Diabetic Ketoacidosis (DKA) in Dogs and Cats

Diabetic ketoacidosis (DKA) is a serious metabolic complication of diabetes mellitus in dogs and cats, characterized by high blood glucose levels, excessive ketone body production, metabolic acidosis, and dehydration. It most commonly occurs in diabetic patients that have become insulin-deficient or insulin resistant, often in the face of concurrent illness or physiologic stress. If not recognized and treated promptly, DKA can rapidly progress to hypovolemic shock, electrolyte abnormalities, and death.

Veterinary professionals must understand the distinct pathophysiologic mechanisms behind DKA—particularly the shift from glucose metabolism to fat metabolism, ketone formation, and buffering depletion—to effectively stabilize and treat affected patients.

A NAVLE Review Article

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Overview

Diabetic Ketoacidosis (DKA) is an acute, life-threatening metabolic decompensation that occurs in patients with underlying diabetes mellitus. It is classically defined by hyperglycemia, ketonemia/ketonuria, and metabolic acidosis, frequently accompanied by dehydration, electrolyte derangements, and acid-base disturbances.

DKA typically represents a decompensated diabetic crisis triggered by insulin deficiency (absolute or relative) and exacerbated by concurrent disease or physiologic stress. In cats, poor diabetic regulation or failure to treat underlying diabetes can precipitate DKA.

Pathophysiology

Insulin deficiency (absolute shortage or insufficient response) prevents glucose uptake into cells, resulting in persistent hyperglycemia and energy starvation at the cellular level.
Cells respond by lipolysis of adipose tissue, leading to large amounts of free fatty acids (non-esterified fatty acids, NEFAs), which are transported to the liver.
In the liver, fatty acids are converted to ketone bodies (mainly β-hydroxybutyrate and acetoacetate), which in normal amounts can serve as alternative fuel. However, when production overwhelms utilization, ketonemia and ketonuria result.
Accumulation of acidic ketone bodies and depletion of buffering bicarbonate leads to anion gap metabolic acidosis.
Osmotic diuresis induced by hyperglycemia and ketonuria causes urinary water and electrolyte losses, contributing to dehydration, hypovolemia, and electrolyte imbalances (notably potassium and phosphorus).
Hypovolemia can impair renal perfusion and glomerular filtration, reducing excretion of glucose and ketones, which further worsens metabolic derangements.

Precipitating Factors / Triggers

While DKA can occur in animals with previously undiagnosed diabetes, more commonly it is triggered by precipitating factors that increase insulin demand or reduce insulin effect:

Concurrent illnesses: pancreatitis, urinary tract infections, pneumonia, other infections.
Insulin omission or underdosing in known diabetic patients.
Physiologic stressors: surgery, trauma, heat stroke, or other stress that increases counter-regulatory hormones (glucagon, catecholamines, cortisol).
Iatrogenic factors: glucocorticoid therapy, infection-induced insulin resistance.

Clinical Presentation

Patients with DKA often present in emergent condition, and clinical signs reflect the combined effects of hyperglycemia, ketonemia, metabolic acidosis, dehydration, and underlying disease.

Common signs include:

Polyuria and polydipsia (PU/PD) — often historical signs of diabetes.
Anorexia or inappetence, vomiting, nausea.
Lethargy or depression, weakness, dehydration, and often weight loss or muscle wasting.
Dehydration and signs of hypovolemia: tacky mucous membranes, delayed capillary refill time, reduced skin turgor.
Acetone or “fruity” breath odor in advanced cases.
Tachypnea or respiratory compensation (Kussmaul breathing or deep, slow respiration) due to metabolic acidosis.
Neurologic signs and collapse or coma in severe cases, especially if acid-base and electrolyte derangements are profound.

In cats, signs may overlap with uncomplicated diabetes (PU/PD, weight loss) but often include significant anorexia, vomiting, and dehydration. Some cats may present in ketoacidotic crisis without a prior diagnosis of diabetes.

Diagnostic Approach

Diagnosis of DKA in veterinary patients relies on a combination of clinical assessment, laboratory diagnostics, and detection of metabolic derangements.

Key diagnostic findings include:

Test / Parameter	Typical Findings in DKA
Blood Glucose	Markedly elevated — often > 300 mg/dL (dogs) or even higher in cats.
Urinalysis	Glucosuria, ketonuria (with acetoacetate or β-hydroxybutyrate), possibly acetone.
Blood Gas / Acid-base	Metabolic acidosis: low bicarbonate, low pH, increased anion gap.
Electrolytes	Often hypokalemia and hypophosphatemia (or total body deficits), although serum values may appear normal or elevated initially. Hyponatremia may be observed.
Hydration / Renal parameters	Evidence of dehydration, azotemia (pre-renal or renal), elevated BUN/creatinine.
Serum ketone measurement	β-hydroxybutyrate (if available) is more reliable than urine dipsticks for ketone quantification.
Additional diagnostics	CBC and biochemistry to assess concurrent disease (e.g. pancreatitis, infection), abdominal imaging as indicated, electrocardiography for electrolyte-mediated arrhythmias.

