Transcript Framingham, Reynolds, CRP Canadian Lipid Guidelines

Thyroid Emergencies
Robina Rana
28th August, 2013
Objectives
• Discuss common thyroid problems:
• Thyroid Emergencies:
– Thyroid Storm
– Myxedema Coma
– Thyrotoxic Periodic Paralysis
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Epidemiology
Presentation
Diagnosis
Management
Relationship between
serum-free thyroxine by
dialysis (FT4) ng/dL and
log10 TSH in
euthyroid,
hyperthyroid,
hypothyroid, and
T4-suppressed euthyroid
individuals.
Spectrum of autoimmune disease of the thyroid gland.
The clinical manifestations of autoimmune disease of the thyroid gland range from
idiopathic myxedema, through nontoxic goiter, to diffuse toxic goiter, or Graves
disease.
Progression of autoimmune disease from one form to another in the same patient
can occasionally occur.
Spectrum of autoimmune disease of the thyroid gland.
The clinical manifestations of autoimmune disease of the thyroid gland range from
idiopathic myxedema, through nontoxic goiter, to diffuse toxic goiter, or Graves
disease.
Progression of autoimmune disease from one form to another in the same patient
can occasionally occur.
Hypothryoidism:
“End stage of untreated or inadequately treated
hypothyroidism”
MYXEDEMA COMA:
Myxedema Coma
• The clinical picture is often that of
– an elderly obese female
– who has become increasingly
withdrawn,
– lethargic, sleepy, and confused.
• The history from the patient may
be inadequate, but the family may
report that
– the patient has had thyroid surgery or
– radioiodine treatment in the past or
– that the patient has previously been
receiving thyroid hormone therapy.
The presentation is one of severe hypothyroidism, with or
without coma
(the term myxedema coma may, therefore, be a misnomer).
Myxedema coma may be precipitated by an
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illness such as a cerebrovascular accident, myocardial
infarction, or
an infection such as a urinary tract infection or pneumonia.
gastrointestinal hemorrhage;
acute trauma;
excessive dehydration; or
administration of a sedative, narcotic, or potent diuretic drug.
A schematic representation of the changes in serum thyroid hormone values with
increasing severity of non thyroidal illness.
A rapidly rising mortality rate accompanies the fall in serum total T4 (TT4) and free T4
(FT4) values.
Pathogenesis of myxedema coma
• The physical findings are not specific. The patient may
be
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semi comatose or comatose
with dry, coarse skin,
hoarse voice,
thin scalp and eyebrow hair,
possibly a scar on the neck, and
slow reflex relaxation time.
Marked hypothermia, with body temperature sometimes falling to as low
as 24°C (75°F), particularly in the winter months.
– Precipitating factors such as pneumonia, urinary tract infection, ileus,
anemia, hypoglycemia, or seizures.
– Fever may be masked by coexistent hypothermia.
– Often there are pericardial, pleural, or peritoneal
effusions.
Remember the Basics;
• High index of suspicion 
– clinical features
• Adherence to ABCs 
– LOC, Vitals (temp, arrhythmia ), IV access, IV fluids,
• Order confirmatory tests 
– Thyroid function tests
– Other pituitary function tests
• Institute early treatment
– Cortisol
– Levothyroxine
• Identify and manage precipitant
Management of Myxedema Coma.
(1) Admit to ICU for
• ventilatory support and
• for intravenous medications.{Oral medications may be poorly absorbed (due to gastric atony or
ileus), and medications should be given intravenously if possible}.
(2) Parenteral thyroxine:
Give a loading dose of 300-400 mcg IV, then maintainance 50-100 mcg IV daily.
(May also give small doses of T3 (liothyronine) , 10 mcg IV every 8 h for the first 48 h if necessary.
but this is usually not necessary, and it may contribute to untoward cardiovascular events.)
(3) Electrolytes:
Water restriction for hyponatremia. Avoid fluid overload.
(4) Limit sedation.
Appropriate reduction in drug dosage.
(5) Glucocorticoids:
Controversial but necessary in hypopituitarism or polyglandular failure.
Dosage: Hydrocortisone, 50-100 mg every 6 h initially and tapered downward over 1 wk. (If initial
serum cortisol was >30 mcg/dL (827.7 nmol/L) corticosteroids are unnecessary.)
(6) Hypothermia:
Do not externally rewarm. (Once myxedema coma is suspected in a hypothermic patient, external
rewarming should be avoided, because this may cause redistribution of blood flow to subcutaneous
tissues and cardiovascular collapse.)
