Melissa S. Wallace, DVM, Diplomate ACVIM
1. Primary Hypoadrenocorticism
a. Clinical presentation
Iatrogenic cases have a history of lysodren therapy or adrenalectomy. Most cases are naturally occurring.
History: waxing and waning lethargy, weakness, or collapse, +/- bloody diarrhea, vomiting, anorexia.
Prolonged capillary refill time, poor peripheral pulse, bradycardia, and possible arrhythmias.
b. Laboratory results
Lymphocytosis and/or eosinophilia (in a stressed animal)
Azotemia, usually prerenal
Inadequate urine concentration
c. Other diagnostic results
Microcardia and reduced pulmonary vasculature on chest radiograph
ECG changes associated with hyperkalemia: e.g. prolonged PR interval, widened QRS complex, absent P waves, sinoventricular rhythm
d. Acute management
Avoid stressful diagnostic procedures!
Start shock treatment with IV 0.9% saline at 90 ml/kg (dog). Give half the shock dose and reassess, continue rate if needed.
Hyperkalemia usually does not require specific therapy other than aggressive saline administration. If a sinoventricular rhythm is present, give 10% calcium gluconate at 0.5 - 1 ml/kg slowly IV to counteract the effects of hyperkalemia on the myocardium. In less severe cases, or in addition to the calcium, you may administer insulin with dextrose and/or sodium bicarbonate, both of which work by shifting potassium intracellularly. Give regular insulin at 0.5 unit/kg IV and immediately give a slow IV bolus of 1 gram of dextrose per unit of insulin administered. Place the same amount of dextrose in the IV fluids to be administered continuously over the next six hours, and monitor the blood glucose of the patient. The dose of sodium bicarbonate is 2.2 mEq/kg as a slow IV bolus. Sodium bicarbonate is the safest, calcium gluconate is the quickest, and the insulin/dextrose is the most effective.
Do an ACTH stimulation test while shock fluids are being administered.
Give glucocorticoids: prednisolone sodium succinate at 20 mg/kg IV (after ACTH stim. samples are drawn) or dexamethasone sodium phosphate at 4 - 8 mg/kg IV.
After shock fluids, continue saline at 120 ml/kg/day (2X maintenance). Adjust the fluid rate based on clinical signs of volume repletion, hydration status and resolution of hyponatremia.
If the patient does not respond adequately to shock treatment, consider colloid therapy (e.g. hydroxyethylstarch at 10 - 20 ml/kg IV). Reduce the daily crystalloid dose by 40%.
Mineralcorticoid therapy does not need to be started until the ACTH stimulation test results are back, as long as the patient is receiving IV fluid support. Choices are oral daily fludrocortisone acetate or injectable desoxycorticosterone pivalate (q ~ 28 days).
2. 'Atypical' hypoadrenocorticism
a. Syndrome description
Some animals are deficient in cortisol but not aldosterone, and therefore do not have typical electrolyte changes. Examples are early primary cases, iatrogenic cases (sudden withdrawal of glucocorticoids, most lysodren overdoses), or secondary to a pituitary deficiency of ACTH.
If the patient is cortisol deficient only, give glucocorticoid but not mineralcorticoid replacement.
Hyperadrenocorticism (complications that may present as emergencies)
1. Pulmonary thromboembolism
Dogs and cats with hyperadrenocorticism may present on an emergency basis with respiratory distress due to pulmonary thromboembolic disease.
b. Diagnosis of PTE
Acute dyspnea, hypoxia, +/- jugular pulse
Normal chest radiograph, or blunting of pulmonary arteries with underperfusion of some lung lobes and overperfusion of others, occasionally pulmonary infiltrates.
Decreased arterial PaO2 (<80 mm Hg) and PaCO2
Evidence of pulmonary hypertension on cardiac echo; scintigraphy scan with abnormal perfusion and normal ventilation; confirmation with pulmonary arteriogram (may not be possible in critical patient).
c. Acute Management
Oxygen and cage rest.
Heparin therapy to prevent further thrombus formation; give an initial dose of 200 IU/kg, followed by 50 - 150 IU/kg TID - QID SC. Adjust the dose to prolong the APTT or ACT is 2 - 2.5 times normal.
+/- warfarin; 0.2 mg/kg loading, followed by 0.05 - 0.1 mg/kg PO SID. Adjust the dose after 3 - 4 days to achieve a PT of 1.5 - 2.5 times normal. Discontinue the heparin gradually after a few days of warfarin therapy.
