DKA

What is diabetic ketoacidosis (DKA)?

DKA is a severe complication of diabetes mellitus (DM) characterized by metabolic acidosis plus hyperglycemia, glucosuria, and ketonemia or ketonuria.

How is diabetic ketosis different from DKA?

Diabetic ketosis is the presence of hyperglycemia, glucosuria, and ketonemia/ketonuria without metabolic acidosis; once there is an accompanying metabolic acidosis primarily due to bicarbonate consumption buffering ketoacids, the condition is termed DKA.

In simple terms, what energy imbalance leads to DKA?

DKA arises from critical insulin inadequacy (absolute or relative) that forces the body to switch from glucose to fatty acids as the main energy source, causing excessive ketone body production and accumulation.

How do excess ketones cause metabolic acidosis in DKA?

Ketones (acetoacetate and β-hydroxybutyrate) are anions of strong acids; each ketone produced generates an equimolar hydrogen ion, which is buffered by bicarbonate. When ketone production overwhelms buffering and metabolic pathways, bicarbonate falls and metabolic acidosis develops.

How does insulin deficiency or antagonism drive the development of DKA?

In DM, decreased insulin production or increased insulin resistance/antagonism leads to reduced glucose utilization, increased gluconeogenesis and glycogenolysis, and activation of hormone-sensitive lipase, which increases free fatty acid release, triglyceride formation, and ultimately ketone body production when acetyl-CoA generation exceeds Krebs cycle capacity.

Why can animals with DKA still have “normal” endogenous insulin levels?

Endogenous insulin levels in dogs with DKA range from low to normal; some have normal levels but still develop DKA due to strong counterregulatory hormone activity and relative insulin deficiency, underscoring that absolute insulin deficiency is not the only mechanism.

What are some key negative effects of metabolic acidosis on the body in DKA?

Metabolic acidosis can cause CNS depression, damage to cardiac myocytes, general tissue necrosis, and contributes to hemodynamic instability.

Which electrolyte abnormalities are commonly seen in DKA?

Total body deficits in sodium and potassium are common, and hypokalemia, hypophosphatemia, and hypomagnesemia frequently develop and complicate treatment; serum sodium may be low, normal, or high depending on concurrent free water losses

How and why are phosphorus and magnesium lost in DKA?

Osmotic diuresis promotes urinary loss of phosphorus and magnesium. Treatment with fluids and insulin without supplementation usually worsens these deficits, leading to hypophosphatemia and hypomagnesemia, which can cause hemolytic anemia, neuromuscular signs, and refractory hypokalemia.

What clinical and ECG signs can suggest hypomagnesemia in DKA?

Generalized weakness, ataxia, seizures, hypertension, and arrhythmias (AF, SVT, VT, VF). ECG changes: prolonged PR interval, wide QRS, depressed ST segment, and peaked T waves before arrhythmias develop.

Which cat breeds are reported to be at increased risk for DM and DKA?

Siamese and Abyssinian cats have been reported as at higher risk for DM and DKA.

Which dog breeds are reported to have increased risk for DM (and thus DKA)?

Schnauzers, Samoyeds, and Keeshonds have been reported to be at increased risk for DM, and thus at risk for DKA.

What are general risk factors for DKA development in diabetic patients?

Undiagnosed or poorly controlled DM

Concurrent illness that increases counterregulatory hormone release

Oral or injectable corticosteroid administration

Other diseases such as pancreatitis, UTIs, hepatic lipidosis, chronic kidney disease, and endocrine disorders.

What are differentials for ketonemia or ketonuria?

Acute pancreatitis, starvation, low-carbohydrate diet, and fever.

What serum β-hydroxybutyrate cutoff supports DKA diagnosis in dogs?

In dogs, blood 3-β-hydroxybutyrate >40.1 mg/dL (>3.88 mmol/L) is ~70% sensitive and 92% specific for diagnosing DKA.

What serum β-hydroxybutyrate cutoff supports or rules out DKA in cats?

In cats, serum 3-β-hydroxybutyrate >26.5 mg/dL (>2.55 mmol/L) is ~94% sensitive and 68% specific for diagnosing DKA, while a concentration <26.5 mg/dL (<2.55 mmol/L) effectively rules out DKA

How do you quickly interpret a blood gas for possible metabolic acidosis in DKA?

First assess pH: pH <7.35 = acidemia.

Base excess (BE) and bicarbonate: BE <–4 and/or HCO₃⁻ below reference (often <18 mEq/L) indicate metabolic acidosis.

If PaCO₂ is elevated (>45 mmHg), a respiratory acidosis is present instead; if metabolic acidosis is present, evaluate the anion gap for high-gap causes (ketones, lactate, uremia, toxins).

Should DKA be managed as an outpatient condition?

No. Hospitalization with intensive treatment and close monitoring is recommended for all DKA patients; outpatient therapy is strongly discouraged except in stable diabetic ketosis without acidosis.

Why are multiple IV catheters often recommended in DKA?

DKA management requires frequent sampling and multiple infusions (fluids, insulin, dextrose, potassium, other supplements). Separate catheters help avoid contamination of blood samples by dextrose or potassium infusions and facilitate safe, efficient therapy.

