Feline endocrine emergencies (Proceedings)


Diabetic ketoacidosis (DKA) is one of the most commonly encountered endocrine emergencies in small animal practice. DKA is typically seen in previously undiagnosed diabetics and less commonly occurs in patients that are on inadequate amounts of insulin.

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is one of the most commonly encountered endocrine emergencies in small animal practice. DKA is typically seen in previously undiagnosed diabetics and less commonly occurs in patients that are on inadequate amounts of insulin. In patients currently receiving insulin, DKA is typically seen in those with a concurrent illness leading to insulin resistance. The pathogenesis of DKA is multifactorial; the four underlying causes include insulin deficiency, diabetogenic hormone excess (catecholamines, cortisol, glucagons, growth hormone), fasting, and dehydration. The interplay between these factors further antagonizes the situation.

Clinical Findings Patients with DKA are divided into those that are "healthy" and those that are sick. Healthy DKAs only display clinical signs typical of diabetes (pu-pd, polyphagia, weight loss) and present without a history of vomiting, anorexia, or lethargy. Typically these patients have only trace-to-small amounts of ketonuria noted. Healthy DKA's can be treated like uncomplicated diabetics.

Sick DKA patients have other systemic signs such as vomiting and lethargy. Physical exam findings may include depression, dehydration, weakness, tachypnea – this may progress to Kussmaul respiration (slow, deep breathing) due to acidosis and an acetone odor to the breath. It is not uncommon for patients in DKA to be presented semicomatose. These patients are true EMERGENCIES!!! Signs may reflect concurrent illnesses as well.

Diagnosis DKA can be rapidly and easily diagnosed. The criteria for establishing this diagnosis include hyperglycemia, glucosuria, ketonuria, and metabolic acidosis. The presence of hyperglycemia which can be documented using a portable glucometer or point-of-care analyzer in combination with glucosuria and ketonuria (detected using urine reagent strips) in a patient with appropriate clinical signs is usually sufficient to establish the diagnosis and begin treatment. Whenever you suspect that a patient may be suffering from DKA, immediately check urine for the presence of both glucose and ketones! Metabolic acidosis can be documented by doing a venous or arterial blood gas. For the purpose of analyzing pH, a venous blood gas is sufficient. Normal pH is 7.35-7.45. Bicarbonate (tCO2) is often included on biochemistry profiles and will be decreased in acidotic patients. A minimum database (CBC, biochemistry profile, complete UA with culture) is crucial to thoroughly rule out any concurrent disorders such as pancreatitis. It may be difficult to initially assess renal function due to the presence of pre-renal azotemia and an osmotic diuresis secondary to the glucosuria.


Fluids and Electrolytes Fluids are the most crucial aspect to treating DKA. Rehydration alone will lower blood glucose concentrations. It is often beneficial therefore to start patients on fluids for a few hours prior to giving insulin. Normal saline is typically considered to be the fluid of choice because patients suffering from DKA are most often whole-body sodium depleted. Dehydration should be corrected over 24 hours. Fluid therapy is critical in treating electrolyte imbalances. Most DKA's are moderately to severely hypokalemic. Their initial blood work may not reflect this deficit. In acidosis, K+ often comes out of the cells as H+ ions move intracellularly, masking severe hypokalemia. As treatment begins to correct the acidosis, the serum K+ concentration will drop. Insulin also causes K+ to move intracellularly. The initial hypokalemia stems from K+ loss through urine and GI and decreased intake due to anorexia. [K+] should be monitored once to twice daily. The rate of supplementation will depend on measured values. If the initial K+ is within normal limits, add 20-40 mEq of K+ to the fluids (½ as KCl, ½ as KPO4). If it is elevated initially, make sure the patient is producing urine & reassess. If it is low, larger amounts of K+ will need to be added. It may be important to calculate the maximum rate of K+ infusion (0.5 mEq/kg/hr) to avoid over-supplementing. Clinical signs of hypokalemia include weakness, ventral flexion of the head and neck, and ileus.

Phosphate moves similarly to K+. Patients in DKA are typically hypophosphatemic due to renal losses. Initial bloodwork may not reveal this as acidosis causes phosphate to move extracellularly. Hypophosphatemia can be life-threatening. If levels fall < 1.5 mg/dl, hemolytic anemia may develop. Phosphate should also be monitored a minimum of once to twice daily. To calculate how much to supplement, you can use the formula: Phosphate supplementation = 0.01-0.03 mmol/kg/hr. However, it is easier to calculate the amount of K+ needed and give ½ as KCl and ½ as KPO4.