Fresh frozen plasma, if animal's ATIII is low
d. The prognosis is grave if the PTE is large.
a. Clinical Presentation
Dogs and cats with hyperadrenocorticism are prone to infections due to the immunosuppressive effects of glucocorticoids. The infections may involve lungs, skin, joints, urinary tract, prostate, heart valves, etc. Classical presentation is fever and shock (poor perfusion, brick red or muddy mucous membranes, tachycardia) in an animal with physical or historical signs of hyperadrenocorticism.
b. Acute Management:
Search for underlying infection; culture the urine, blood, and joint fluid if indicated. Once stable, radiograph the chest, and ultrasound the heart valves, kidneys, etc.
Treat for septicemia and shock with IV crystalloids, IV broad-spectrum bacteriocidal antibiotics, +/- glucocorticoids.
Monitor response: peripheral pulse, capillary refill time, CVP, blood pressure, heart rate, temperature, urine output, and mental status. If response is poor, use colloid therapy.
If patient is still hypotensive after appropriate volume replacement and colloids, consider pressor or inotropic support (e.g. dopamine, dobutamine).
c. Prognosis is guarded to good.
3. Neurological signs
Dogs or cats with pituitary macroadenomas may present with signs related to the space-occupying mass in addition to the endocrine manifestations. Neurological signs are usually initially subtle, but on an emergency basis a patient may present with confusion, decreased level of consciousness, pacing, ataxia, head pressing, blindness, seizures, or coma. Common differentials include a side effect of lysodren, another type of brain tumor, or a cerebral vascular accident (stroke).
b. Acute management
If the diagnosis is a pituitary macroadenoma there is no truly effective therapy at this stage of the disease. However, because other brain tumors may be resectable or respond more quickly to radiation therapy, and a stroke may improve over time, initial therapy for cerebral edema with mannitol (1 g/kg IV over 20 - 30 minutes) is indicated. High dose short-acting steroids should be considered. Try methylprednisolone sodium succinate 30 mg/kg IV followed by 15 mg/kg IV two and six hours later.
c. The prognosis is grave.
1. Clinical presentation
a. Syndrome description
Clinical signs, when present, are a result of secretion of catecholamines (e.g. norepinephrine, epinephrine) by an adrenal medulla tumor. These tumors may be benign or malignant, but are often invasive. The signs often wax and wane or are vague. Sometimes, the clinical presentation is secondary to tumor embolism or hemorrhage from invasion of the tumor into a major abdominal vessel (e.g. vena cava). This disease tends to afflict geriatric patients. It is uncommon in dogs and rare in cats.
b. Clinical signs and physical examination findings
Generalized weakness, episodic collapse
Anxiety, restlessness, panting
Heart disease (hypertrophic cardiomyopathy, arrhythmias)
Pallor, weak pulses
c. Acute management
Supply oxygen and cage rest if needed.
Monitor blood pressure, blood gases, ECG
Start alpha blocker therapy with phenoxybenzamine (0.5 - 1.5 mg/kg BID to effect) to block the effects of catecholamine release if the diagnosis is strongly suspected based on signs, blood pressure, echocardiogram, ECG, and abdominal ultrasound.
It may also be necessary to use a beta-blocker such as propranolol to control tachyarrhythmias. Start this after alpha blockade to avoid severe hypertension.
Avoid drugs which exacerbate catecholamine effects (e.g. halothane, atropine)
d. Prognosis is guarded to poor.
Hyperparathyroidism, Hypervitaminosis D, and Hypercalcemia
a. Types of hyperparathyroidism
Primary - usually a parathyroid gland adenoma in a geriatric dog or cat.
Secondary - usually from chronic renal failure - does not cause the syndrome discussed here.
Tertiary - usually from chronic severe renal failure.
b. Hypervitaminosis D
Toxic - from ingestion of a vitamin D containing rodenticide (Rampage®, Quintox®).
Iatrogenic - from oversupplementation of vitamin D
2. Clinical presentation
a. Physical signs
The clinical signs are from hypercalcemia, which is a result of either too much parathyroid hormone or too much vitamin D. These syndromes are distinctly different, particularly in phosphorus balance, but the emergency management is usually the same.
Signs of hypercalcemia are lethargy, polyuria/polydipsia, anorexia, vomiting, and weakness.
3. Acute management
a. Confirm the hypercalcemia; spurious hypercalcemia is common
b. Fluid therapy
If the total calcium exceeds 14 mg/dL, the ionized calcium exceeds 7 - 8 mg/dL, or the calcium x phosphorus product exceeds 55, start IV 0.9% saline.
Give maintenance (60 ml/kg/day) plus replacement of dehydration (% dehydration x B.W.(kg) x 1000 = ml of fluid) over 6 - 24 hours (depending on severity of hypercalcemia and clinical signs).
After rehydration, continue diuresis by giving 2 times maintenance (120 ml/kg/day) of saline IV.
