Transcript Hyperthyroidism by Dr Sarma

HYPERTHYROIDISM
A Practical Approach to Dx. and
Rx.
PROF. BIKHA RAM DEVRAJANI
MB,FCPS,FACP,FRCP
LUMHS JAMSHORO

A 27 years unmarried lady presented with the
history of weight loss increased appetite ,
sweating and palpitation
 Q what is D/D ?
THYROID GLAND
Clinical Exam. of Thyroid

Have patient seated on a stool / chair

Inspect neck before & after swallowing

Examine with neck in relaxed position

Palpate from behind the patient

Remember the rule of finger tips

Use the tips of fingers for palpation

Palpate firmly down to trachea

Pemberton’s sign for RSG
Where to look for Thyroid ?
Clinical Anatomy of Thyroid
Clinical Exam of Thyroid
Clinical Exam of Thyroid
Clinical Exam of Thyroid
Thyromegaly
Hyperthyroidism

A hyper metabolic biochemical state
 It is a multi system disease with
 Elevated levels of FT4 or FT3 or both
 What is thyrotoxicosis ?
 What is hyperthyroidism ?
 What are the various causes ?
 How to differentiate the causes ?
 What is the appropriate treatment ?
Causes of Hyperthyroidism
1.
2.
3.
4.
5.
6.
7.
8.
9.
Graves Disease – Diffuse Toxic Goiter
Plummer’s Disease – Toxic MNG
Toxic phase of Sub Acute Thyroiditis - SAT
Toxic Single Adenoma – STA
Pituitary Tumours – excess TSH
Molar pregnancy & Choriocarcinoma (↑↑ βHCG)
Metastatic thyroid cancers (functioning)
Struma Ovarii (Dermoid and Ovarian tumours)
Thyrotoxicosis Factitia ; INF, Amiodarone,
SSRIs
Graves Disease

The most common cause of thyrotoxicosis (50-60%).
 Organ specific auto-immune disease
 The most important autoantibody is
– Thyroid Stimulating Immunoglobulin (TSI) or TSA
– TSI acts as proxy to TSH and stimulates T4 and T3
 Anti thyro peroxidase (anti-TPO) antibodies
 Anti thyro globulin (anti-TG) Anti Microsomal and
other
 Autoimmune diseases - Pernicious Anemia, T1DM
 RA, Myasthenia Gravis, Vitiligo, Adrenal
insufficiency.
Graves Disease
I 123 or TC 99m Normal v/s Graves
Graves Disease
Toxic Multinodular Goiter (TMG)








TMG is the next most common hyperthyroidism - 20%
More common in elderly individuals – long standing
goiter
Lumpy bumpy thyroid gland
Milder manifestations (apathetic hyperthyroidism)
Mild elevation of FT4 and FT3
Progresses slowly over time
Clinically multiple firm nodules (called Plummer’s
disease)
Scintigraphy shows - hot and normal areas
Toxic Multinodular Goiter (TMG)
Toxic Multinodular Goiter (TMG)
Sub Acute Thyroiditis (SAT)

SAT is the next most common hyperthyroidism – 15%

T4 and T3 are extremely elevated in this condition

Immune destruction of thyroid due to viral infection

Destructive release of preformed thyroid hormone

Thyroid gland is painful and tender on palpation

Nuclear Scintigraphy scan - no RIU in the gland

Treatment is NSAIDs and Corticosteroids
Toxic Single Adenoma (TSA)

TSA is a single hyper functioning follicular thyroid
adenoma.

