Transcript Hyperthyroidism and Thyroid Storm

Hyperthyroidism and
Thyroid Storm
Tintinalli Chapter 215
12/15/05
Prepared by Trent W. Smith
Lecture by Dr. Klien MD
Normal Thyroid State
• Synthesis and release of thyroid hormone
is controlled by TSH relaesed form the
anterior pituitary
• TSH is controlled by the release of thyroid
releasing hormone (TRH) from the
hypothalmus and a negative feedback
loop to the pituitary
• Thyroid hormone production s dependent
on adequate adequate iodine intake
Normal Thyroid State
• Thyroid hormone is reversible bound to
various proteins including thyroninebinding globulin (TBG)
• Free unbound portions are biologically
active
• T4 is the predominant circulating hormone
• T4 is deiodinated to t3
• T3 is biologically more active than T4 but
has a shorter half-life
Hyperthyroidism
• Occurs in in all ages
– Uncommon under the age of 15
• 10 x’s more common in women (1/10,000)
• Graves disease is the most common etiology
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80% of cases in the U.S.
Common in the 3rd and 4th decades
Caused by autoimmune thyroid-stimulating antibodies
Associated with diffuse goiter, opthalmopathy, and
local dermopathy
Hyperthyroidism
• Toxic multinodular and toxic nodular
goiters are the next most common
etiologies
– Usually occurs in older populations
– Commonly with previous history of goiter
– Often with milder symptoms of thyrotoxicosis
Hyperthyroidism
• Amiodarone-induced thyrotoxicosis (AIT)
– Amiodarone is iodine rich and may cause
both hyper and hypothyroidism
– Difficult to treat because of incomplete
understanding of mechanism
– Two major forms exists
• Type 1 occurs with a normal thyroid
• Type 2 occurs with a abnormal thyroid
– Tx. Varies based on the the type
Hyperthyroidism
• Hyperthyroidism resembles a state of
increased adrenergic activity despite a
normal or low serum cortisol level
• Classic complaints include heat
intolerance, palpitations, weight loss,
sweating, nervousness, and fatigue
Hyperthyroidism
Symptoms
Signs
Weaknes
Goiter/thyroid burit
Fatigue
Hyperkinesis
Heat intolerance
Opthalmopathy
Nervousness
Lid retraction/stare
Increased sweating
Lid lag
Tremors
Tremor
Palpitations
Warm moist skin
Weight loss
Hyperreflexia
Hyperdefication
Tachycardia/arrhythmia
Dyspnea
Systolic hypertension
Menstrual abnormalities
Widened pulse pressure
Hyperthyroidism
• Confirmed by thyroid function test
– Elevated free T4 and Low TSH
– In some cases of graves disease T4 may be
normal and TSH decreased but the patient
appears thyrotoxic
– T3 level should be done to rule out T3
toxicosis
– Hypothyroidism secondary to pituitary
adenoma will have elevated TSH levels
Hyperthyroidism
• Treatment
– Palliative treatment of mild hyperthyroidism is
accomplished using B-blockers
• Most commonly used is propanolol
– Treatment of Graves diseases include longterm use of antithyroid medications,
radioactive iodine, or subtotal thyroidectomy
– Type I AIT is treated with methimazole and
potassium perchlorate
– Type II AIT is treated with glucocorticoids
Hyperthyroidism
• Treatment cont.
– Toxic multinodular goiter and solitary
adenomas may be treated with radioiodine
therapy
– Thryoiditis is usually self limited and therapy
is rarely needed
Thyroid Storm
• A life threatening hypremetabolic state due to
hyperthyroidism
• Mortality rate is high (10-75%) despite treatment
• Usually occurs as a result of previously
unrecognized or poorly treated hyperthyroidism
• Thyroid hormone levels do not help to
differentiate between uncomplicated
hyperthyroidism and thyroid storm
Thyroid Storm
• Preciptatnts of Thyroid Storm (tabel 215-4)
Infection
Trauma
DKA
MI
CVA
PE
Surgery
Withdrawal of thyroid
med
Iodine administration
Palpation of thyroid
gland
Ingestion of thyroid
hormone
Unknown etiology (2025%)
Thyroid Storm
• Clinical features
– The most common signs are fever,
tachycardia out of proportion to the fever,
altered mental status, and diaphoresis
– Clues include a history of hyperthyroidism,
exophthalmoses, widened pulse pressure and
a palpable goiter
– Patients may present with signs of CHF
Thyroid Storm
• Clinical features cont.
