Thyrotoxicosis

THYROTOXICOSIS

Presented by:Tanvi Singla

Thyrotoxicosis “clinical syndrome that results when

tissues are exposed to high levels of circulating thyroid hormones.”

Hyperthyroidism Other causes like excessive ingestion of thyroxine, release of hormone in ovarian tumors

CLINICAL TYPES

Primary thyrotoxicosis (Grave’s disease)

Secondary thyrotoxicosis (Toxic nodular goitre)

Solitary toxic nodule Hyperthyroidism due to rarer

causes

DIFFUSE TOXIC GOITRE

Grave’s disease (S/S & diffuse vascular goitre appears simultaneously)

Primary thyrotoxicosis 8 times more common in females Hyperthyroidism more severe than secondary Cardiac failure rare

FEATURES: FEMALE

Female with strong family predisposition (50%)

Extra thyroidal manifestation Middle or young age (30-50 yr) Autoimmune disorder (evidence :demonstration

of TSH R auto – antibodies in the circulation)

human Leukocyte antigen(HLA) and T- lymphocyte may contribute

Enlargement of gland is diffuse.

•Pretibial myxoedema• Proximal myopathy• Acropachy• Ophthalmoplegia

PATHOGENESIS : autoimmune

Acini lined flattened cuboidal epithelium, filled with homogenous colloid

Hyperplasic empty acini, which are lined by high columnar epithelium

C/F:

Most significant being:

weight loss despite good appetite

tiredness

heat intolerance Others being:

emotional instability

palpitations

diarrhoea

EXAMINATION GPE: underweight

Thyroid gland:

Site : Swelling in the lower part of the front of the neck.

Size : slight to moderate enlargement.

Shape : symmetrical.

Surface: smooth.

Skin overlying: is warm.

Special character : moves up & down with deglutition.

Consistency : soft or firm

Edge: well defined.

Pulsations & thrills : are detected usually at the upper poles

CNS signs

Insomnia Tremors of tongue and outstretched

hands Agitation Exaggerated reflexes

Cutaneous Changes

Moist warm extremities Profuse sweating & flushed face Falling of hairs Clubbing of fingers & toes Soft and brittle nails

Pretibial myxoedema B/L, non pitting edema, ± a/w

clubbing aka thyrotoxic dermopathy Seen in thyrotoxicosis pt. treated

with surgery or antithyroid drugs Always a/w exophthalmos Cause : deposition of myxomatous

tissue(GAG’s) mainly in pretibial region

Skin – dry coarse and swelling due to obliterated lymphatics by mucin

CVS

More in elderly PULSE

Rate : Sleeping pulse up to 100 – 120/ min Character : water - hammer character

Rhythm: cardiac arrythmias are superimposed on sinus tachycardia as disease progresses.

Stages of development of cardiac arrythmias in thyrotoxicosis

Multiple extrasystoles Paroxymal atrial tachycardia Paroxysmal atrial fibrillation Persistent atrial fibrillation

(non responsive to digoxin)

(V) Eye manifestations :

A. Exophthatmos ( > 50 % of cases ) :

TYPES :

a)Apparent ( mild = false) exophthalmos : widening of the palpebral fissure due to spasm of Muller's muscle.

b)True exophthalmos : actual protrusion of the eyeballs.

It is an autoimmune disease

Infiltration of retro bulbar tissue with inflammatory cells & fluids with varying degree of spasm of upper eyelid as LPS is partly innervated by symapthetic fibresProbably due to cross- reaction of thyroid antigen & eye (Schwartz )

C.T showing infiltration of Retro bulbar spacesTrue exophthalmos

With widdened palpebral apperture and

clearly seen sclera

Classification of eye changes in Graves’ disease

Class Definition

0 No signs or symptoms.

1 Only signs, no symptoms. (Signs limited to

upperlid retraction, stare, lid lag.)