Differential diagnoses include uncomplicated diabetes mellitus, hyperosmolar hyperglycemic syndrome (especially in cats), renal disease, gastrointestinal disease with vomiting/diarrhea, and other causes of metabolic acidosis.

Treatment and Management

DKA is a medical emergency that necessitates intensive, hospital-based management, frequent monitoring, and a stepwise therapeutic approach. The main therapeutic goals are to restore perfusion and hydration, correct metabolic derangements, reduce hyperglycemia, manage acidosis, and treat or identify underlying trigger conditions.

Key therapeutic steps include:

Fluid therapy
- Begin with isotonic crystalloids (e.g. 0.9% NaCl) to address dehydration, restore vascular volume, and correct electrolyte imbalances.
- Careful reassessment of hydration status, perfusion, and electrolyte needs is essential.
Insulin therapy
- Regular insulin is the treatment of choice in DKA and should only be administered after initial fluid resuscitation to avoid precipitous drops in blood glucose and worsening of electrolyte shifts.
- Constant Rate Infusion (CRI) regimens are commonly used; Merck provides protocols (e.g. 2.2 U/kg for dogs or 1.1 U/kg for cats in 250 mL saline, with adjustments based on serial glucose measurements).
- Goal is to gently reduce the rate of decline in blood glucose — ideally no more than 50–100 mg/dL per hour — to avoid cerebral edema or hypoglycemia.
Electrolyte supplementation
- Potassium: Hypokalemia is frequently seen or will worsen with insulin therapy; potassium supplementation is critical once renal function and urine output are adequate.
- Phosphorus: Hypophosphatemia is common and can contribute to muscle weakness and hemolysis; supplementation may be required.
- Monitoring sodium and chloride is important, but supplementation must be done cautiously to avoid rapid osmotic shifts.
Acid-base management
- The metabolic acidosis of DKA often corrects with fluid and insulin therapy alone. Bicarbonate therapy is controversial and usually reserved for severe acidosis (e.g. pH < 7.0) or if acidosis is not improving with standard therapy.
Addressing concurrent or precipitating conditions
- Identifying and treating underlying diseases (e.g., pancreatitis, infections, renal disease, Addison’s, or diabetic management lapses) is critical to resolution and prevention of relapse.
- Antibiotics, antiemetics, analgesia, nutritional support, and gastrointestinal protection may all be required depending on individual patient needs.
Nutritional support
- Once vomiting has resolved and the cat or dog is stable, feeding should be reintroduced carefully to avoid further metabolic derangements and to support recovery. The timing and type of nutrition vary by species and patient status.

Monitoring and Reassessment

Close monitoring is essential throughout hospitalization to guide therapy and detect complications:

Serial blood glucose every 1–2 hours during insulin CRI, transitioning to longer intervals once stable.
Frequent electrolytes (K⁺, P⁺, Na⁺, Cl⁻) and blood gas / bicarbonate monitoring.
Urine output and hydration status.
Clinical status, including neurologic function, hydration, perfusion, vomiting, and appetite.
Monitoring for hypoglycemia, overcorrection of glucose, or rebound hyperglycemia.
Monitoring for therapy-related complications such as hypokalemia, hypophosphatemia, cerebral edema, fluid overload, or electrolyte-induced arrhythmias.

Complications and Prognosis

Complications of DKA and its management can be significant:

Hypokalemia — persistent or worsened by insulin therapy, potentially causing muscle weakness, ileus, or cardiac arrhythmias.
Hypophosphatemia — can lead to hemolysis, muscle weakness, and respiratory compromise.
Cerebral edema or neurologic deterioration if blood glucose is corrected too rapidly.
Hypoglycemia if insulin is over-corrected or if nutritional support is inadequate.
Pulmonary edema or volume overload, particularly in patients with compromised cardiac or renal function.

Prognosis is variable and depends on timely diagnosis, aggressive and appropriate therapy, and the severity of concurrent disease. Cats and dogs with severe DKA, delayed treatment, or significant concurrent illness have a guarded to poor prognosis. However, with early intervention and adequate management, many patients can recover from DKA and resume diabetic care.

NAVLE High-Yield Points

For NAVLE exam preparation, veterinary students should focus on the following high-yield takeaways for DKA:

DKA is a decompensated diabetic emergency characterized by hyperglycemia, ketonemia/ketonuria, and metabolic acidosis combined with dehydration.
Fluid therapy must precede insulin therapy to avoid worsening hypovolemia or precipitating central nervous system complications.
Insulin should be administered carefully — constant rate infusion (CRI) of regular insulin is standard, and blood glucose should not be lowered too quickly (limit ~50–100 mg/dL/h).
Potassium supplementation is critical from the early phase of therapy because insulin-driven intracellular shifts and osmotic diuresis can cause or worsen hypokalemia.
Phosphorus supplementation may be required to avoid complications such as hemolysis or respiratory muscle weakness.
Look for and treat concurrent diseases (e.g. infections, pancreatitis, insulin omission) which may have precipitated the DKA episode.
Recognize that cats may present in DKA without prior diagnosis of diabetes and may have more prominent GI signs and dehydration.
Be alert for treatment complications such as cerebral edema, hypoglycemia, and electrolyte disturbances.