– Common GI symptoms include diarrhea and
hyperdefication
– Apathetic thyrotoxicosis is a distinct
presentation seen in the elderly
• Characteristic symptoms include lethargy, slowed
mentation, and apathetic facies
• Goiter, weight loss , and proximal muscle
weakness also present
Thyroid Storm
• Diagnosis
– Thyroid storm is a clinical diagnosis based
upon suspicion and treated empirically
– Lab work is non specific and may include
Leukocytosis, hyperglycemia, elevated
transaminase and elevated bilirubin
Thyroid Storm
• Treatment
– Initial stabilization includes airway protection,
oxygenation, fluids and cardiac monitoring
– Treatment can then be divided into 5 areas:
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General supportive care
Inhibition of thyroid hormone synthesis
Retardation of thyroid hormone release
Blockade of peripheral thyroid hormone effects
Identification and treatment of precipitating events
Thyroid Storm
• Drug Treatment of Thyroid Storm (table 216-6)
– Decrease de novo synthesis:
• Porpythiouracil
• Methimazole
600-1000mg PO initially, followed by 200-250 mg q 4 hrs
40 mg PO initial dose, then 25 mg PO q6h
– Prevent relases of hormone (after synthesis blockade intiated)
• Iodine
• Lithuim
Iaponoric acid (Telepaque) 1 gm IV q8h for the first 24 h, then
500 mg bid or Potassium iodide (SSKI) 5 drops PO q6h or Lugol
solution 8-10 drops PO q6h
800-1200 mg PO every day
– Prevent peripheral effects:
• B-Blocker
• Guanethidine
• Reserpine
Propanolol (IV) titrate 1-2 mg q 5min prn (may need 240-480mg
PO q day) or Esmolol (IV) 500 mcg/kg IV bolus, then 50-200
mcg/kg per min maintenance
30-40 mg PO q 6 h
2.5-5 mg IM q4-6h
• Other consideration:
• Corticosteroids
• Antipyretics
Hydrocortisone 100 mg IV q 8 h or
dexamethosone 2 mg IV q 6 hr
Cooling blanket
acteaminophen 650 mg PO q 4-6h
Thyroid Storm
• Treatment cont
– Propranolol has the additional effects or blocking
perpheral conversion of T4-T3
– Avoid Salicylates because it may displace T4 from
TBG
– If the patient continues to deteriorate despite
appropriate therapy circulating thyroid hormone may
be removed by plasma transfusion, plasmapheresis,
charchoal plasmaperfusion
– Remember you must not administer iodine until
the synthetic pathway has been blocked
Thyroid Storm
• Disposition
– Admit to the ICU
Hypothyroidism and
Myxedeam Coma
Tintinalli Chapter 215
12/15/05
Prepared by Trent W. Smith
Lecture by Dr. Klien MD
Hypothyroidism
• Occurs when there is insufficient hormone
production or secretion
• Occurs more frequently in women (0.6 to 5.9 %)
• The most common etiologies are
– Primary thyroid failure due to autoimmune diseases
(Hashimoto thyroiditis is the most common)
– Idiopathic causes
– Ablative therapy
– Iodine deficiency
• May be transient
– Pathophysiology is unclear but may be viral in nature
Hypothyroidism
• Etiologies of Hypothyroidism
– Primary
• Autoimmune etiologies
– Hashimotos is the most common
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Idopathic
Post ablation (surgical, radioiodine)
Post external radiation
Thryoiditis (subacute, silent, postpartum)
– Postpartum thyroiditis occurs within 3-6 months and occurs in
2- 16 % of women
– Self limited etiologies, often prededed by hyperthroid phase
• Infiltrative disease (lymphoma, sarcoid, amyloidosis,
Tuberculosis
• Congenital
Hypothyroidism
• Etiologies of Hypothyroidism
– Post Partum
• Occurs 3-6 months post partum and occurs in 2-16% of
women
– Secondary (pituitary)
• Neoplasm
• Infiltrative Dz.
• Hemorrhage
– Tertiary (hypothalamic)
• Neoplasm
• Infiltrative Dz.
Hypothyroidism
Etiologies of Hypothyroidism
– Drugs
• Amiodarone
– Occurs in 1-32% of patients
– Most likely due to the large amount of iodine released in the
metabolism of the drug which inhibits thyroid hormone
synthesis, release, and conversion of T4 to T3
• Lithium
– Acts similarly to iodine and inhibit thyroid hormone release
• Iodine (in patients with pre-existing autoimmune disease)
• Antithyroid medication
Hypothyroidism
• Clinical Features
– The typical symptoms of hypothyroidism
include fatigue, weakness, cold intolerance,
constipation, weight gain, and deepening of
voice.
– Cautaneous signs include dry, scaly, yellow
skin, non-pitting, waxy edema of the face and
extremities (myxedema): and thinning
eyebrows
Hypothyroidism
• Clinical Features cont.