(7) Treat the precipitating illness (eg, pneumonia or urinary tract infection).
Mortality from myxedema coma was about 80%.
Prior to the recognition of the need for intravenous T4 and for
respiratory support, Currently, the mortality is about 20%
Predictors of acute mortality include
– level of consciousness,
– lower Glasgow scores, and
– higher APACHE II (acute physiology and chronic health evaluation)
scores
• Higher mortality is also associated with
– increased age,
– cardiac complications,
– and high-dose thyroid hormone replacement (500 g/d of L-T4 or–75
g/d of L-T3). The latter presumably reflects the increased metabolic
demand attendant to high dose replacement in the setting of limited
physiologic reserve.
• Persistent hypothermia and bradycardia, despite therapy, are
associated with a poor prognosis.
Laboratory tests useful in the differential diagnosis of hyperthyroidism
An acute life-threatening exacerbation of thyrotoxicosis.
THYROID STORM / THYROID CRISIS:
Thyroid Storm:
• It accounts for 1% to 2% of hospital
admissions for thyrotoxicosis.
• It occurs in a patient with
– Predisposition to hyperthyroidism
• a history of Graves disease who has discontinued anti
thyroid medication or
• in a patient with previously undiagnosed
hyperthyroidism.
– Precipitants
• Non thyroid related
Thyroid Storm—Precipitating Factors.
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Withdrawal of antithyroid drugs
Severe infection
Diabetic ketoacidosis
Myocardial infarction
Cerebrovascular accident
Cardiac failure
Surgery
Parturition
Trauma (eg, hip fracture)
Radioiodine (rare)
Drug reaction
Iodinated contrast medium
• The clinical picture is that of ;
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an acute onset of hyperpyrexia (with temperature >40°C [104°F]),
sweating,
marked tachycardia often with atrial fibrillation,
nausea,
vomiting,
diarrhea,
agitation,
tremulousness, and
delirium.
The presence of jaundice is considered a poor prognostic sign.
Occasionally, the presentation is
“apathetic without the restlessness and agitation”,
but with symptoms of weakness, confusion, cardiovascular and
gastrointestinal dysfunction, and hyperpyrexia.
Diagnosis is largely based on the clinical
findings;
• Serum T4, free T4, T3, and free T3 are all elevated, and
TSH is suppressed.
These findings are not different from what is seen in other patients
with hyperthyroidism, but the difference is in the setting.
• It is thought that thyroid storm represents an
exacerbation of thyrotoxicosis associated with
– a shift of T4 from the bound to the free compartment with
an increase in free T3 and T4, as well as
– an exaggerated response to a surge of catecholamines that
results from the stress of the precipitating event.
• The cause of death is usually cardiac arrhythmia and
failure.
• Liver function abnormalities are often seen, as is
leukocytosis, even in the absence of infection.
Remember the Basics;
• High index of suspicion 
– clinical features
• Adherence to ABCs 
– LOC, Vitals (temp, arrhythmia ), IV access, IV fluids,
• Order confirmatory tests 
– Thyroid function tests
– Other pituitary function tests
• Institute early treatment
• Identify and manage precipitant
The therapeutic regimen typically consists of multiple
medications, each of which has a different mechanism
of action:
• A beta-blocker
– to control the symptoms and signs induced by increased
adrenergic tone
• A thionamide
– to block new hormone synthesis
• An iodine solution
– to block the release of thyroid hormone
• An iodinated radiocontrast agent (if available)
– to inhibit the peripheral conversion of T4 to T3
• Glucocorticoids
– to reduce T4-to-T3 conversion,
– promote vasomotor stability, and
– possibly treat an associated relative adrenal
insufficiency
Effects of Antithyroid Drugs.
(THIONAMIDES)
1. Propylthiouracil(PTU)
2. Methimazole(Tapazole)
 Inhibition of thyroid hormone
synthesis
 a reduction in intrathyroidal
immune dysregulation
 Reduction of the peripheral
conversion of thyroxine to
triiodothyronine.
(in the case of propylthiouracil)
*Tyrosine-Tg denotes tyrosine residues in thyroglobulin, I+ the
iodinating intermediate, and TPO thyroid peroxidase.
Cooper DS. N Engl J Med 2005;352:905-917.
Management of Thyroid Storm.
