Hyperthyroidism is a condition where the thyroid gland produces excess thyroid hormones, leading to thyrotoxicosis or hypermetabolism. It is more common in women and the clinical types include diffuse toxic goiter (Graves' disease), toxic nodular goiter, and toxic nodule. Symptoms include fatigue, emotional changes, heat intolerance, weight loss and palpitations. Signs include tachycardia, sweaty palms, eye signs like lid retraction, and goiter. Treatment options are antithyroid medications, surgery, or radioactive iodine, with the goal of restoring normal thyroid hormone levels. Complications after thyroid surgery can include bleeding, respiratory issues, nerve injury, thyroid dysfunction,
2. Hyperthyroidism
It is a set of disorders that involve
excess synthesis and secretion of
thyroid hormones (T3 and T4) by the
thyroid gland, which leads to the
hypermetabolic condition of
thyrotoxicosis.
3. Thyrotoxicosis
The term thyrotoxicosis refers to the
physiological effects or clinical syndrome of
hypermetabolism that results from excess
circulating levels of T3 ,T4 or both.
Thyrotoxicosis is eight times more common
in women than in men.
5. Diffuse toxic goitre
Usually occurs in younger women and is
frequently associated with eye signs.
The syndrome is that of primary thyrotoxicosis.
7. Toxic nodular goitre
o A simple nodular goitre is present for a long
time.
o Usually in the middle-aged or elderly,
infrequently is associated with eye signs.
o The syndrome is secondary thyrotoxicosis.
o Hyperthyroidism is due to autonomous thyroid
tissue.
8. Toxic nodule
A toxic nodule is a solitary overactive nodule.
It is autonomous and its hypertrophy and
hyperplasia are not due to TSH-Rab.
TSH secretion is suppressed by the high level of
circulating thyroid hormones.
11. Primary thyrotoxicosis
1. Hyperthyroidism is usually more severe and
goitre is diffuse and vascular.
2. Onset is abrupt.
3. Orbital proptosis, ophthalmoplegia and pretibial
myxoedema is present.
4. Thrill and a bruit may present.
5. Cardiac failure is rare.
12. Secondary thyrotoxicosis
1. Hyperthyroidism is not severe and goitre is
nodular.
2. Onset is insidious.
3. Eye signs other than lid lag and lid spasm (due
to hyperthyroidism) are very rare.
4. Cardiac failure is rare or atrial fibrillation is
present.
15. Eye Signs
1.Lid retraction:
Here upper eyelid is higher than normal.
2. Von Graefe’s sign (Lid Lag’s):
It is inability of the upper eyelid to keep pace
with the eyeball when it looks downwards to
follow the examiners finger.
3.Joffroy’s sign:
Absence of wrinkling on forehead when patient
looks up
16. 4. Stellwag’s sign:
Absence of normal blinking. It is due to widening of
palpebral fissure due to lid retraction and also due to
contraction of voluntary part of levator palpebrae
superioris muscle.
5. Moebius sign: It is lack of convergence of eyeball.
6.Naffziger’s sign:
With patient in sitting position and neck fully extended,
protruded eyeball can be visualized when observed
from behind.
17. Thyrotoxicosis should always be considered
in:
a. Children with a growth spurt, behaviour
problems or myopathy.
b. Tachycardia or arrhythmia in elderly.
c. Unexplained diarrhea.
d. Loss of weight.
18. Principles of treatment of thyrotoxicosis
1.Antithyroid drugs
Common use are carbimazole and propylthiouracil.
Advantages. No surgery and no use of radioactive
materials.
Disadvantages. Treatment is prolonged and the
failure rate is at least 50 per cent. With milder
cases being treated for only 6 months and severe
severe cases for 2 years before stopping therapy.
19. 2. Surgery
In diffuse toxic goitre and toxic nodular goitre with
overactive internodular tissue.
Advantages
1. The goitre is removed, cure is rapid and high if
surgery has been adequate.
Disadvantages
1. Recurrence of thyrotoxicosis-5%.
2. Risk of permanent hypoparathyroidism and
nerve injury when subtotal thyroidectomy is
carried out.
3. There is a risk of permanent hypoparathyroidism
and nerve injury.
20. 3. Radioiodine
It destroys thyroid cells reduces the mass of functioning
thyroid tissue to below a critical level.
Advantages.
No surgery and no prolonged drug therapy.
Disadvantages.