– Cardiac findings include bradycardia,
enlarged heart, and low-voltage
electrocardiogram
– Paresthesia, ataxia, and prolongation or
DTR’s are characteristic neurologic findings
– See table below for more complete list
Hypothyroidism
• Symptoms and Signs or Hypothyroidism (table 216-2)
Symptoms
Signs
Fatigue
Hoarseness
Weight Gain
Hypothermia
Cold intolerance
Periobital puffiness
Depression
Delayed relaxation of ankle
jerks
Menstrual irregularities
Loss of outer third of eyebrow
Constipation
Cool, rough, dry skin
Joint Pain
Nonpitting edema
Muscle cramps
Bracycardia
Infertility
Peripheral Neuropathy
Hypothyroidism
• Treatment
– Most patient with uncomplicated symptomatic
Hypothyroidism may be referred to the
primary physician for further evaluation and
initiation of treatment
– If hypothyroidism is due to a secondary
etiology initiation of thyroid hormone therapy
may exacerbate preexisting adrenal
insufficiency
Myxedema
• Myxedema is a rare life threatening
decompensation of hypothyroidism
– Usually in individuals with long-standing
hypothyroidism
– Most often seen in the winter months
– More common in elderly women with
underdiagnosed or undertreated
hypothyroidism
Myxedema
• Precipitating events include
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Infection
CHF
Trauma
CVA
Exposure to cold
Drugs
• Sedatives
• Lithium
• Amiodarone
Myxedema
• In addition to the clinical features of hypothyroidism
patients may present with
– Hypothermia
– Altered metal status
• Coma, delusions, and psychosis (myxedema maddness)
– Hyponatremia
• Dilutional secondary to decreased free-water clearance
– Hypoglycemia
• Secondary to impaired gluconeogenesis
– Hypotension
– Bradycardia
– Respiratory Failure
• Secondary to decreased strength of respiratory muscle
• Hypercapnia and hypoxia is common
Myxedema
• Diagnosis
– Must have high clinical suspicion
– Commonly has Hx. Of hypothyroidism
– Delcine in function is usually insidious in
onset
Myxedema
• Diagnosis cont
– Laboratory evaluation may reveal
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Anemia
Hyponatremia
Hypoglycemia
↑ Transaminases
↑ CPK
↑ LDH
↓Po2 and ↑PCo2 on ABG’s
Myxedema
• Diagnosis cont.
– EKG may reveal
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Sinus Bradycardia
Prolonged QT interval
Low voltage
Flattened or inverted T waves
Myxedema
• Treatment (see table 216-5 below)
– No prospective studies on optimal therapy have been
done thus treatment recommendations are not
uniform
– Airway stabilization with adequate oxygenation and
ventilation or vital
– Cardiovascular status must be monitored closely
– Hypothermic patients should be gradually rewarmed
with gentle passive external rewarming
• Hypotension from reversal of hypothermic vasoconstriction
should be avoided
Myxedema
• Treatment cont.
– Hyponatremia typically responds to fluid
restrictions. Severe cases may require
hypertonic saline with lasixs
– Vasopressors are usually ineffective and
should only be used in severe hypotension
– Lovothyroxine 300-500 mcg slow IVP
followed by 50-100 mcg daily
Myxedema
• Treatment cont.
– L-triiodothyronine 25 mcg IV or orally q 8 h is a
alternative
• This dose should be halved in patients with cardiovascular
disease
– Hydrocortisone 100 mg IV q 8 hours should
be given
• Send baseline cortisol level to lab if possible
– Precipitating causes should be sought and
treated
Myxedema
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Treatment of Myxedema Coma (table 216-5)
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Recognition
Supportive therapy including ventilatory support
Thyroid replacement
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Glucocorticoid
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Gentle fluid restriction for dilutional hyponatremia
Hypertonic saline for severe hyponatremia
Hypoglycemia
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Prevent additional loss
Passive external rewarming
Electrolyte correction
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Hydrocortisone: 100 mg IV q8h
Hypothermia
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Lovothyroxine 300-500 mcg slow IVP followed by 50-100 mcg daily or
T3 25 mcg IV or PO q 8 hrs
Dextrose-containing IV fluids
Monitoring
Aggressive treatment of presipitating causes
Admit patient to a monitored setting
Myxedema
• Disposition
– Admit to appropiately monitored bed
Questions
• 1. Hyperthyroidism is Characterized by
which of the following
– A. Fatigue
– B. Palpitations
– C. Weight Loss
– D. Heat intolerance
– E. All the above
• 2. The most common etiology of
hyperthyroidism is
– A. Toxic Multinodular
– B. Graves
– C. Toxic Nodular
– D. Amiodarone induces
• 3. Typical Feature of Hyperthyroidism
include
– A. Fatigue
– B. Weakness
– C. Constipation
– E. Cold Intolerance
– F. All the above
• 4. T or F Hyperthyroidism is more common
in women
• 5. T or F Hypothyroidism is more common
in women
• 6. T or F Mild hyperthyroidism may be
treated with B-blockers
•
Answers 1. E 2. B 3. F 4.T 5.T 6.T