Thyrotoxicosis, or hyperthyroidism, is caused by excessive thyroid hormones. It can be primary, resulting from conditions like Graves' disease, or secondary, from a toxic multinodular goiter or toxic adenoma. Graves' disease is an autoimmune disorder caused by antibodies that stimulate the thyroid. Symptoms include hypermetabolism, nervousness, and eye changes. Diagnosis involves thyroid function tests, ultrasound, and radioactive iodine uptake. Treatment options are antithyroid medications, radioactive iodine therapy, or surgery. Complications can include thyroid storm, which is a medical emergency requiring aggressive treatment.

1. Thyrotoxicosis
Dr.Sundarprakash Sivalingam
Associate Professor in surgery

2. Definition
• Thyrotoxicosis is the biochemical and clinical complex that results
when the tissues are presented with excessive quantities of the
thyroid hormones.

3. Classification
1. Primary thyrotoxicosis
Graves disease
Diffuse toxic goiter
2. Secondary thyrotoxicosis
Plummer’s disease
3. Toxic nodule
4. Other causes

4. Causes of hyperthyroidism
• Graves disease (Primary Thyrotoxicosis)
• Thyrotoxicosis in Multinodular goitre (Secondary Thyrotoxicosis)
• Toxic adenoma
• Thyroiditis
• Subacute
• Lymphocytic
• Drug induced
• Thyrotoxicosis factitia
• Jod Basedow thyrotoxicosis— Iodide induced
• Autoimmune thyroiditis or de Quervain’s thyroiditis.
• Neonatal thyrotoxicosis.
• Struma ovarii.
• Drugs like amiodarone

5. Primary thyrotoxicosis
• Graves' disease
• an autoimmune disorder
• caused by thyroid-stimulating antibodies directed at the TSH on
follicular cells.

6. Pathogenesis
• The exact cause of Grave’s disease is unknown but
several immunological phenomena have been
observed.
• There is an increased frequency in HLA B8-DR3 in
Caucasians with this disease.
• A circulating antibody, which stimulates the TSH
receptors mimicking all effects of TSH is the patho-
genetic event in Graves' disease.
• The thyroid gland is diffuse and smoothly enlarged
with an increased vascularity.
• On microscopy, the epithelium is tall (columnar) with
minimal colloid present.
• Prominent infoldings of hyperplastic epithelium.
• Lymphocytic infiltration may be seen in the thyroid.

7. Clinical Features
• Symptoms :-
o Hypermetabolism:-
heat intolerance
excessive sweating
hunger
weight loss.
o Adrenergic discharge:-
nervousness
emotional lability
insomnia
tremors
psychosis
oCardiac:-
Dyspnea
palpitations
enhancement of angina pectoris
cardiac failure
oGastrointestinal:-
diarrhea
Increased appetite
oMuscular:-
Proximal muscle weakness
Menstruation:-
oligomenorrhea and amenorrhea and
abortions or failure to conceive .

8. Examination
• Patient appears anxious, restless and fidgety.
• Warm skin
• Moist palm
• The hair is fine and silky.
• A fine tremor of the fingers and tongue is characteristic.
• Cardiovascular manifestations
wide pulse pressure
tachycardia
atrial arrhythmias
systolic murmurs
cardiomegaly
sometimes heart failure.
• Splenomegaly also may be present.
• A diffusely enlarged thyroid gland is seen. A bruit is generally present over the gland signifying that the patient
is thyrotoxic.
• Skin Dermopathy is uncommon and usually occurs over the dorsum of the legs or feet and is termed pretibial
myxedema. The affected area is raised, thickened and may be hyperpigmented.

9. Eye signs
"DR Joffroy may validate symptoms"
Dalrymple sign:- rim of sclera is seen all around the cornea,
on looking straight forward.
Rosenbach's sign:- fine tremor of the upper eyelids on
slight closure of the eye.
Joffroy's sign:-lack of wrinkling of the forehead when a
patient looks upward.
Moebius sign:- lack of convergence on looking to near
object.
Von Graefe's sign (lid lag sign):-lagging of the upper eyelid
on looking downward without movinh the head.
Stellwag's sign:-staring look with infrequent blinking.

10. Toxic Multinodular Goiter (Plummer's Disease)
• Toxic multinodular goiter is a consequence of longstanding simple goiter.
• Commonly seen in endemic areas.
• The transition from nontoxic to toxic nodule involves the development of functional
autonomy, i.e. some nodules become independent of TSH stimulation.
• In both endemic and sporadic goiters, administration of iodides may lead to the
development of thyrotoxicosis.
• Toxic multinodular goiter is a disease of the aging or elderly and is less severe than
Graves' disease( Jod-Basedow phenomenon).
• An enlarged nodular thyroid is palpable sometimes with compressive symptoms-
dysphagia or dyspnea.
• Cardiovascular involvement is more common and may manifest as arrhythmias (atrial
fibrillation) or congestive cardiac failure precipitated by thyrotoxicosis.
• Weakness and wasting are predominant with loss of appetite. This listlessness of the
patient is called apathetic thyrotoxicosis.

11. Toxic Adenoma
• Autonomously functioning thyroid nodules (AFTN) are nodules that
function independently of the normal pituitary-thyroid negative
feedback control mechanism.
• Autonomously functioning thyroid nodules usually produce
hyperthyroidism and suppress TSH secretion by the pituitary.Hence,
the extranodular tissue becomes functionally inactive.
• Most AFTN become clinically manifest when the diameter exceeds 3
to 4 cm in size.