Hypomagnesemia, while commonly present in DKA, rarely requires therapy. Typically, the hypomagenesemia will resolve without specific treatment as the ketoacidosis resolves. Clinical signs referable to hypomagnesemia are not seen unless total levels are < 1 mg/dl and ionized levels are ,<0.5 mg/dL. Hypomagnesemia should be treated in patients with refractory hypokalemia or hypocalcemia. Other clinical signs that may be seen due to low magnesium are non-specific and include lethargy, anorexia and weakness.

Acid-base status Correcting hypoperfusion with appropriate fluid therapy is very beneficial for correcting the acidosis. Most patients won't require specific therapy for their acidosis. If the patient is extremely depressed and has a pH < 7.1 or a CO2 < 12 mEq/L, bicarbonate therapy should be considered. Any efforts to change pH should be done slowly so as not to cause rapid alterations in the pH of the CSF. Dose: mEq bicarb = body weight (kg) x 0.4 x (12 – patient's bicarb) x 0.5. Give this over 6 hours and then reassess.

Insulin therapy It is crucial that cats receive insulin as part of their therapy for DKA. In some cats, it is possible to lower blood glucose concentrations into the 200s (mg/dL) purely through rehydration and without concurrent insulin treatment. While tempting to do so, patients need insulin in order to resolve ketosis. It may be necessary to place the cat on 2.5% dextrose in order to administer insulin.

Many clinicians use an intermittent intramuscular regime. Regular insulin is used because it has a rapid onset and a brief duration of effect. An initial dose of 0.2 U/kg IM is followed by subsequent doses of 0.1 U/kg IM q 2hr. BG should not drop faster than 50-75 mg/dl/hr! Hyperglcemia typically resolves in 4-8 hr whereas it may take 1-2 days to resolve ketosis. Once the patient is eating and otherwise stable, switch to longer acting insulin such as glargine.

A constant low-dose intravenous infusion of regualr insulin can also be done. Add 1.1 U/kg of regular insulin to a 250 ml bag of 0.9% saline. Insulin binds to plastic so it is crucial to run out the first 50 ml of the insulin-containing fluid prior to administering it to the cat. The insulin-containing fluid is initially administered at 10 ml/hr. As the blood glucose concentration drops, the rate of infusion can be lowered. This route requires extremely close supervision. It is imperative that the infusion's rate be lowered or discontinued all-together as the blood glucose concentration drops. As the patient stabilizes and blood glucose concentrations drop to more acceptable levels (200-250 mg/dL), the cat can be switched over to intermittent intramuscular or subcutaneous injections. Alternatively, the cat can continue on the CRI until it is ready to be switched over to long-lasting insulin. Lispro insulin has been used successfully as an IV infusion to treat DKA in dogs; Lispro insulin still requires study to see if it is safe and effective treatment for DKA in cats.

Blood Glucose and Dextrose

The goal is to keep the BG in the 100-300 range. The dextrose in the fluids and the dose of insulin administered will have to be adjusted to achieve this. Patients initially need to have their BG checked q 2 hours and changes made accordingly. As glucose concentrations stabilize, they can be monitored less frequently.

A study presented in 2010 at ACVIM found that cats in DKA treated with a combination of SQ glargine and IM regular insulin resolved their metabolic acidosis faster than cats treated with an IV regular insulin protocol. There was no difference in mortality, length of hospital stay or resolution of ketonemia.

Hyperosmolar Nonketotic Diabetes Mellitus (HONKDM)

This is a less common complication of DM, however it is not uncommon in cats. It has a similar pathogenesis to DKA with a relative deficiency in insulin. For the hyperosmolar syndrome to develop, some functioning beta cells must still be producing insulin. The existence of some insulin prevents the formation of ketones. Excessive dehydration leads to a decrease in GFR which leads to a decrease in glucose excretion. Hyperglycemia worsens and causes an increase in plasma osmolality. Increased plasma osmolality draws water out of cerebral neurons → obtundation → less water intake → vicious cycle.

HONKDM is characterized by:     1) severe hyperglycemia (BG > 600 mg/dl)     2) hyperosmolarity > 350 mOsm/kg [2(Na + K) + 0.05(glucose) + 0.33(BUN)]     3) dehydration and     4) lack of ketones.

These patients may still be acidotic despite their lack of ketones because 1) -hydroxybutyrate is a ketone which is not detected with urine strips (to detect, add a drop of H2O2 to the urine) and 2) lactic acidosis is the end product of anaerobic metabolism of glucose. One study of cats suffering from HONKDM found that the vast majority (90%) of cats suffered from an extremely serious, concurrent disease such as renal disease or heart failure.

Clinical Findings Patients typically are quite depressed, even comatose. Weakness may have been present for several weeks prior to presentation. Prior to lethargy and depression, cats will have a preceding history consistent with DM including polyuria-polydipsia, polyphagia and weight loss.