If fluid therapy does not significantly improved hypercalcemia within 24 hours, and the calcium is in excess of 15 mg/dL, consider drug therapy.
c. Drug therapy
Furosemide at 5 mg/kg IV. In severe cases, this can be followed by a constant rate infusion of 5 mg/kg/hr IV. Moderate cases may respond to less aggressive therapy, such as 2 - 4 mg/kg BID IV, SC, or PO. Avoid dehydration by adjusting IV fluid rate as needed.
Sodium bicarbonate can be given, especially if concurrent acidosis is present. This will lower the ionized calcium, which is the important goal. Give 1 - 2 mEq/kg as a slow IV bolus, or place in an infusion over 6 hours. Avoid the creation of a severe metabolic alkalosis, which can causes significant morbidity.
Glucocorticoids may reduce hypercalcemia in some cases, but may interfere with the diagnosis of an important differential (lymphosarcoma) and exacerbate other differential diagnoses (blastomycosis, osteomyelitis). Give prednisone 1 - 2.2 mg/kg BID SC or PO.
Calcitonin may be helpful in patients with cholecalciferol rodenticide toxicity. Give 4 - 8 IU/kg SC BID.
The prognosis is good for primary hyperparathyroidism with surgery, guarded to good for cholecalciferol toxicity depending on severity and finances, and grave for chronic end-stage renal failure (unless hemodialysis or transplant is provided).
1. Clinical presentation
Primary hypoparathyroidism occurs uncommonly in young adult dogs. In cats it is rare, usually seen in young adult to middle aged cats. Iatrogenic hypoparathyroidism is more common in older cats after bilateral thyroidectomy for hyperthyroidism, or in dogs after parathyroidectomy.
Another common cause of hypocalcemia is periparturient tetany, which is a combination of inadequate calcium mobilization and excess calcium loss.
The signs of hypoparathyroidism are due to hypocalcemia.
Signs are weakness, a stilted gait, muscle tremors, apparent anxiety or irritability, pruritis of the ears and face (cats), and tetanic convulsions.
2. Acute management
Stop tetanic convulsions with a slow (15 minutes) bolus of 10% calcium gluconate IV at 0.5 - 1.5 ml/kg to effect.
For periparturient tetany, after the bolus above, give an equal amount of calcium gluconate SC, diluted with saline to 5%, and send the pet home on oral calcium carbonate supplementation. Do not allow the offspring to nurse for 24 hours, and send milk replacer and bottles home with the owner.
For primary or iatrogenic hypoparathyroidism, start an IV constant rate infusion of calcium gluconate in saline or a balanced electrolytes solution (check for precipitation if lactate or acetate is present) at a rate of 60 - 90 mg/kg/day of elemental calcium. 10% calcium gluconate = 9.3 mg/ml of elemental calcium.
Initiate vitamin D therapy with calcitriol at 0.03 - 0.06 ug/kg/day. Alternatively, use dihydrotachysterol at a loading dose of 0.03 mg/kg/day divided, tapering to 0.01 - 0.02 mg/kg/day after 2 - 3 days of therapy. With either drug, monitoring of calcium and frequent dosage adjustments are necessary during initial regulation. Formulation of the drug into small doses by a pharmacist is usually necessary.
1. Clinical presentation
a. Hyperthyroid Cats
Typical signs include weight loss, tachycardia, polyphagia, polyuria, polydipsia, nervousness, irritability, G.I. signs, and a poor hair coat. Rarely, anorexia and lethargy are reported. A palpable thyroid nodule(s) is usually present, along with tachycardia and a heart murmur, gallop, or arrhythmia. Rarely, a cat may have striking ventroflexion of the neck.
Cats may present in a "thyroid storm" with severe tachycardia, open-mouthed breathing, hypoxia, and a "panic-attack" mental status. These cats may become aggressive and/or hysterical with handling.
b. Hyperthyroid Dogs
Hyperthyroidism is rare in the dog, and is usually caused by an overdosage of thyroid hormone supplementation, or a thyroid tumor. The tumors are usually palpable and often malignant. Signs are similar to the cat.
c. Acute Management
Reduce stress! Too much handling or restraint (blood draws, catheter placement, radiographs) will exacerbate catecholamine release, and can precipitate a stroke or a fatal cardiac arrhythmia.
Give supplemental oxygen and cage rest. Do not attempt to place an oxygen face mask on a hypoxic 'thyroid storm' cat!
Start a beta-blocking agent ASAP. Propranolol is the drug of choice because it blocks both the peripheral and cardiac effects of thyrotoxicosis, while more cardiac specific beta-blocking agents (e.g. atenolol) do not block the peripheral effects. Dose: Cat 1 - 2 mg/kg BID - TID; Dog 0.2 - 1 mg/kg BID - TID, to effect.
