Myxedema Coma

Chapter 73 Myxedema Coma



Rebecka S. Hess, DVM, DACVIM



KEY POINTS



• Myxedema coma is a misnomer. Many patients in a hypothyroid crisis are not comatose and do not have myxedema.

• Myxedema coma is difficult to diagnose, because it is rare and the clinical and clinicopathologic abnormalities may be nonspecific.

• Rottweiler dogs are at increased risk for a hypothyroid crisis.

• Concurrent disease, most commonly infection (pneumonia), may increase the risk for a hypothyroid crisis. Treatment with steroids, nonsteroidal medication, or surgery may also increase the risk for a hypothyroid crisis.

• Myxedema, obesity, mental dullness, hypercholesterolemia, and nonregenerative anemia are observed in many, but not all, dogs in a hypothyroid crisis.

• Intravenous (IV) administration of levothyroxine at a dosage of 5 μg/kg q12h is a safe and effective treatment for dogs in a hypothyroid crisis.

• Subjective improvement in mentation or ambulation occurs within 24 to 30 hours of IV levothyroxine administration in most dogs.

• When treated appropriately with supportive care and IV levothyroxine, most dogs with myxedema coma respond well and are discharged from the hospital.


INTRODUCTION


Canine myxedema coma is a rare, life-threatening complication of hypothyroidism.1-7 In human beings the name myxedema coma is considered a misnomer, because human patients with this condition are rarely comatose and do not usually have myxedema.8,9 Diagnosis of myxedema coma is difficult because it is rare, and therefore little is known of the condition.1 Diagnosis is further complicated by nonspecific clinical signs. Recognition of an acute hypothyroid crisis in dogs that do not have coma or myxedema may advance the understanding and improve the outcome of dogs with suspected myxedema coma.1



PATHOPHYSIOLOGY


The pathophysiology of myxedema coma is incompletely understood. Thyroid hormones regulate cell function in many organs by binding intranuclear receptors and promoting expression of various enzymes.10 Thyroid hormones exert chronotropic and inotropic effects in the heart, as well as catabolic, metabolic, calorigenic, and developmental effects in other organs.10 Therefore decreased thyroid hormone function has a profound effect on many body systems. The clinical hallmarks of myxedema coma in human beings are altered mental status, inadequate thermoregulation, decreased respiratory and cardiovascular function, and concurrent disease.9,11


In human beings, altered mental status may be limited to disorientation, confusion, or lethargy.9 Coma is unusual.8,9 In dogs, clinical signs such as disorientation and confusion may be difficult to appreciate. Although most dogs in a hypothyroid crisis have mental dullness, coma upon initial examination is uncommon.1,2,4-6 The pathophysiology of altered mental status is multifactorial and may be a result of decreased blood flow to the brain, hyponatremia, or lack of a direct effect of thyroid hormone on the brain.9


The pathophysiology of altered thermoregulation resulting in hypothermia is likely also multifactorial. Inadequate thyroid hormone function in the hypothalamus may result in inability to regulate body temperature.9 Additionally, a decrease in the calorigenic effect of thyroid hormones contributes to hypothermia.9 The body temperature of some individuals with myxedema coma may appear to be normal because of a concurrent infection and a fever.9


Hypoventilation develops secondary to decreased respiratory system responsiveness to hypoxia and hypercapnia, and may be complicated by obese body condition, muscle weakness, pneumonia, pericardial or pleural effusion, and ascites.11 In the heart, thyroid hormones increase the number of β-adrenergic receptors and their affinity to catecholamines, thereby increasing the inotropic and chronotropic effects of catecholamines.10 Hypothyroid cardiomyopathy is also caused by an increase in α-myosin heavy chains (MHC), which have decreased adenosine triphosphatase (ATPase) activity, and a decrease in β-MHCs, which have more adenosine triphosphatase activity.10 These changes result in hypothyroid cardiomyopathy typified by impaired left ventricular function or atrial fibrillation.12,13 During a hypothyroid crisis, cardiovascular dysfunction is characterized by bradycardia, decreased cardiac contractility, cardiac enlargement, and hypotension, although diastolic hypertension has also been documented.11


Concurrent disease may prevent normal compensatory mechanisms from responding appropriately to a hypothyroid crisis, and may therefore be involved in the pathophysiology of myxedema coma.9 Absence of concurrent disease in most cases of hypothyroidism may explain why myxedema coma remains rare.


When myxedema does occur, it is thought to develop secondary to accumulation of the glycosaminoglycan hyaluronic acid in the dermis.6,14 Impaired renal perfusion secondary to decreased cardiovascular function results in inability to excrete water and contributes to development of edema.11 Excessive secretion of antidiuretic hormone may also contribute to fluid retention and edema in some patients.15



RISK FACTORS


Rottweiler dogs are at increased risk for myxedema coma.1 Most dogs with myxedema coma are of middle age (median 6 years, range 4 to 10 years).1 The age of dogs with myxedema coma is not significantly different from the age of other hypothyroid dogs. Female dogs do not appear to be at increased risk compared with other hypothyroid dogs, although myxedema coma is more common in women than in men.1,8,11 Dogs with untreated hypothyroidism are at increased risk.1-6


Most dogs with myxedema coma have a concurrent disorder, most commonly an infection.1 In a recent report of seven dogs in a hypothyroid crisis, concurrent disease was diagnosed in five.1 Infection was diagnosed in four of the seven dogs.1 Three of the four dogs with infection had aspiration pneumonia. Additional infections included foreign body keratoconjunctivitis, pyometra, severe bilateral otitis, and pyoderma.1 The most commonly observed concurrent infections in humans with myxedema coma are pneumonia, influenza virus, urinary tract infection, and sepsis.8


Glucocorticoids were administered to three dogs with myxedema coma within 1 month of a hypothyroid crisis.1,5 Oral prednisone at a dosage of 0.55 mg/kg q12h lowers the concentration of thyroid hormones in dogs.16 Nonsteroidal antiinflammatory medications (carprofen and flunixin meglumine) were used in conjunction with glucocorticoids in one dog in a hypothyroid crisis.1 Nonsteroidal antiinflammatory drugs (NSAIDs) may cause suppression of thyroid stimulating hormone (TSH) secretion.17 It is therefore possible that administration of glucocorticoids to dogs with untreated hypothyroidism may increase the risk of myxedema coma. An association between NSAIDs, or other thyroid hormone synthesis–altering drugs, and canine myxedema coma may become apparent in the future.


Surgery increases the risk of myxedema coma in human beings and has been reported in three dogs with myxedema coma.1,6 It is possible that surgery compromises the ability of normal cardiovascular and pulmonary compensatory mechanisms to respond to a hypothyroid crisis, and therefore increases the risk for such a crisis.8


Other factors that increase the risk of myxedema coma in human beings include burns, carbon dioxide retention, gastrointestinal hemorrhage, hypoglycemia, infection, hypothermia (most cases are diagnosed during the winter), stroke, trauma, and various medications including anesthetics, barbiturates, β-blockers, diuretics, narcotics, phenothiazines, and tranquilizers.8

Related posts:

  1. Deteriorating Mental Status
  2. Hyperthermia and Fever
  3. Ventilator-Associated Lung Injury
  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Myxedema Coma

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