Metabolic Nightmares: Diabetic KetoAcidosis and hyperosmolar Syndrome

Complications of Diabetes Mellitus

Diabetic ketoacidosis and less commonly hyperosmolar syndrome are serious complications of diabetes mellitus. Both conditions can be challenging to treat although in the short term they have differing prognoses that may have impact when managing the case.

Pathogenesis of Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis (DKA) is a severe complication of unregulated or undiagnosed diabetes mellitus (DM). It can be associated with either an absolute or relative deficiency of insulin. Previously well regulated diabetic cases may develop DKA due to the presence of comorbidities such as urinary tract infections, pyoderma, neoplasia, pancreatitis etc. even in the face of regular insulin injections as a result of peripheral insulin resistance. Although many cases of DKA will be known diabetics a number will present without a previous diagnosis of diabetes, especially cats, although careful questioning will reveal a history consistent with the condition.
Hyperglycaemia caused by a combination of decreased tissue utilisation and increased hepatic glucose production results in an osmotic diuresis resulting in intracellular, interstitial and intravascular dehydration to various degrees depending on the severity. Ketoacids worsen diuresis causing volume depletion and decreased glomerular filtration rate. Diuresis results in loss of solutes including sodium, phosphorus, magnesium, chloride and potassium leading to whole body depletion. Volume contraction worsens hyperglycaemia.
Ketoacids are direct stimulators of the chemoreceptor trigger zone, causing nausea and vomiting. This cycle continues and worsens dehydration contributing to clinical signs.

Hyperosmolar Syndrome

Hyperosmolar syndrome is a rare condition. It develops in a state of glucose deficiency that results in increased hepatic glucose production and decreased glucose utilisation but ketosis is minimal to absent. This is thought to be due to the presence of adequate amounts of insulin to prevent lipolysis but not to prevent hepatic glucogenesis. There is typically very severe hyperglycaemia (30- 80mmol/l) which is often associated with some degree of renal impairment, which may be pre-existent or prerenal. The clinical signs are typically neurological ranging from mild depression to coma depending on the severity and duration of the hyperglycaemia. Neurological derangements are associated with cerebral parnechymal dehydration associated with hyperglycaemia. The prognosis is guarded. A recent paper looking at cats presenting with hyperosmolar syndrome reported a long-term survival rate of 12% with the majority of cases dying or euthanased within the first 10 hours of hospitalisation. [...]