9

K
Phos
Na

ideally buffered solution not Saline

Question 10

Can you bolus cats with DKA?

Answer 10

Flow rates appropriate for shock therapy should be used for cats with severe signs of dehydration and poor perfusion. However, the flow rate should be reduced if depression worsens, because cerebral edema is a possible complication.

Question 11

What moves with glucose after insulin administration?

Answer 11

Insulin administration allows the translocation of glucose from the extracellular to the intracellular space in glucose-sensitive tissues (especially skeletal muscle and adipose tissue).
This translocation of glucose is accompanied by water, potassium, and phosphate

Question 12

Why is phosphate important in DKA?

Answer 12

Hypophosphatemia can be present at the time of diagnosis but more commonly develops with insulin treatment in anorexic cats. Hypophosphatemia can result in hemolytic anemia if phosphate concentrations decrease to less than 0.3 to 0.45 mmol/L=
Some cats require a blood transfusion if packed cell volume drops substantially. This condition may occur despite supplementation with phosphate.

Cannot be mixed with buffered solutions as it binds with the Ca

Question 13

What is DKA?

Answer 13

• Life-threatening complication of DM
• Results from a combination of factors:
- insulin deficiency (relative or absolute)
- counter regulatory hormones (insulin resistance)
- osmotic diuresis
• Risk factors
- undiagnosed DM
- inadequate insulin dose/frequency/missed dose(s)
- concurrent disease
• The majority patients have concurrent disease

Question 14

What is the typical signalment of DKA?

Answer 14

• Cats >8yo, most 10-14yo
• Risk factors in cats senior age, male gender, obesity, Burmese breed of European blood lines, physical inactivity
• Median age of dogs with DKA 8y; no sex or breed
predisposition

Question 15

What are the typical clinical signs of DKA?

Answer 15

• History of PU/PD, weight loss (may not be noticed by owner, increasing risk)
• Acute onset lethargy, hypo/anorexia, vomiting +/- diarrhoea
+/- CNS depression

Question 16

How do you diagnose DKA?

Answer 16

• Hyperglycaemia (usually >24mmol/L)
• Glucosuria
• Arterial/venous pH <7.30-7.35; HCO3- <12mmol/L
• Ketoaemia/uria
dipstick negative for ketones? - then use POC device to measure plasma β-HB

N.B when patient is getting better, they produce less B-HB and more acetone so dipstick may look like the pet is getting worse

Question 17

What are the typical concurrent diseases with DKA?

Answer 17

• Dogs – approximately 70% of cases including pancreatitis, bacterial UTI (20%), HAC
• Cats – acute necrotising pancreatitis, sepsis, AKI
Suspect in cats ini within 1-3d of treatment

Question 18

What are the goals of treatment (in order)

Answer 18

• Restore intravascular volume
• Correct dehydration
• Electrolyte and acid-base disturbances
• Decrease glucose concentrations

Question 19

What is the most important tx for DKA when presenting

Answer 19

Fluid therapy
• Isotonic – NaCl 0.9%, Hartmann’s, no studies proving benefit of either
• Corrects dehydration concurrently improving glycaemia
• Rate dependent on clinical assessment - don’t go too high - 1-2xm as v fast can lead to cerebral oedema
• Weigh twice daily; account for 0.5-1% loss per day due to fasting

Question 20

Outline Na in DKA

Answer 20

• With rare exceptions, all dogs and cats with DKA have
significant deficits in total body sodium - even if bloods don’t show this
• Hyperglycaemia => free water in IVS => effective decrease in Na+.
Correct by adding 1.6mmol/L to the measured Na+ for every 5.6mmol/L the plasma glucose exceeds normal range
• Do not correct Na+ imbalance at a rate that exceeds
0.5mmol/L/h (or can lead to central pontine myelinolysis)

Question 21

Outline K in DKA

Answer 21

• Total body deficit
• Potassium can be decreased, normal or increased at
presentation
• Supplement before starting insulin therapy if normo- or hypokalaemic at presentation
• Do not exceed 0.5mmol/kg/h (risk of cardiac arrhythmia)

Question 22

Outline the use of insulin

Answer 22

• Inhibits lipolysis, gluconeogenesis and glycogenolysis; promotes utilisation of glucose and ketones by tissues
• Low-dose regular insulin (CRI vs IM)
• Ideally initiate within 4h of starting IVFT
• BG should be measured hourly initially and the insulin dose adjusted accordingly
• Aim to slowly decrease BG to the range of 10-14mmol/L, preferably over 6-10h (ideally 2.8-4mmol/L/h)

usually takes 48-72 hours to lose all ketones after insulin started

Question 23

What is the IM insulin protocol

Answer 23

• 0.2 IU/kg initially
• 0.1 IU/kg one hour later
• 0.05-0.2 IU/kg/h (depending on rate of BG decline) until BG ≤14mmol/L
• 0.1-0.4 IU/kg SC q4-8h (if adequate hydration)
• Add glucose to IVFT (2.5-5% solution), maintaining BG between 8-15mmol/L
• Start lente insulin (dog) or porcine zinc insulin (cat) once the patient is eating, drinking and off IVFT (initial dose 0.1-0.3 IU/kg)

Question 24

What is the CRI insulin protocol?

