Diabetic Ketoacidosis (DKA)

• Presentation of diabetic ketoacidosis

  Often newly diagnoses diabetics. Usually middle-aged to older animals.

  Since diagnosis - PUPD hasn’t resolved, weight loss has continued. Progressive lethargy, anorexia and vomiting.

  Clinically these patients are often dehydrated and hypovoalemic through fluid loss.

  Other signs: abdominal pain (pancreatitis common), hepatomegaly (diabetic hepatopathy in dogs, hepatic lipidosis cats). BCS, mental dullness.
• Diagnosis of diabetic of ketoacidosis

  Usually straight-forward - history and clinical signs are a strong clue.

  Diabetes M -> Hyperglycaemia and glucosuria.

  Ketones -> b-hydroxybutyrate is the most abundant.

  • Blood ketones is ideal; usually tests for b-hydroxybutyrate.
  • Urine ketones less ideal; usually for acetoacetate so false negatives.

  Metabolic acidosis -> blood gas machine
• Treatment of diabetic ketoacidosis - fluid therapy.

  Hypovolaemia/ dehydration and metabolic acidosis mask the true extent of electrolyte disturbances - in particular potassium and phosphate.

  Use Hartmann’s

  Restore volume status and hydration rapidly - arguably restore deficit quickly over 6-12 hours.

  Reduces glucose significantly alone (mechanism not fully understood).

  Reveals true extent of electrolyte disturbances allowing treatment.
• Treatment of diabetic ketoacidosis - electrolytes

  As hydration restores hypokalaemia and hypophsophataemia may unmask:

  • Severe hypokalaemia - profound muscle weakness and respiratory arrest when extreme.
  • Severe hypophosphataemia - weakness, myocardial depression, arrhythmias and haemolysis or seizures.
• Treatment of diabetic ketoacidosis - hypokalaemia

  Potassium supplementation - dose rate dependant on severity (table in formulary) - CRI or spiked fluids.

  High rates can cause bradyarrythmias - at highest doses, consider ECG monitoring

  Monitor and adjust q4-6 hour.
• Treatment of diabetic ketoacidosis - hyperphosphataemia

  CRI of potassium phosphate 0.0-0.12 mM/kg/hr.

  • Take care as contains potassium too.
• Treatment of diabetic ketoacidosis - hyponatraemia

  Sodium is pushed intracellularly in response to hyperglycaemia.

  • Maintains normal osmolality.

  As glucose corrects - sodium should also correct.
• Treatment of diabetic ketoacidosis - hypocalcaemia

  Only correct if clinical signs noted e.g. muscle twitching/tremors.

  Usually corrects with fluid therapy and restoration of renal perfusion.

  Dose rates in the formulary.
• Treatment of diabetic ketoacidosis - hypoglycaemia

  Once hydration is restores, focus switches to switching of ketogenesis and as a by product, achieving normoglycaemia (mild hyperglycaemia) until the patient begins eating, drinking and is BAR.

  This is via regular neutral insulin administration or insulin CRI.

  Once the patient is eating (any food at this point) and stable then slowly switch back to routine insulin regimen as per long term DM control.

  If the patient is persistently anorexic - consider tube feeding.
• Prognosis of diabetic ketoacidosis

  Survival to discharge - 70% (good but nor perfect)

  <10% dogs relapse.

  Up to 40% cats relapse.
• Euglycaemic DKA - overview

  A significant risk with using sodium-glucose Cl transport 2 inhibitors.

  These promote loss of glucose and sodium into urine - promoting hypovolaemia and reducing glucose available for energy metabolism. Only use in cats that are type 2.

  Some cats can exhaust their islet cells and have no insulin -> severe negative energy balance -> ketogenesis and acidosis. However urinary losses of glucose mean they are euglycaemic/ normoglycaemic - easy to miss.
• eDKA - diagnosis

  Recent introduction of an SGLT2 inhibitor:

  • 1/15 risk!
  • <14 days after starting treatment.

  Clinical signs consistent with DKA e.g. anorexia/vomiting.

  Ketones in the blood urine, acidosis, normoglycaemia.
• eDKA - treatment

  Same principle as DKA, fluid therapy followed by low dose insulin therapy.

  • However - glucose supplementation (5%) is immediate as they are eyglycaemic.
  • Insulin is started despite blood glucose <7.5mmol/l
  • After cessation of drug - urinary glucose loss continues for 2-3 days, so glucose supplementation must continue.
• Hyperglycaemic Hyperosmolar syndrome - overview

  Pathogenesis is similar to DKA, but a small amount of insulin and hepatic glucagon resistance reduce lipolysis, so ketones are not elevated. However peripheral insulin resistance in tissue still stimulates gluconeogenesis and glycogenolysis mobilising glucose.
• Hyperglycaemic Hyperosmolar syndrome - diagnosis

  BG > 33.3mmol/l

  Absence of urinary ketones.

  Serum osmolality > 350mOsm/kg
• Hyperglycaemic Hyperosmolar syndrome - Treatment

  Fluid therapy is key, however rapid correction of hyperglycaemia (and hypernatraemia) lead to an osmotic gradient across the blood brain barrier - rapid cerebral oedema is possible -> seizure, coma And death.

  Therefore - aim to restore deficit over 24-48 hour, but monitor glucose and sodium very closely.
• Hyperglycaemic Hyperosmolar syndrome - monitoring

  Both of these sets of Pateints are intesive and require regular blood sampling/ glucose monitoring.

  Blood sampling - central venous catheter:

  • Requires 24 hour nursing care, so hospitalised setting is ideal.
  • However, no reason can not be done in 1st opinion hospital.

  Glucose monitoring - freestyle Libra