Supportive care
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Fluids
Oxygen
Cooling blanket
Acetaminophen (Aspirin should be avoided, because it will displace T4 from thyroid
hormone—binding globulin, resulting in an increase in FT4
• Multivitamins
• If indicated, antibiotics, digoxin to treat a-fib and heart failure
Specific measures
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Propranolol, 40-80 mg orally every 6 h ( adrenergic blockade)
Propylthiouracil, 150 mg every 6 h, or methimazole, 20 mg every 8 h; may be administered
per rectum if oral route is unavailable
INORGANIC IODINE: inhibit thyroid hormone synthesis but also block the conversion of T4 to T3,.
• Saturated solution of potassium iodide, 5 drops (250 mg) orally twice daily; or
• iopanoic acid, 0.5 g IV or orally twice daily; or
• iohexol, 0.6 g (2 mL of Omnipaque 300) IV twice daily
Dexamethasone, 2 mg every 6 h ( for adrenal support and decrease FT4 FT3 )
Cholestyramine or colestipol, 20-30 g/d ( interferes with enterohepatic circulation of T4)
Thyrotoxic periodic paralysis (TPP) is a rare but frightening thyroid
emergency.
THYROTOXIC PERIODIC PARALYSIS:
Thyrotoxic Periodic Paralysis
The usual clinical presentation is of an
• Asian male (male:female ratio approximately 17:1)
• with symptoms of untreated hyperthyroidism
• who awakens at night or in the morning with flaccid ascending paralysis.
• Typically, there is a history of vigorous exercise and/or a large highcarbohydrate meal before retiring.
• There is usually no family history of periodic paralysis, but there may be a
family history of autoimmune thyroid disease.
The acute episode may be complicated by cardiac arrhythmias due to the
concomitant presence of hypokalemia.
The illness has also been reported to occur in Native Americans, African
Americans, and in individuals of Mexican or South American descent, but
these ethnic groups are affected rarely.
The paralysis initially
– involves the lower extremities but
– progresses to the girdle muscles,
– followed by the upper extremities.
• Proximal muscle groups are affected to a greater
extent than distal.
• Facial and respiratory muscles are usually spared.
• Sensory function, bowel and bladder function
are not affected.
• Deep tendon reflexes are depressed or absent.
Pathogenesis of thyrotoxic periodic paralysis;
The differential diagnosis of TPP includes
• familial periodic paralysis,
• Guillain-Barré syndrome, and
• acute intermittent porphyria.
The diagnosis is based on the
• absence of a family history,
• the characteristic presentation,
• the presence of hyperthyroidism due either to Graves disease or toxic nodular
goiter (other types of hyperthyroidism have been implicated as well), and
• usually a low serum potassium level.
• The electromyogram, performed while the patient is experiencing weakness,
– shows myopathic changes with reduced amplitude of compound muscle
action potentials. These do not change in amplitude after administration of
intra-arterial low-dose epinephrine (distinguishes from familial periodic
paralysis).
• Electrocardiograms show changes associated with
– hypokalemia,
– tachycardia,
– increased QRS voltage,
– first-degree heart block, and,
– on occasion, serious ventricular arrhythmias.
Management of Thyrotoxic Periodic Paralysis.
With appropriate treatment, recovery is rapid, and once the thyrotoxicosis is controlled, the
paralysis will not recur
(1) Oral potassium supplement cautiously (if needed); monitor serum K+
(2) Oral propranolol (60 mg every 6 h) blocks the -adrenergic stimulation of Na+-K+ ATPase.
(3) Antithyroid drug therapy should be started immediately, even though it takes time to bring the patient into a
euthyroid state.
Avoid:
• IV potassium (important to be cautious if administering intravenous potassium, which may raise total body potassium to toxic
levels as the episode resolves.
• IV glucose which stimulates insulin secretion and worsens hypokalemia,
(ie, crystalloid fluid replacement only)
• Adrenergic agonists (eg, isoproterenol) which promote movement of potassium into the intracellular
compartment and exacerbate the problem
• Acetazolamide, which has been shown to reduce frequency of attacks in familial periodic paralysis, may worsen attacks
of thyrotoxic periodic paralysis and should be avoided.
Conclusion
• Myxedema coma: • Thyroid storm:
– Passive warming
– Load Synthroid
• Daily IV
– Start Hydrocortisone
– Look for inciting event
– Control heart rate
• B-blockade
• Calcium channel
blockade
– Thionamide therapy
– Look for inciting event
• Thyrotoxic
Periodic
Paralysis:
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With appropriate
treatment,
recovery is rapid,
and once the
thyrotoxicosis is
controlled, the
paralysis will not
recur
Thank You