Answer 24

• To prepare: add 2.2 IU/kg (dog) or 1.1 IU/kg (cat) regular insulin to 250mL NaCl 0.9%. Discard approx. 50mL before connecting
• Use separate IV from that used for IVFT/KCl
supplementation
• Start at 10mL/h. Adjust as indicated based on hourly BG

Question 25

Outline phosphorous in DKA

Answer 25

• Plasma phosphorous may be normal, decreased or
increased at presentation; intracellular tissue phosphorous is usually depleted
• Hypophosphataemia often clinically silent
• Cats – haemolytic anaemia
• Report of stupor and seizures in one dog
• Supplementation recommended if serum phosphorous <0.5mmol/L
• Overly aggressively phosphorous supplementation may lead to hypocalcaemia, tetany and soft tissue mineralisation

Question 26

Outline Mg in DKA

Answer 26

Clinical signs of magnesium deficiency:
- arrhythmia, weakness, seizures, refractory hypocalcaemia and hypokalaemia
Suspect if refractory low Ca or K
• Measurement of total magnesium concentration is unlikely to reflect active plasma magnesium status
• Administer only to patients that have documented decreased ionised magnesium
• Most dogs with DKA have normal-increased iMg at
admission
• Magnesium deficiency present in some cats
Doesn’t normally affect progression of DKA

Question 27

How do you deal with concurrent disease?

Answer 27

• Most common co-morbidities include acute or chronic
pancreatitis, bacterial infection, cholangiohepatitis, CKD,
cardiac disease and insulin antagonism induced by hormonal disorders (HAC, dioestrus [rare with acromegaly])
• Diagnostic imaging; urine culture
• Modifications in therapy and/or additional therapy may be required
• Insulin therapy should never be delayed or discontinued
• Stop exogenous glucocorticoid therapy unless life threatening immune-mediated disease
• Bitches with pyometra or in confirmed dioestrus should undergo OVH as soon as safely possible
• Only test for HAC once patient stable, eating and electrolyte derangements/metabolic acidosis have resolved

Question 28

What blood monitoring should be done and how frequently?

Answer 28

• Demeanour/HR/RR/hydration status q2-4h
• BG q1-2h
• Blood-gas/electrolytes q6-8h
• Phosphorous q8-12h
• Magnesium? – if refractory hypokalaemia
• Aim to gradually return biochemical parameters to normal over 36-48h

Question 29

What is the prognosis for DKA patients?

Answer 29

• Most dogs (70%) treated for DKA survive to be discharged from the hospital with a median hospitalisation time of 6 days
- at least 7% of dogs develop recurrent episodes of DKA
- dogs with co-existing HAC are less likely to be discharged from hospital
- the degree of base deficit is associated with outcome
• Prognosis in cats highly dependent on presence and
management of concurrent disease. Mortality (referral) ranges from 18-36%. Higher survival rates (up to 100%) are reported in uncomplicated cases
• Diabetic cats with DKA no less likely to achieve remission

Question 30

How is hyperglycaemic hyperosmolar syndrome different?

Answer 30

• Severe hyperglycaemia >33mmol/L and serum osmolality >320mOsm/kg
• Compared to DKA, patients are more dehydrated, less acidaemic and have lower [counter-regulatory hormone]
• 2°or concurrent disease precipitate development
• To calculate osmolality: 2 x (Na+ + K+) + glucose + urea
• Treatment as per DKA
• Mortality 38-65%
almost all cats with hyperosmolar hyperglycemia have other serious diseases concurrently, including kidney failure or neoplasia (but are less likely to have pancreatitis)

Question 31

How is the pathophysiology of hyperosmolar hyperglycaemia different?

Answer 31

Cats commonly have normal to elevated sodium concentrations, and because they have poor glomerular filtration, glucose concentrations are typically twice as high as in cats with DKA or uncomplicated diabetes

Therefore, cats with hyperosmolar hyperglycemia have substantially higher calculated total and effective osmolarity than cats with DKA or uncomplicated diabetes, so that there is potential for large fluid shifts when intravenous fluids are administered, which means that if plasma osmolarity or glucose concentrations are lowered before intracellular glucose and osmolarities have equilibrated, a concentration gradient develops between plasma and intracellular fluid. If marked, this can cause catastrophic effects such as cerebral edema