Thyroid Emergencies

Hypothyroidism
Symptoms

• Nervous system • Cardiovascular

– Forgetfulness and mental
slowing
– Paresthesias
– Carpal tunnel syndrome
– Ataxia and decreased
hearing
– Tendon jerk slowed with
prolonged relaxation
phase
– Bradycardia
– Decreased cardiac output
– Pericardial effusion
– Reduced voltage on EKG
and flat T waves
– Dependent edema
 Hypothyroidism
Symptoms
• Gastrointestinal
– Constipation
– Achlorhydria with
pernicious anemia
– Ascitic fluid with high
protein
• Renal
– Reduced excretion of water
load
• Hyponatremia
– Decreased renal blood flow
and glomerular filtration
• Pulmonary
– Responses to hypoxia and
hypercapnia are decreased
– Pleural effusions high
protein
• Musculoskeletal
– Arthralgia
– Joint effusions
– Muscle cramps
– CK can be elevated
• Anemia
– Normochromic normocytic
– Megaloblastic
• Pernicious anemia
 Hypothyroidism
Symptoms
• Skin and hair • Metabolism
– Loss of lateral eye brows – Hypothermia
– Dry, cool skin – Intolerance to cold
– Facial features – Increased cholesterol and
• Coarse and puffy triglyceride
• Reproductive system • Decreased lipoprotein
receptors
– Menorrhagia from – Weight gain
anovulatory cycles
– Hyperprolactinemia
• No inhibition of thyroid
hormone
 Myxedema Coma

• Is the end stage of long standing severe

hypothyroidism characterized by altered mental
status, hypothermia & symptoms related to slowing
of function in multiple organs.

• It is a medical emergency carrying mortality rate of

30-50%.
 Myxedema Coma
Diagnosis
• Defective • Precipitating illness or
thermoregulation event
– Normal body temperature – Exclude pulmonary or
with sepsis urinary tract source
– Trauma
• Age
– Stroke
– Most are elderly
• Decreased ability to
– Hypoglycemia
compensate – Hypothermia
– CO2 narcosis
– Diuretics
– Sedatives
– Tranquilizers
– Winter season
– Drug overdose
 Clinical features
• Prototypical patient is an elderly female with long
standing history of hypothyroidism.

• The hallmarks of myxedema coma are decreased

mental status and hypothermia, but hypotension,
bradycardia, hyponatremia, hypoglycemia, and
hypoventilation are often present as well.
• Neurologic manifestations — Despite the name
myxedema coma, patients frequently do not present in
coma but do manifest lesser degrees of altered
consciousness.
• This usually takes the form of confusion with lethargy
and obtundation.
• Alternatively, patient may have prominent psychotic
features, so-called myxedema madness.
• Untreated, patients will progress to coma.
• Focal or generalized seizures may occur, sometimes
due to concomitant hypoglycemia or hyponatremia.
Cardiovascular abnormalities-

• Severe hypothyroidism is associated with

bradycardia, decreased myocardial contractility, a
low cardiac output, and sometimes hypotension.

• Pericardial effusion may be present.

• Its clinical manifestations include diminished heart

sounds, low voltage on electrocardiogram (ECG),
and a large cardiac silhouette on chest radiograph.
Hypothermia-

• The low body temperature may not be recognized

initially, because many automatic thermometers do
not register frankly hypothermic body temperatures.

• The severity of the hypothermia is related to

mortality in severe hypothyroidism; the lower the
temperature, the more likely a patient is to die.
Hypoventilation -

• Hypoventilation with respiratory acidosis results primarily

from central depression of ventilatory drive with
decreased responsiveness to hypoxia and hypercapnia.

• Other contributing factors include respiratory muscle

weakness, mechanical obstruction by a large tongue,
and sleep apnea.

• Some patients require mechanical ventilation.

• Airway management may be complicated by

myxedematous infiltration of the pharynx
 Laboratory evaluation
• TSH
• Free thyroxine (T4)
• Cortisol
• Blood glucose levels
• Arterial blood gases
• CBC
• Electrolytes
• KFT
 Key laboratory findings
• Reduced free T4
• High TSH (primary hypothyroidism)
• Low or high normal TSH(central
hypothyroidism)
• Low blood sugar
• Hyponatremia
• Hypercapnia with respiratory acidosis
• Hypoxemia
• leukocytosis
 Treatment and emergency
management
• Secure airway and obtain iv access
• ICU admission
• Thyroid hormone
• Glucocorticoids
• Supportive measures
• Appropriate management of coexisting
problems (eg, infection)
• Cardiovascular support
– Dilute fluids should be avoided in hyponatremic
patients to prevent a further reduction in the plasma
sodium concentration.
– Fall in blood pressure is ominous
• Look for GI bleed, MI, over diuresis or iatrogenic
vasodilatation
• Endocrine support
– Hydrocortisone 100 mg Q8 hrs
• Treat possible coexisting primary or secondary adrenal
insufficiency
• Stop once cortisol level is confirmed to be normal.
• Body temperature support
– Poikilothermic
– No aggressive warming
• Vasodilatation= vascular collapse
– Passive warming
• Respiratory support
– Intubation may be needed
– If HCT <30%, transfuse
• Provide adequate perfusion and oxygen carrying capacity
• Thyroid hormone therapy
– 300-500 mcg i.v. Levothyroxine bolus then,

– 50-100 mcg IV Qday

• Lower doses for smaller people or older at risk for
cardiac events

• IV to bypass poor absorption in the bowel

– Alternately give T4 and T3 due to decreased T3

conversion
• 200-300 mcg T4 then 50 mcg/day bolus

• 5-20 mcg T3 then 2.5-10 mcg Q8 hrs

• Addition of Levothyroxine causes
– Increase in cardiac index 1-2 days
– TSH falls 32% in 24 hrs
– Serum T3 levels increased on 3rd day
– Reversal of blunted ventilatory responses 7 days
• Obtain Free T4- 3 days after initiation of
therapy to make sure it is increasing
– Adjust to normalize value
• Once tolerating PO can change to oral
therapy
– Increase IV dose by 40% for oral dosing
• ie: IV 100 mcg then 140 mcg PO