Benign monoclonal tumor that usually is larger than 2.5 cm

It is the cause in 5% of patients who are thyrotoxic

Nuclear Scintigraphy scan shows only a single hot nodule

TSH is suppressed by excess of thyroxines

So the rest of the thyroid gland is suppressed
Toxic Single Adenoma (TSA)
Nucleotide
Scintigraphy
Age and Sex

Age
– Graves disease
20 to 40
– Toxic MNG
> 50 yrs
– Toxic Single Adenoma
35 to 50
– Sub Acute Thyroiditis
Any
age

Sex M : F ratio
– Graves Disease
1: 5 to 1:10
– Toxic MNG
1: 2 to 1: 4
Nucleotide Scintigraphy
Clinical Features
1.
Those that occur with any type of
thyrotoxicosis
2.
Those that are specific to Graves disease
3.
Non specific changes of hyper metabolism
Common Symptoms
1.
2.
3.
4.
5.
6.
7.
8.
9.
Nervousness
Anxiety
Increased perspiration
Heat intolerance
Tremor
Hyperactivity
Palpitations
Weight loss despite increased appetite
Reduction in menstrual flow or oligomenorrhea
Common Signs
1.
2.
3.
4.
5.
6.
7.
8.
Hyperactivity, Hyper kinesis
Sinus tachycardia or atrial arrhythmia, AF, CHF
Systolic hypertension, wide pulse pressure
Warm, moist, soft and smooth skin- warm handshake
Excessive perspiration, palmar erythema,
Onycholysis
Lid lag and stare (sympathetic over activity)
Fine tremor of out stretched hands – format's sign
Large muscle weakness, Diarrhea, Gynecomastia
Specific to Graves Disease
1.
2.
3.
4.
Diffuse painless and firm enlargement of thyroid gland
Thyroid bruit is audible with the bell of stethoscope
Ophthalmopathy – Eye manifestations – 50% of cases
 Sand in eyes, periorbital edema, conjunctival edema
(chemosis), poor lid closure, extraocular muscle
dysfunction, diplopia, pain on eye movements and
proptosis.
Dermoacropathy – Skin/limb manifestations – 20% of cases
 Deposition of glycosamino glycans in the dermis of the
lower leg – non pitting edema, associated with erythema
and thickening of the skin, without pain or pruritus called
(pre tibial myxedema)
Clinical Presentations
MNG and Graves
Huge Toxic MNG
Diffuse Graves Thyroid
Higher grades of Goiter
Toxic MNG
(Diffuse) Graves
Grade IV Toxic MNG
Huge Toxic MNG
Huge Toxic MNG
Thyroid Ophthalmopathy
Proptosis
Lid lag
Ophthalmopathy in Graves
Periorbital edema and chemosis
Ophthalmopathy in Graves
Occular muscle palsy
Laka Laka Laka
Severe Exophthalmia
Thyroid Dermopathy
Pink and skin coloured papules, plaques on the shin
Graves with Acropathy
Graves Goiter
Acropathy
Thyroid Acropathy
Clubbing and
Osteoarthropathy
Onycholysis
Non specific changes
Hyperglycemia, Glycosuria
2. Osteoporosis and hypercalcemia
3. ↓ LDL and Total Cholesterols