2 Soft tissue involvement (s/s).

3 Proptosis

4 Extraocular muscle involvement(diplopia)

5 Corneal involvement.

6 Sight loss (optic nerve involvement).

Severe cases are marked by pappiloedema and corneal ulceration referred to as malignant exophthalmos

Spasm and retraction usually disappears when hyperthyroidism is controlled – B adrenergic drugs

Sleeping propped up and lateral tarsorrhaphy help protect the eye

Prednisolone – improvement has been reported….intraorbital not preferred.

When the eye is in danger…orbital decompression reqd

Toxic nodular goitre Simple, nodular goitre

present for a long time before the hyperthyroidism

Middle aged or elderly Eye symptoms rare Usually nodules are

inactive and interthyroid tissue is overactive

If 1 or more nodules are active – hyperthyroidism is due to autonomous tissue

Toxic nodule

Solitary overactive nodule Autonomous Hypertrophy not due to

TSH-Rab Normal surrounding thyroid

tissue is inactive due to suppressed TSH secretion bcoz of high , level of circulating hormones

TREATMENTNON SPECIFIC – Rest and Sedation.

SPECIFIC – Medical intervention

Surgical intervention

Radioiodine

ANTI – THYROID DRUGS Carbimazole, Propyluracil, Methimazole B – adrenergic blockers – proranolol,

nadolol Iodides – dec vascularity of the gland

only used as immediate preoperative measure

Drugs help maintain euthyroid state for a long time in hope of spontaneous remission

Block Cvs

effects

Regime Start with 10mg carbimazole- 3 or 4 times a day

…. Latent interval – 2 weeks

When pt. becomes euthyroid, decrease the dose to 5mg- 2 to 3 times a day for 6 to 24 months

Alternative regime- BLOCK AND REPLACEMENT THERAPY

Inhibit all T3 T4 production with high dose and then give maintainence dose of 0.1 – 0.15mg of thyroxine daily

decreased risk of iatrogenic thyroid insufficiency and less follow up required

Adv : no surgery and no use of radioactive

Disadv: prolonged t/t and failure rate about 50%.

aplastic anemia and agranulocytosis Poor prognosis: large gland size,

severity of disease nad TSH-Rab levels

RADIO-IODINE Destroys thyroid cells Reduces mass of thyroid tissue below a

critical level Slow response.. substantial

improvement expected in 8 – 12 wks.. If not repeat dose

Higher dose – thyroid failure in 6mnths Lower dose result in insufficiency Due to sublethal damage to cells not

damaged by t/t

SURGERY Indicated in- severe diffuse toxic goitre

- toxic nodular goitre with overactive

internodular tissue

-toxic nodule Cures by reducing overactive mass Subtotal thyroidectomy- long term followup Total or near total thyroidectomy- immediate

thyroid failure with life long thyroxine replacement… SIMPLIFIES FOLLOW UP

Adv: Goitre is removed, cure is rapid and cure rate is high if surgery has been adequate

Disadv: recurrence in 5% cases

risk of permanent hypothyroidism

nerve injury

young women – cosmetic issues

Structure

Each lobePear shaped2 *1*1 inches

Its apex lies atLevel of oblique lineOf thyroid cartilage& base reach 5th. Or 6th. Tracheal

ring

Isthmus lies on2nd. ,3rd. ,4th ,Tracheal rings

Pyramidal lobeIt is connected to hyoid bone

By fibrous band ( levator glandulae )

thyroid

2 capsules :*true C.T. capsule around gland*false outer capsule from pretracheal fascia

Pretracheal fascia

1- arterial :

Blood supply

• superior thyroid artery• Branch from E.C.A..

