DKA SA

Presenting signs

·    Often newly diagnosed diabetics, middle-aged/older animals

·    Since diagnosis – unresolved PUPD, continued weight loss

·    Progressive lethargy, anorexia, V+

·    Dehydrated, hypovolaemic

·    Other signs:

o  Abdominal pain – pancreatitis common

o  Hepatomegaly – due to diabetic hepatopathy (dogs), hepatic lipidosis (cats)

o  BCS loss (but might still be obese)

o  Mental dullness – due to headache

Pathophysiology

·    Reduced insulin ® reduced glucose uptake into cells ® metabolic deficit

·    Glucagon ® lipolysis ® fatty acids ® acetyl CoA ® ketones produced by liver

·    Ketones = acetoacetate, B-hydroxybutyrate, acetone

o  Acetoacetate and BHB are acidic ® metabolic acidosis

·    Metabolic acidosis + inadequate cellular energy ® inappetence, nausea, reduced mentation, V+

o  ® dehydration, renal hypoperfusion, electrolyte derangements ® death

§ If animal inappetent – accelerates process

·    Insulin levels not always low – consider other concurrent disease leading to IR, through increased cortisol, catecholamines or glucagon

Diagnosis

·    History and clinical signs good indicator

·    Diabetes mellitus – hyperglycaemia + glucosuria

·    Measure ketones – test BHB in blood

o  Differentiate from hyperglycaemic hyperosmolar syndrome – HGHOS has high glucose but no ketoacidosis

·    Metabolic acidosis – use blood gas/EPOC

·    POCUS – rule out other diseases, may see collapsed heart due to hypovolaemia

·    Haematology – anaemia, neutrophilia with L shift, incr. Heinz bodies in cats

·    Biochemistry – incr. ALP/AST (hepatic effects, jaundiced), electrolyte abnormalities

·    Urinalysis – bacteriuria

Treatment

·    Fluid therapy

o  Hypovolaemia/dehydration and acidosis mask extent of electrolyte disturbances – will see once animal hydrated

o  Hartmann’s, over 6-12h, monitor electrolytes closely (every 2h)

·    Electrolytes, once hydration restored

o  As hydration restores, hypokalaemia and hypophosataemia may unmask

§ Severe hypoK – muscle weakness, respiratory arrest

§ Hypophos – weakness, myocardial depression, arrhythmias, haemolysis, seizures

o  Treat these as appear:

§ Low K – CRI potassium supplementation (monitor for bradyarrhythmias)

§ Low phos – CRI potassium phosphate (don’t give too quickly

§ Low Na – should correct itself as glycose corrected

§ Low Ca – only correct if CS seen (muscle twitch/tremours) – Ca bolus

§ Low Mg – treat if V+ or regurgitation

·    Correct hyperglycaemia – give insulin until patient begins to eat/drink and is BAR

o  Via insulin CRI or neutral insulin administration – CRI better as can adjust as blood glucose improves

o  Once patient eating and stable, can switch back to routine insulin regime as per long term DM control

o  If persistently anorexic/not eaten for 24-48h – consider feed tubing

·    Other considerations

o  In pain/headache – opioid for analgesia

o  Maropitant if V+/nauseous

o  Consider concurrent diseases:

§ Dogs: cushings, pancreatitis, UTI

§ Cats: hepatic lipidosis, pancreatitis, chronic renal failure, neoplasia, infection

Prognosis

·    Relapse common

·    Consider euthanasia

Hyperglycaemic hyperosmolar syndrome

·    Rare form of DKA – still have small amount of insulin

·    Diagnosis: hyperglycaemia but no ketones

·    Treatment:

o  Fluid therapy – over 24-48h, monitor glucose and Na, and monitor for neurological signs

§ If too rapid correction of hyperglycaemia and hypernatraemia ® osmotic gradient across BBB ® cerebral oedema ® seizure, coma, death

o  Start insulin treatment once normovolaemic and hydrated

·    Prognosis – not great in long term