1. Isotope facilities must be available.
2. The patient must be quarantined ,avoid
pregnancy and close physical contact
particularly with children.
3. Eye signs may be aggravated.
21. Surgery for thyrotoxicosis
Preoperative preparation:
Preparation is as an outpatient and only rarely
need admission.
Aims is to make the patient biochemically
euthyroid.
Clinical assessment:
a. Improvement in previous symptoms.
b. Objective signs weight gain, lowering of the
pulse rate.
c. Thyroid function tests.
22. Preoperative preparation cont’d
• Antithyroid drugs; Carbimazole 30–40 mg per
day is the drug of choice.
• When euthyroid (after 8–12 weeks), the dose
may be reduced to 5 mg 8-hourly.
• The last dose of carbimazole is given on the
evening before surgery.
24. Thyroidectomy; steps
A curved skin crease incision is made
midway between the notch of the thyroid
cartilage and the suprasternal notch.
Flaps of skin, subcutaneous tissue and
platysma are raised upwards to the
superior thyroid notch and downwards to
the suprasternal notch.
The deep cervical fascia is divided in the
midline between the sternothyroid muscles
down to the plane of the thyroid capsule.
25. Operative steps
The sternothyroid muscle is mobilised off
the thyroid lobe.
Middle thyroid veins passing directly into
the internal jugular vein require ligation and
division.
The branches of the superior thyroid artery
splay out over the upper pole and ligated.
26. Operative steps
The lobe is then free to rotate medially out
of its bed.
The recurrent laryngeal nerve should be
identified.
Inferior thyroid artery is ligated.
27. Operative steps
Resection of each lobe is carried out,
absolute haemostasis is secured by ligation
of individual vessels and by suture of the
thyroid remnants to the tracheal fascia.
Pretracheal muscles and cervical fascia are
sutured, a negative suction drain kept in nd
the wound closed in layers.
31. Postoperative complications
1.Haemorrhage:
a. Deep to deep fascia b. Subcutaneous.
Produces tension hematoma due to slipping of
the ligature of the superior thyroid artery, from a
thyroid remnant or a thyroid vein.
Treatment:
Opening of the wound.
Evacuation of hematoma.
Ligature of the bleeding vessels.
32. 2.Respiratory obstruction due to
Laryngeal edema as a result of
• Tension hematoma
◦ Endotracheal intubation & surgical handling
• Collapse / kinking of the trachea.
• Bilateral recurrent nerve paralysis.
Treatment:
• Release of haematoma.
• Intubation if necessary.
33. Complications cont’d
3. Recurrent laryngeal nerve paralysis and
voice change:
• May be unilateral or bilateral, transient or
permanent.
• If a RLN is injured during surgery and the
transected ends are identified, they should
be reanastomosed.
Voice and cord function should be assessed at
first follow-up 4 weeks postoperatively.
34. RLN
Unilateral:
•Vocal cord lies in cadaveric position
•Hoarseness of voice & aspiration of liquids.
•Ineffective cough
Bilateral:
•Aspiration
•Ineffective cough
•Bronchopneumonia
35. Treatment
Unilateral:
• Speech therapy
• Medialise of cord
• Teflon paste injection
• Thyroplasty type 1
• Muscle or cartilage implant
• Arthrodesis of arytenoid joint
37. Complications cont’d
4.Thyroid insufficiency
5.Parathyroid insufficiency
6.Thyrotoxic crisis
7.Wound infection: Cellulitis.
8.Hypertrophic or keloid scar: If the incision
overlies the sternum and in dark skinned
individuals.
9.Stitch granuloma: If non-absorbable, particularly
silk is used.
38. Thyrotoxic crisis (storm)
• This is an acute exacerbation of
hyperthyroidism.
• It occurs if a thyrotoxic patient has been
inadequately prepared for thyroidectomy
and is now extremely rare.
40. Treatment
Symptomatic and supportive:
• Aministration of intravenous fluids, cooling
the patient with ice packs, oxygen,
• Diuretics for cardiac failure, digoxin for
uncontrolled atrial fibrillation, sedation and
intravenous hydrocortisone.
41. Specific treatment
• Carbimazole 10–20 mg 6-hourly.
• Lugol’s iodine 10 drops 8-hourly by mouth
or sodium iodide.
• 1g i.v. Propranolol intravenously (1–2 mg)
or orally (40 mg 6-hourly) will block -
adrenergic effects.