– Inferior thyroid artery– Branch from thyrocervical trunk– Which is branch of 1st. Part of subclavian

OthersThyroid artery from aorta ( may be absent )

Accessory tracheal & esophageal braches

2- venous :

Superior thyroid veindrain to I.J.V.

middle thyroid veindrain to I.J.V.

inferior thyroid veinsdrain to left innominate vein

The middle thyroid veinIs the shortest soit is the

1st To be ligated

Superior laryngeal nerve

internal laryngeal nerve Sensory to m.m of

Larynx above vocal cords

external laryngeal nerve

Motor to cricotyroidMuscle

Injury causes voice weaknessIt is closely related

To Superior thyroid artery

Right R.L.N.Turns around 1st. PartOf subclavian artery

Left R.L.N.Turns around arch of

aorta

Both supply all Intrinsic musclesOf larynx except (cricothyroid )

& m.m below vocal cordsInjury causes vocal cord paralysis

Surgical anatomy From superficial to deep:

SkinPlatysma (a muscle in superficial fascia

of neck)Investing layer of deep cervical fasciaPre-tracheal layer of deep cervical

fasciaStrap muscles of neck (thin flat

muscles)

Preoperative preparation

Make patient euthyroid

CARBIMAZOLE regime (8-12wks)

Alternate: B adrenergic blocking drugs

abolish clinical manifest. of toxic state

propranolol(40mgTDS) or nadolol(160mg OD)

rapid response.. Operation can be arranged within few days

continue therapy for 7 days postoperatively

Investigations

Full blood count (CBC) Serum Urea, Electrolytes, Creatinine Thyroid Function tests Laryngoscopy Thyroid antibodies Serum calcium estimation Radio-iodine (99mTc / 131I) scan of thyroid

INFORMED CONSENT FOR THE SURGERY IS

ESSENTIAL

Technique

GA with endotracheal intubation Pt. is supine with table tilted at 15° at the

head end to reduce venous engorgement (reverse trendelenburg)

Sand bag placed transversely under the shoulder

Neck extended Apply tension to skin, platysma and

strap msls for easy dissection.

Curved skin incision made midway between notch of thyroid cartilage and suprasternal notch

Flaps of skin, s/c, platysma raised upwards to superior thyroid notch and downwards to suprasternal notch

Exposing the gland

Investing fascia divided in the midline Strap msls divided only if large area to be

exposed Sternohyoid msl is mobilised off the thyroid

lobe taking care to stay close to msl and outside capsule

Pretracheal fascia opened Gland is exposed

Dealing with vessels Arteries before veins (to prevent venous

engorgement) Vessels clamped, divided and ligated Superior thyroid artery ligated close to the

upper pole of the gland. This is to prevent damage to external

laryngeal nerve.

Inferior thyroid artery is similarly dealt with faraway from the lower pole of the gland

This is to safeguard recurrent laryngeal nerve.

They are not routinely ligated to preserve parathyroid function

Then superior, middle and inferior thyroid veins are dealt with in a similar manner.

i

SUBTOTAL THYROIDECTOMY

TRANSECTED ISTHMUSLobe resected from medial and lateral surface to produce a V shaped suture

4-5gm left

In total thyroidectomy , complete excision of gland with autoimplantation of parathyroid gland

Parathyroid glands

Identified by careful inspection If inadvertently or unavoidbly excised or

devasularised Should be fragmented and auto-

transplanted immediately within sternoclenomastoid muscle

Absolute hemostasis secured by ligation of individual vessels and by suture of thyroid remnants to tracheal fascia

Pretracheal msls and cervical fascia are sutured and wound closed

Complications Hemorrhage Respiratory obstruction Recurrent laryngeal nerve paralysis-Hoarseness

of voice Hypocalcemic tetany (due to accidental removal

of parathyroid glands during total thyroidectomy) Wound infection: This may manifest after 48

hours of surgery Thyroid insufficiency Thyrotoxic crisis Hypertrophic / Keloid scar Stitch granuloma

Post operative care Transient hypocalcemia – oral Ca+2

maybe necessary….if severe then 10ml IV Ca+2 gluconate 10% given

Screen parathyroid insufficiency – serum Ca+2 measured 4-6wks after operation

Recurrent thyrotoxicosis common – lifelong follow up