4. Atrial fibrillation, LVH, ↑ LV EF
5. Hyper dynamic circulatory state
6. High output heart failure
7. H/o excess Iodine, amiodarone, contrast
dyes
1.
FREE THYROXINE or FT4
Nine Square Approach
PRIMARY
HYPERTHYROID
LOW
NORMAL
HIGH
THYROID STIMULATING HORMONE - TSH
FREE THYROXINE or FT4
Nine Square Approach
SUB CLINICAL
HYPERTHYROID
LOW
NORMAL
HIGH
THYROID STIMULATING HORMONE - TSH
Diagnosis
1.
Typical clinical presentation
2.
Markedly suppressed TSH (<0.05 µIU/mL)
3.
Elevated FT4 and FT3 (Markedly in Graves)
4.
Thyroid antibodies – by Elisa – anti-TPO,
TSI
5.
ECG to demonstrate cardiac manifestations
6.
Nuclear Scintigraphy to differentiate the
causes
Algorithm for Hyperthyroidism
Measure TSH and FT4
 TSH, FT4 N
 TSH,  FT4
Primary (T4)
Thyrotoxicosis
Measure FT3
 TSH,  FT4
N TSH, FT4 N
Pituitary Adenoma
FNAC, N Scan
Features of Grave’s
Yes
Rx. Grave’s
No
 RAIU
Low RAIU
Single Adenoma, MNG
High
T3 Toxicosis
Normal
Sub-clinical Hyper
F/u in 6-12 wks
Sub Acute Thyroiditis, I2, ↑ Thyroxine
Laboratory Diagnosis
Serum T3, T4, FT3, FT4
Sensitive TSH assay
Serum TRAb
Test of TRH irritation
Radioactive iodine uotake:
Normal: 3h 5-25%, 24h 20-45%, peak at 24h
Thyroid scan: 131I, 99mTc
Diagnosis
 Symptoms
 Signs
 Laboratory examination
Differential diagnosis
 Other causes of thyrotoxicosis
 Anxiety neurosis or mania
 Some states of hypermetabolism without
thyrotoxicosis: severe anemia, leukemia, etc.
 Cardiac disease: atrial fibrillation, angina
 Pheochromocytoma
 Other causes of ophthalmoplegia (myasthenia
gravis) and exophthalmos (orbital tumor)
 Others: COPD, DM, cirrhosis of the liver.
Treatment Options
1.
Symptom relief medications
2.
Anti Thyroid Drugs – ATD
 Methimazole, Carbimazole
 Propylthiouracil (PTU)
3.
Radio Active Iodine treatment – RAI
Rx.
4.
Thyroidectomy – Subtotal or Total
5.
NSAIDs and Corticosteroids – for SAT
Symptom Relief
Rehydration is the first step
2. β – blockers to decrease the sympathetic excess
 Propranalol, Atenelol, Metoprolol
3. Rate limiting CCBs if β – blockers
contraindicated
4. Treatment of CHF, Arrhythmias
5. Calcium supplementation
6. SSKI or Lugol solution for ↓ vascularity of the
gland
1.
Anti Thyroid Drugs (ATD)
Imp. considerations
Methimazole
Propylthiouracil
Efficacy
Very potent
Potent
Duration of action
Long acting BID/OD
Short acting QID/TID
In pregnancy
Contraindicated
Safely can be given
Mechanism of action
Iodination, Coupling
Iodination, Coupling
Conversion of T4 to T3
No action
Inhibits conversion
Adverse reactions
Rashes, Neutropenia Rashes, ↑Neutropenia
Dosage
20 to 40 mg/ OD PO
100 to 150mg qid PO
How long to give ATD ?