12. Primary thyrotoxicosis Secondary thyrotoxicosis
Etiology—Autoimmune Not autoimmune
Enlargement of goiter is diffuse, firm or soft Bosselated or nodular not uniform
Onset is abrupt Insidious
Hyperthyroidism is usually severe Hyperthyroidism usually mild
Cardiac failure is rare Cardiac failure or multiple extrasystole,
paroxysmal atrial tachycardia,
paroxysmal atrial fibrillation, or persistent atrial
fibrillation
Eye signs common Except lid lag and retraction other eye signs are
not seen
No pre-existing goiter Pre-existing nodular goiter for a long duration
Usually younger women Usually middle aged or elderly
The entire gland is overactive Internodular thyroid tissue is overactive, rarely
one or more nodules
also may be overactive
Presence of bruit Bruit need not be present
. It is due to abnormal thyroid stimulating
antibodies (TSAb)
No such antibodies (it is due to over activity of
nodules)
Can be managed by, drugs, radioiodine,
and surgery
Surgery is the treatment of choice after control of
the toxicity
Manifestations not due to hyperthyroidism
pretibial myxedema may occur
Not seen

13. Other Varieties of Thyrotoxicosis
1. Thyrotoxicosis factitia :- It results from ingestion of large amounts
of thyroid hormone. The syndrome is usually seen in women with
underlying psychiatric disorder and in hospital personnel.
2. Trophoblastic Tumor :- Patients with choriocarcinoma or
hydatidiform mole frequently display elevations of serum total and
free T. and T 3 concentrations. A circulating thyroid stimulator of
trophoblastic origin, possibly hCG, causes thyroid hyperfunction.
Ectopic thyroid tissue with widespread functioning metastasis of
thyroid carcinoma or struma oveaii may occasionally give rise to
thyrotoxicosis.

14. Investigations
1. Thyroid function tests
2. Ultrasound of thyroid
3. Radio-iodine uptake study
4. Thyroid antibodies

15. Treatment
• Medical therapy
• Radioiodine ablation
• Surgery

16. Medical Therapy
• Antithyroid drugs
• Carbimazole (CBZ)
• Methimazole
• propylthiouracil (PTU)
• belonging to the thioureas group
• also blocks the conversion of T4 to T3 in the peripheral tissues.
• PTU is started at a dose of 100 mg
• CBZ at a dose of 10 to 20 mg thrice daily.
• Most patients become euthyroid within 4 to 8 weeks of therapy. The dose is then
reduced to a maintenance dose.

17. • Iodides
• It is the fastest acting thyroid inhibitor.
• It reduces iodide transport, oxidation and organification and to block the release of
T4 and T3 from the thyroid gland.
• The preparations used include Lugol's iodine (3 to 5 drops thrice daily). 5% sol has
5% iodine and 10% pot iodide.
• The major use of iodide is in preoperative preparation and in the management of
thyrotoxic storm.
• Beta-blockers
• block beta-adrenergic receptors and provide relief from symptoms like tremors,
palpitations, anxiety and heat intolerance.
• decrease the heart rate, cardiac output and oxygen consumption in thyrotoxicosis.
• The drugs used are propranolol (40 to 180 mg/day) or atenolol (25 to 100 mg/day).
• contraindicated in patients with congestive cardiac failure, asthma and diabetes.

18. Radioiodine Therapy
• Radioiodine is simple and economical therapy.
• Indicated in patients above 40 years, especially those who fail to respond to
antithyroid drugs and failures of surgery.
• Contraindicated during pregnancy and lactation and in severe thyrotoxicosis or in
patients with large or malignant thyroids.
• A dose that will deliver about 5,000 to 8000 rads to the thyroid will be effective in
ameliorating the hyperthyroidism in Graves' disease.
• The patients should be euthyroid prior to radioiodine therapy to prevent thyroid
storm. Thyroid function gradually declines beginning in 2 to 3 weeks.
• The main drawbacks are hypothyroidism, risk of carcinogenesis, and
teratogenicity after the use of radioiodine, though the precise likelihood of the
latter two remain contentious.

19. Surgical Therapy
• The objective of thyroidectomy is complete and permanent control of
thyrotoxicosis.
• The patients should be euthyroid before operation, with antithyroid drugs that
should be continued up to the day of surgery.
• Lugol's iodine, in the preoperative preparation, will reduce the vascularity of the
gland. The preparation is necessary to reduce the risk of thyroid storm.
• Subtotal thyroidectomy is commonly performed leaving 4 to 8 gm of residual
thyroid tissue.
• Total thyroidectomy should be considered in patients with infertility and Graves'
disease with coexisting eye disease.

20. Complications of surgery
a. Postoperative hemorrhage leading to the development of tension
hematoma and respiratory distress.
b. Respiratory obstruction caused by laryngeal edema,
c. Recurrent laryngeal nerve injury.
d. Hypoparathyroidism that may be temporary or permanent.
e. Thyrotoxic storm.
f. Hypothyroidism.
g. Wound problems-infection and keloid.

21. Thyrotoxic Crisis (or Thyroid Storm)
• A thyroid storm is a life-threatening situation rarely encountered nowadays owing
to the good preoperative preparation for thyrotoxicosis.
• It may be noticed after operation when the patient has tachycardia, fever, and
mental confusion.
• Dehydration from vomiting and fever be present and may progress on to coma.
• It may also occur in medical conditions like infection, trauma or radiation
thyroiditis.
Treatment
• The patient is treated in the acute phase with a fluid replacement, anti-thyroid
drugs, beta blockers and Lugol's iodine through a nasogastric (NG) tube. They
should also receive steroids. Sedation and correction of hyperpyrexia are
important.