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Endocrine emergencies (Proceedings)

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Oct 01, 2008

Diabetic Ketoacidosis (DKA)

DKA is one of the more common endocrine emergencies seen in veterinary emergency centers throughout the US. It is mostly seen in newly diagnosed diabetics, or ones that have a reason for insulin resistance, such as Pyelonephritis, pancreatitis, or underlying disease.

Pathophysiology

Because glucose can not enter into cells from a lack of insulin (relative or absolute), ketones are synthesized from fatty acids as a substitute for energy. This results in severe acidosis and severe electrolyte abnormalities. The ketone bodies that are formed are beta hydroxybutyrate, acetoacetic acid, or, acetone. The diagnosis is based on evidence of metabolic acidosis (usually pH < 7.3), hyperglycemia, glucosuria, and ketonuria. The ketone strips that recognize ketone bodies in the urine are manufactured to recognize acetoacetic acid, rather then the more commonly formed ketone acid in DKA, beta hydroxybutyrate. This can be overcome by adding hydrogen peroxide to the urine, and then testing with the strip, which will convert the beta hydroxybutyrate to acetoacetic acid.

The synthesis of ketone bodies occurs from 2 units of acetyl-CoA, which condense to from acetoacetyl-CoA in multiple organs. This is then converted to acetoacetate by deacylase in the liver. The liver then converts acetoacetate to beta hydroxybutyrate and acetone. Ketone bodies are metabolized with difficulty in the liver and then enter the blood stream. The initiation of ketone bodies comes from acetyl-CoA, which is the result of B-oxidation of fatty acids. The lack of insulin and increased counter regulatory hormones (mainly glucagon, also catecholamines, glucocorticoids, and growth hormone) results in increased fatty acid oxidation, and hence excess production of acetyl-CoA.

The acidosis results mainly from the formation the of the ketone acids, but also the vomiting, dehydration, and volume contraction contribute. The electrolyte abnormalities most commonly noted in DKA patients are hypokalemia, hypophosphatemia, hyper- or hyponatremia, and hypomagnesemia. No matter what the values on the chemistry panel reveal, patients presenting with DKA are whole body potassium and phosphorous depleted. Hypokalemia results from acidosis, osmotic diuresis, ketonuria, vomiting, and extracellular fluid volume expansion from hyperglycemia. Depending on the severity of hypokalemia, clinical signs can range from muscle weakness, paralysis, respiratory and cardiac depression. Hypophosphatemia can result from metabolic acidosis and renal losses, and during initial therapy with insulin (drives into cells). Clinical signs of deficiency include weakness, respiratory and cardiac dysfunction, hemolytic anemia, decreased tissue oxygenation (loss of 2,3-DPG). Sodium alterations are due to losses through vomiting, diuresis, and the acidosis. Clinical signs of deficit or excess result in altered mental status.

Tests

As with any sick animal a minimum database and diagnostic imaging should be performed. We would recommend a CBC, chemistry with lytes (Na, K, Cl, Mg, Ca, Phos), urinalysis, urine culture (many have urinary tract infections), 3 view chest radiographs, and abdominal ultrasound.

Treatment



Fluids are the most important part of therapy for DKA. Patients suffering from this disease are volume depleted, and fluids alone will dilute out the glucose concentration and help to re-establish renal perfusion to excrete glucose, and correct acid base disturbances. Any replacement crystalloid fluid will help to accomplish these goals, although 0.9%NaCl is the fluid of choice (helps with sodium and chloride losses). Potassium supplementation is also required to replace the hypokalemia that is present, and this can be worsened when insulin therapy is commenced. It is vital to calculate the maximum rate of potassium infusion (0.5 mEq/kg/hr) for the patient to avoid over-supplementing during the treatment process. See chart below for starting recommendations, although the maximum infusion rate is sometimes required. If the patient also has significant hypomagnesemia, the this must be addressed before the hypokalemia will resolve. If the phosphorous is also low then an easy way to supplement, is to give ½ the potassium supplemented as potassium phosphate. The rate of phosphorous supplementation can be 0.01-0.03 mmol/kg/hr.