Treatment Similar treatment as for DKA. Imbalances must be corrected very slowly. Fluid therapy is typically either 0.9% NaCl or 0.45% NaCl. Caution must be exercised to not decrease osmolarity too quickly. Decrease it by ½ - 1 osmol/hour. The goal should be to correct dehydration over 36 hours. Insulin therapy should be delayed for a few hours to allow for some correction of dehydration, electrolyte imbalance, renal function, and stabilization of blood pressure. While patients may still be hypokalemic, this abnormality does not tend to be as severe as in DKA because they do not have as great of an osmotic diuresis. Patients with hyperosmolar diabetes may be hyperphosphatemic depending on the azotemia. Hypophosphatemia is less of a concern in HONKDM. Insulin therapy is the same as for DKA, but extreme caution should be exercised to avoid precipitously dropping blood glucose concentrations and thus osmolality.. These patients must be monitored very closely! Monitor urine output, electrolytes and renal values 1-3 times daily. The prognosis for HONKDM is guarded, particularly if there is a serious concurrent disease.

Hyperthyroidism -Thyroid Storm

Thyroid storm is a term used in human medicine to describe a life-threatening multisystemic disturbance due to elevated thyroid hormone levels. In humans, thyroid storm is usually associated with a precipitating event such as infection, surgery or trauma. There are 4 main features to the clinical picture in humans: 1) fever 2) tachycardia or supraventricular arrhythmias 3) central nervous system symptoms 4) gastrointestinal symptoms. Humans suffering from a "thyroid storm" have a very high mortality rate. It is currently debated whether feline patients suffer from a similar "thyroid storm". Certainly cats suffer from thyrotoxicosis (elevated thyroid hormone levels).

Clinical signs Thyrotoxic cats may display a variety of clinical signs. Historically, owners may complain of polyphagia with weight loss, vomiting, diarrhea, polyuria-polydipsia and behavior changes such as irritability. More emergent clinical signs include evidence of respiratory distress such as open-mouth breathing and tachypnea. The cat may be so stressed that he/she appears "panicked" and becomes extremely agitated with handling. Physical examination typically reveals a palpably enlarged thyroid gland. A gallup rhythm or cardiac murmur is frequently auscultated. Many hyperthyroid cats suffer from cardiac hypertrophy. If the cat has progressed to heart failure, evidence of pulmonary edema such as crackles or pleural effusion such as dullness of the lung fields may be auscultated. Thyrotoxicosis may result in thromboembolic disease, often manifested in cats as a "saddle thrombus" with the cat presenting for acute paraplegia. Acute blindness secondary to retinal detachment due to systemic hypertension may be present. Severe hypokalemia or thiamine deficiency may result in muscle weakness and ventroflexion of the neck.

Treatment It is critical to avoid stressing the cat as much as possible. If one is available, place the cat in an oxygen cage to provide supplemental oxygen. Most other ways of delivering supplemental oxygen such as nasal cannulas or face-mask are too stressful for these fragile cats. Cats displaying cardiac manifestations should be immediately treated with a beta-blocker such as atenolol (6.25-12.5 mg/cat/day) or propanolol (2.5–5 mg/cat q 8-12 hr or 0.02 mg/kg IV slowly). Production of thyroid hormone will need to be addressed. Methimazole (2.5-5 mg/cat q 12 hr) inhibits the organification of iodide, thus preventing the synthesis of new thyroid hormone. It may take up to a week however to see a decline in serum T4 levels. In critical cases, it may be necessary to block the secretion of already formed hormone. Iopanoic acid, a lipid-soluble radiographic contrast agent, blocks peripheral conversion of T4 to T3. The dose is 50-200 mg/cat BID PO. The systemic effects of thyrotoxicosis must also be addressed. Most of these cats will be hypovolemic so intravenous fluid therapy should be considered. Fluids will help treat pyrexia if that is a component of the presentation as well. Severe pyrexia may require additional cooling methods such as fans or cool water baths (if that doesn't excessively stress the cat). Potassium and vitamin B supplementation should be administered in cats displaying cervical ventroflexion. In humans suffering from "thyroid storm" glucocorticoids are recommended to decrease circulating hormone levels. The use of glucocorticoids has not been evaluated for this purpose in cats.

Blindness Systemic hypertension may result from hyperthyroidism. Systemic hypertension may result in a variety of ophthalmic problems including retinal detachment, hemorrhage or edema. It is important to consider hyperthyroidism as an underlying etiology in any cat that presents for acute blindness. Systemic hypertension may be documented at the same time that hyperthyroidism or it may not manifest for many months, even after initiation of treatment for hyperthyroidism.

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