Why should insulin therapy not be started immediately with fluids?

Insulin shifts water and potassium into cells, potentially worsening intravascular volume depletion and electrolyte derangements. Ideally, patients receive IV fluids for ~2–4 hours until intravascular volume is restored (normalized HR/BP, CRT, warm extremities, good pulses) before starting insulin.

When should insulin therapy ideally be started in DKA?

Insulin therapy should typically begin between 2 and 6 hours after initiating fluid therapy, once intravascular volume is restored. Starting insulin too early may worsen hypovolemia and electrolytes; starting it too late (>6 hours) is associated with slower resolution of DKA.

Is the CRI dose different in cats?

Historically cats were dosed at 1.1 U/kg in the bag, but this is no longer recommended; a CRI dose of 2.2 U/kg in the bag has been associated with faster resolution of hyperglycemia and ketonemia without adverse effects.

How should insulin CRI be given relative to sampling lines?

The insulin CRI should run through a separate catheter from the blood sampling line, to avoid contamination and falsely low or high glucose readings. Dextrose and potassium solutions should also be kept out of the sampling lumen.

How is regular insulin used once BG <250 mg/dL in the IM protocol?

Once BG <250 mg/dL, give 0.1–0.3 U/kg SC every 6–8 hours until ketosis resolves; withhold insulin if BG <80 mg/dL.

What is the hybrid insulin protocol for cats with DKA using glargine + regular insulin?

SC glargine 0.25 U/kg q12h plus IM regular insulin 1 U IM q6h if BG >250 mg/dL. Dextrose 2.5% is added to fluids if BG 80–249 mg/dL, and a 0.5 mL/kg bolus of 50% dextrose plus 5% dextrose in fluids is used if BG <80 mg/dL. This combination has been associated with faster resolution of hyperglycemia and ketonemia and shorter hospital stays compared with low-dose CRI in some studies.

When should DKA patients be transitioned to long-acting insulin?

Once the patient is eating, vomiting is controlled, and ketosis has resolved or markedly improved, they can be transitioned from CRI/IM protocols to a long-acting SC insulin regimen

What initial long-acting insulin doses are commonly used in cats post-DKA?

A typical starting dose is 0.5–1 U/cat SC twice daily of glargine or protamine zinc insulin, regardless of previous insulin dose, since insulin requirements may change after DKA.

What initial long-acting insulin doses are commonly used in dogs post-DKA?

In dogs, a common starting dose is 0.25–0.5 U/kg SC twice daily of porcine insulin zinc suspension (Vetsulin/Caninsulin) or neutral protamine Hagedorn (NPH) insulin.

s bicarbonate therapy routinely recommended in DKA?

No. In most cases, appropriate fluid and insulin therapy will correct acidosis.

Bicarbonate therapy is controversial, can worsen hypokalemia, and may cause paradoxical CNS acidosis due to CO₂ generation, especially in hypoventilating patients

When might bicarbonate therapy be considered in DKA?

It may be considered when plasma bicarbonate is <12 mEq/L with severe metabolic acidosis and decompensation, after careful risk–benefit assessment.

What is the “glargine-only” DKA protocol described in cats, and why might it be used?

It uses intermittent IM and SC glargine alone (no regular insulin), with dosing adjusted based on blood glucose, while cats are maintained on IV fluids. It reduces cost by using a single long-acting insulin vial that can be dispensed at discharge, helpful for clinics that rarely treat DKA.

What are potential risks or limitations of the glargine-only protocol for feline DKA?

Less frequent glucose and electrolyte monitoring increases risk of undetected hypoglycemia, arrhythmias, or hemolytic anemia. In one small retrospective study, 15/15 cats survived without clinical hypoglycemia, but 100% were hypokalemic, 80% became hypophosphatemic (42% of those needed phosphorus supplementation), and 2 required transfusions for hemolytic anemia.

What is the overall short-term prognosis for dogs and cats with DKA?

Most studies report that about 70% of dogs and cats with DKA survive to hospital discharge. Median hospitalization time is typically ~5–6 days.

What factors are associated with poorer outcomes in dogs with DKA?

Anemia, hypocalcemia, and more severe acidemia at presentation are associated with worse prognosis and higher mortality in dogs

What factors are associated with poorer outcomes in cats with DKA?

Azotemia, hypermagnesemia, and hyperbilirubinemia at presentation have been associated with worse prognosis in cats.

• High Mg usually means kidneys can’t excrete it, which = significant AKI/CKD, often with hyperphosphatemia, acidosis, and other electrolyte derangements — a classic multi-organ failure picture.

How common are recurrent DKA episodes in dogs and cats?

At least ~7% of dogs and ~18% of cats with DKA will experience a recurrent DKA episode.

What is euglycemic DKA (eDKA), and when should we suspect it in cats?

eDKA is diabetic ketoacidosis with normal or only mildly elevated blood glucose; in cats, it has been reported with sodium–glucose cotransporter-2 inhibitors (e.g., bexagliflozin), especially during periods of decreased caloric intake or concurrent disease. Any SGLT2-treated diabetic cat with lethargy, anorexia, vomiting, or dehydration should be promptly checked for ketones and acid–base status, even if blood glucose is not markedly elevated.