Reduction of thyroid hormones takes 2-8 weeks

Check TSH and FT4 every 4 to 6 weeks

In Graves, many go into remission after 12-18 months

In such pts ATD may be discontinued and followed up

40% experience recurrence in 1 yr. Re treat for 3 yrs.

Treatment is not life long. Graves seldom needs
surgery

MNG and Toxic Adenoma will not get cured by ATD.

For them ATD is not the best. Treat with RAI.
Radio Active Iodine (RAI Rx.)

In women who are not pregnant

In cases of Toxic MNG and TSA

Graves disease not remitting with ATD

RAI Rx is the best treatment of hyperthyroidism in
adults

The effect is less rapid than ATD or Thyroidectomy

It is effective, safe, and does not require hospitalization.

Given orally as a single dose in a capsule or liquid
form.

Very few adverse effects as no other tissue absorbs RAI
Radio Active Iodine (RAI Rx.)
 I123
is used for Nuclear Scintigraphy (Dx.)
 I131
is given for RAI Rx. (6 to 8 milliCuries)

Goal is to make the patient hypothyroid

No effects such as Thyroid Ca or other malignancies

Never given for children and pregnant/ lactating
women

Not recommended with patients of severe
Ophthalmopathy

Not advisable in chronic smokers
Surgical Treatment




Subtotal Thyroidectomy, Total Thyroidectomy
Hemi Thyroidectomy with contra-lateral subtotal
ATD and RAI Rx are very efficacious and easy – so
Surgical treatment is reserved for MNG with
1. Severe hyperthyroidism in children
2. Pregnant women who can’t tolerate ATD
3. Large goiters with severe Ophthalmopathy
4. Large MNGs with pressure symptoms
5. Who require quick normalization of thyroid function
Preoperative Preparation

ATD to reduce hyper function before surgery

βeta blockers to titrate pulse rate to 80/min

SSKI 1 to 2 drops bid for 14 days

This will reduce thyroid blood flow

And there by reduce per operative bleeding

Recurrent laryngeal nerve damage

Hypo parathyroidism are complications
Dietary Advice

Avoid Iodized salt, Sea foods

Excess amounts of iodide in some
–
Expectorants, x-ray contrast dyes,
– Seaweed tablets, and health food
supplements
– These should be avoided because
– The iodide interferes with or
complicates the management of both
ATD and RAI Rx.
Summary of Hyperthyroidism
Hyperthyroidism
Graves (TSI Ab
Age
%
Enlarged Pain
RAIU Treatment
20 - 40
60% Diffuse
None
↑↑
ATD – 18 m
Toxic MNG
> 50
20% Lumpy
Pressure
↑
RAI, Surgery
Single Adenoma
35 - 50
5%
None
±
RAI, ATD
Yes
↓↓
NSAID, Ster.
eye, dermo, bruit)
Single
S Acute Thyroiditis Any age 15% None
TSH is markedly low, FT4 is elevated
Thyrotoxicosis Factitia

Excessive intake of Thyroxine causing thyrotoxicosis

Patients usually deny – it is willful ingestion

This primarily psychiatric disorder

May lead to wrong diagnosis and wrong treatment

They are clinically thyrotoxic without eye signs of
Graves

High doses of Thyroxine lead to TSH suppression

This causes shrinkage of the thyroid

Stop Thyroxine and give symptom relief drugs

A 27 years unmarried lady presented with the
history of weight loss increased appetite ,
sweating and palpitation
 Q what is D/D ?
Case # 1
A patient complains of “sandy” sensation in his
eyes,weight loss, and a tremor. His extraocular muscles
are inflammed. His thyroid is diffusely enlarged and
non tender.
The most likely diagnosis is
a. Iodine deficiency
b. Sub-acute thyroiditis
c. Multinodular goiter
d. Graves’ disease
e. Silent thyroiditis
Case # 2
A 55 year old woman is anxious, irritable, frequent
semi solid stools and she reports weight loss of 5 kgs in
the past six months. She was having a lumpy bumpy
painless swelling in her neck for past 20 years.
The most likely diagnosis is
a. Iodine deficiency goiter
b. Sub-acute thyroiditis
c. Multinodular goiter
d. Graves’ disease
e. Solitary toxic adenoma
Case # 3
A 60 year patient from a mountain region complains of
constipation. He has a heart rate of 60, dry thick skin,
and a tongue that has scalloped edges from teeth
indentation. He has a goiter.
The most likely diagnosis is
a. Iodine deficiency
b. Subacute thyroiditis
c. Graves’ disease
d. Silent thyroiditis
Case # 5
A 72 year old man complains of tremor and inability to
concentrate. On exam, he has a heart rate of 100 beats
per minute. He has a large goiter with many nodules. He
has a fine tremor. His serum T4 is very high and TSH is
very low.
Treatments that are likely to improve his symptoms are
a. Iodine therapy
b. Ethanol injection of his thyroid (PEI)
c. 6 weeks of Methimazole
d. Radio Active Iodine therapy
Case # 6
In Nuclear Scintigraphy Scan I123 uptake is very high
in
the thyroid of patients with
a. Silent thyroiditis
b. Single functional adenoma
c. Sub-acute thyroiditis
d. Acute ingestion of animal thyroid extract
e. Graves’ disease
Hypothyroidism and
Myxedeam
Coma
PROF.BIKHA RAM DEVRAJANI
MB,FCPS,FACP
INCHARGE MEDICAL UNIT IV
LUMHS JAMSHORO
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




