Myxedema coma pathophysiology: Difference between revisions

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==Associated Conditions==
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Revision as of 00:25, 10 October 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Pathophysiology

  • Myxedema coma occurs as a result of long-standing, undiagnosed, or undertreated hypothyroidism.
  • Myxedema coma is usually precipitated by a systemic illness.

Triggers

  • Myxedema coma can result from any of the causes of hypothyroidism, most commonly chronic autoimmune thyroiditis.
  • Myxedema coma can also occur in patients who had thyroidectomy or underwent radioactive iodine therapy for hyperthyroidism.
  • Rare causes may include secondary hypothyroidism and medications such as lithium and amiodarone.

Pathogenesis

  • Thyroid hormone plays an important role in cell metabolism.
  • Long-standing hypothyroidism is associated with reduced metabolic rate and decreased oxygen consumption, which affects all body systems. [5]
  • Reduced metabolism results in hypothermia.
  • Reduced metabolism and decreased oxygen also results in decreased drug metabolism leading to overdosing of medications particularly sedatives, hypnotics, and anesthetic agents; this can precipitate myxedema coma.
  • Even in severe hypothyroidism a balance of metabolic homeostasis is achieved through adaptive neurovascular mechanisms. However in conditions such as respiratory or urinary tract infections, cardiac, acute myocardial infarction or stroke interfere with this adaptive mechanisms by decreasing the blood volume and ventilation triggering myxedema coma.
 
 
 
 
 
 
 
 
Hypothyroidism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Precipitating Factor
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
T4
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↓ Intracellular T3
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypothalamus
 
Respiratory
 
 
 
Cardiovascluar
 
Renal
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↓ thermogenesis
 
Hypercapnia
Hypoxia
 
 
 
↓ inotropic
bradycardia
 
↓ Volume status
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypothermia
 
Hypoventilation
 
 
 
↓ Cardiac output
↓ blood volume
 
↓ GFR
↑ ADH
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Alteration of mental state
 
Cerebral anoxia
 
 
 
↓arterial pressure/shock
 
Hyponatremia
Edema
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Myxedema Coma
 
 
 
 
 
 

The following table summarizes the various effects of reduced thyroid hormone on different organ systems

Organ System Effect due to Decreased Thyroid Hormone Manifestation
Cardiovascular
  • Cardiac contractility is impaired
    • Leading to reduced stroke volume
    • Low cardiac output
    • Bradycardia
    • Hypotension
  • Reduced stroke volume
    • Accumulation of fluid rich in mucopolysaccharides within the pericardial sac
  • Hypotension
  • Narrowed pulse pressure
  • Edema
  • Pericardial effusions
Neurologic
  • Altered brain function due to
    • Reduced oxygen delivery and consumption
    • Decreased glucose utilization
    • Reduced cerebral blood flow.
  • Altered consciousness
Pulmonary
  • Central depression of ventilatory drive
    • Hypoxia
    • Hypercapnia
  • Hypoventilation
Renal
  • Reduced glomerular filtration rate because of
    • Low cardiac output
    • Peripheral vasoconstriction
    • Rhabdomyolysis
  • Low volume stimulates
    • Antidiuretic hormone impairs water excretion leading to hyponatremia
Gastrointestinal
  • Mucopolysaccharide infiltration and edema results in
    • Malabsorption
    • Gastric atony
    • Impaired peristalsis
    • Paralytic ileus
    • Megacolon
  • GI bleeding
  • Ascites
  • Constipation
Hematologic
  • Coagulopathy
    • due to decrease in production of factors V, VII, VIII, IX, and X
  • Hemorrhage and vitamin B12 deficiency
  • Bleeding
  • Anemia

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Gross Pathology

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References