1. Hypothyroidism in dogs as an emergency
a. Myxedematous Coma
In very rare canine cases, severe hypothyroidism can present with a "myxedematous crisis". These dogs have chronic and severe untreated hypothyroidism with classic clinical signs, in addition to the "crisis". The syndrome is characterized by a tragic facial expression with nonpitting edema of the face and head, hypothermia, bradycardia, hypotension, hypoventilation, and extreme weakness, stupor, or coma. The mortality rate is high.
b. Acute treatment
Supportive care for coma; temperature regulation, frequent turning, padded cage, skin care, bladder management as needed.
Fluid therapy for circulatory support. Monitor for hypoxia, hypoglycemia, and hypotension and treat each as needed.
Start sodium levothyroxine supplementation, which must be given initially by injection, preferably IV, at a dose of 5 ug/kg q 12 hours.
Animals with diabetes mellitus that are receiving insulin therapy or oral hypoglycemic agents may develop hypoglycemia. The clinical signs are initially subtle (drowsiness, confusion, weakness, an uncoordinated gait) and become more severe if not addressed (collapse, tremors, seizures, coma).
b. Acute management
Home management of mild cases involves feeding of simple sugars such as honey or corn syrup. If the pet is able to eat a meal, that is helpful.
For clinic cases, give 50% dextrose (diluted to a 20% solution) at ¼ - ½ gram per kilogram as a slow IV bolus, and then add 50% dextrose to a balanced electrolyte solution to make a 5% dextrose solution and administer as an IV drip. Give this fluid at a maintenance rate (60 ml/kg/day).
If the patient is dehydrated or was obtunded for a prolonged period of time, increase the fluid rate accordingly.
1. Clinical Signs
Signs of insulinoma are directly related to low blood glucose (CNS effects predominantly) and resemble an insulin overdose, although a gradual onset or waxing and waning history is typical.
Muscle weakness, confusion, apparent incoordination, collapse and seizures are all possible signs.
The history may include improvement after feeding or oral administration of simple sugars, and a worsening with fasting and/or exercise.
Some patients with chronic insulinoma develop a peripheral neuropathy characterized by muscle atrophy, weakness, decreased reflexes and decreased proprioception. Acutely correcting the blood glucose will not result in recovery of these deficits, although removal of the tumor might improve the condition.
2. Other Differential Diagnoses for Hypoglycemia
a. Iatrogenic - insulin overdose or oral hypoglycemic agents
b. Hepatic failure or portosystemic shunt
c. Juvenile hypoglycemia
3. Acute Management
a. Start diagnostics
If the patient is hypoglycemic at the time of presentation, draw a blood sample for serum insulin measurement prior to the treatment of the hypoglycemia, and submit both the insulin and blood glucose sample to the laboratory.
b. Correct hypoglycemia
If the patient is having a seizure or is in a coma, administer a slow IV bolus of dextrose as for insulin overdose (see section on diabetes mellitus). Give only enough to control the signs. Proceed to the next step.
For all patients with moderate to severe clinical signs; add dextrose to a balanced electrolyte solution and administer at a maintenance rate (60 ml/kg/day) by a constant rate infusion.
The dextrose should be that amount needed to control the clinical signs and keep the patient's blood glucose above 60 mg% and below 120 mg%. The amount is anywhere from 2.5% - 20% dextrose in the solution. Giving more dextrose than necessary is not helpful, and may exacerbate insulin secretion by the tumor.
Highly concentrated solutions of dextrose (above 5%) are quite hypertonic and should be given by a central catheter.
Mild clinical signs may be managed by feeding the pet; see below.
Feed the patient frequent small amounts of high calorie, high protein pet food, such as Nutritional Recovery Formula or Hill's A/D.
4. Management of Intractable Seizures Secondary to Hypoglycemia
Some patients will not respond to administration of dextrose because they have cerebral necrosis and edema.
Give a bolus of diazepam to attempt to stop the seizure (0.5 - 1 mg/kg IV), and place on a diazepam IV drip at 2.5 - 20 mg/hour (depending on patient size and response) as a constant rate infusion.
Cerebral edema may be treated with 20% or 25% mannitol at 1 g/kg IV over 20 minutes.
Intractable hypoglycemia (in spite of dextrose administration) and cerebral edema may both be helped by glucocorticoid administration. Give prednisolone sodium succinate at 30 mg/kg IV followed by dexamethasone at 0.1 mg/kg IV BID. Administering glucocorticoids may obscure the diagnosis and worsen the prognosis if the patient turns out not to have an insulinoma.