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, are characteristic neurologic
findings
– See table below for more complete list
Hypothyroidism

Symptoms and Signs or Hypothyroidism
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 Coma
Introduction

Myxedema coma still has a high mortality rate
(despite intensive treatment).
Clinical Manifestations
Reduced level of consciousness.
 Seizures.
 Other features of hypothyroidism.
 Hypothermia (up to 74oF).
 There may be a history of treated hypothyroidism
with poor compliance, or the patient may be
previously undiagnosed.

Clinical Manifestations

Myxedema coma almost always occurs in the
elderly and is usually precipitated by factors that
impair respiration, such as:
– Drugs (esp. sedatives, anaesthetics, antidepressants).
– Pneumonia.
– Congestive heart failure.
– Myocardial infarction.
– Gastrointestinal bleeding.
– Cerebrovascular accidents.
– Sepsis.
– Exposure to cold.
Elevated TSH
Measure Free T4
Normal
Low
Subclinical
hypothyroidism
Primary
hypothyroidism
TPOAb+ or
symptomatic
T4 treatment
TPOAb–, no
symptoms
Annual follow up
TPOAb+
Autoimmune
hypothyroidism
T4 treatment
TPOAb–
Rule out other
causes of
hypothyroidism
Normal TSH
Pituitary disease suspected?
No
Yes
No further testes
Measure free T4
Low
Normal
No further tests
Rule out drug effects,
sick euthyroid syndrome,
then evaluate anterior
pituitary function
Pathogenesis
Hypoventilation, leading to hypoxia and
hypercapnia, plays a major role in pathogenesis.
 Hypoglycemia and dilutional hyponatremia also
contribute to the development of myxedema coma.

Treatment
Levothyroxine – single intravenous bolus of 500 g,
and usually continued at a dose of 50–100 g.
OR
 Liothyronine (T3) intravenously or via NG tube, dose
range from 10 – 25 g every 8 to 12 h.

– T4  T3 conversion is impaired.
– Excess dose has the potential to provoke arrhythmias.
OR
Treatment

Combine levothyroxine (200 g/d) and liothyronine
(25 g) as a single, initial intravenous bolus
followed by daily treatment with levothyroxine (50 to
100 g/d) and liothyronine (10 g every 8 h).
Supportive therapy should be provided to correct
any associated metabolic disturbances.
 External warming is indicated only if the
temperature is <30oC, as it can result in
cardiovascular collapse.

Treatment
Space blankets should be used to prevent further
heat loss.
 Parenteral hydrocortisone (50 mg every 6 h), as
there is impaired adrenal reserve in profound
hypothyroidism.
 Any precipitating factors should be treated,
including the early use of broad-spectrum
antibiotics, pending the exclusion of infection.

Treatment
Ventilatory support with regular blood gas analysis
is usually needed during the first 48 h.
 Hypertonic saline or intravenous glucose may be
needed if there is hyponatremia or hypoglycemia.

– Hypotonic intravenous fluids should be avoided because
they may exacerbate water retention secondary to
reduced renal perfusion and inappropriate vasopressin
secretion.
Treatment
The metabolism of most medications is impaired,
and sedatives should be avoided if possible or used
in reduced doses.
 Blood levels should be monitored, when available,
to guide medication dosage.

Algorithm for Thyroid Nodule
Thyroid Nodule
Low TSH
Normal TSH
TC 99 Nuclear Scan
Hot Nodule
RAI Ablation,
Surgery or
ATD
FNAC or US
guided biopsy
Cold Nodule
4%
Malignant
Surgery
10%
69%
Suspicious or
follicular Ca
Benign
T4
suppression
Cyst
17%
Non diagnostic –
repeat FNAC
Surgery or
Cytology

A 27 years unmarried lady presented with the
history of weight loss increased appetite ,
sweating and palpitation
 Q what is D/D ?
Case # 4
A 25 year old woman is three months pregnant. She
has a large goiter. Her exam is otherwise normal.
Her thyroid tests are normal.
You recommend
a. Cassava five times weekly
b. Fish three times weekly
c. Formula milk for the baby when it is
born
d. A very low salt diet
THYROID DISEASE
IN PREGNANCY
Physiologic
Changes in Pregnancy

Free thyroxine levels remain within the normal
range during pregnancy (though total
thyroxine levels are increased secondary to
increased TBG.)
 TSH decreases slightly in first trimester.
 The thyroid gland increases slightly
in size during pregnancy.
Hypothyroidism

Untreated patients with hypothyroidism
rarely conceive and carry a pregnancy.
 Treated hypothyroidism usually has
no associated pregnancy complications.
Hypothyroidism

Some patients will require increased
levothyroxine doses during their pregnancies.
 Monitor thyroid function tests each trimester
and at other clinically indicated times.
 Prenatal vitamins can decrease the absorption
of levothyroxine.
Hyperthyroidism

95% of hyperthyroidism in pregnancy
is secondary to Graves’ Disease.
 A good pregnancy outcome can be
expected in patients with good control.
Hyperthyroidism

Untreated hyperthyroidism is associated
with decreased fertility, an increased rate
of miscarriage, intrauterine growth retardation
(IUGR), premature labor, and perinatal
mortality.
 Poorly controlled thyrotoxicosis is associated
with thyroid storm especially at labor and
delivery.
Hyperthyroidism

Beta Blockers and PTU can be safely used
in pregnancy and in nursing mothers.
 PTU crosses the placenta but does not usually
cause fetal hypothyroidism and goiter unless
used in high doses.
 Treatment goals favor mild hyperthyroidism
over hypothyroidism.
Hyperthyroidism Grave’s Disease

Like other immune mediated diseases
in pregnancy, Grave’s disease tends to
improve
in the third trimester.
 Exacerbations may occur in the first trimester
and postpartum.
Hyperthyroidism Grave’s Disease

Neonatal and fetal thyrotoxicosis may occur
because of transplacental passage of thyroid
stimulating antibodies.
Postpartum Thyroiditis

Postpartum thyroiditis is a destructive
autoimmune thyroiditis that begins with
a period of hyperthyroidism followed by
a period of hypothyroidism. The gland is
often enlarged.
 There is usually complete recovery but a
chance
of recurrence in subsequent pregnancies exists.
Postpartum Thyroiditis

80-85% of patients will have positive
antithyroid antibodies.
 A radioactive iodine uptake scan can
differentiate postpartum thyroiditis from
an exacerbation of Graves’ Disease.
Postpartum Thyroiditis

Postpartum thyroiditis in an important
consideration in women with postpartum
depression.
Hyperemesis Gravidarum

Hyperemesis is associated with abnormal
thyroid function tests in a significant number
of cases.
 Hyperthyroidism may be the cause of
hyperemesis or hyperemesis may be the cause
of the hyperthyroidism.
Thyroid Nodules

New thyroid nodules should be aggressively
investigated during pregnancy because of a
high incidence of malignancy.
Thyroid Investigations

Radioactive Iodine is contraindicated in
pregnancy.
 Nursing mothers who have radioactive iodine
uptake scans should pump and discard their
milk for 48-72 hours after the test.
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:





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
600-1000mg PO initially, followed by 200-250 mg q 4 hrs
 Methimazole
40 mg PO initial dose, then 25 mg PO q6h
– Prevent relases of hormone (after synthesis blockade intiated)
 Iodine
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
 Lithuim
800-1200 mg PO every day
– Prevent peripheral effects:
 B-Blocker
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
 Guanethidine
30-40 mg PO q 6 h
 Reserpine
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
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