HEPATIC ABSCESS

GOITER

DR SYED UBAID Associate professor of surgery

INTRODUCTIONDiseases of the thyroid gland invariably leads to enlargement of the gland.The term GOITER is applied to any enlargement of the thyroid gland regardless of the cause.

GOITERThe normal thyroid gland is impalpable. The term goitre (from the Latin guttur = the throat) is used to describe generalised enlargement of the thyroid gland. A discrete swelling (nodule) in one lobe with no palpable abnormality elsewhere is termed an isolated (or solitary) swelling. Discrete swellings with evidence of abnormality elsewhere in the gland are termed dominant nodule.

Classification of thyroid swellings Simple goitre (euthyroid) Toxic goiter Neoplastic Inflammatory Other (Amyloid)

Classification of thyroid swellingsSimple goitre (euthyroid) 1.Physiological Pubertal ,Pregnancy 2.Diffuse hyperplastic Multinodular goitreToxic goiter 1.Diffuse (Graves disease) 2.Multinodular 3.Toxic adenomaNeoplastic 1.Benign 2.Malignant

Classification of thyroid swellingsInflammatory 1. Autoimmune Chronic lymphocytic thyroiditis Hashimotos disease2.Granulomatous (De Quervains thyroiditis)3. Fibrosing (Riedels thyroiditis)4. Infective Acute (bacterial thyroiditis,viral thyroiditis, subacute thyroiditis) Chronic (tuberculous, syphilitic)

Simple goiterAetiology Simple goitre may develop as a result of stimulation of the thyroid gland by TSH, Inappropriate secretion from the anterior pituitary a microadenoma In response to a chronically low level of circulating thyroid hormones. 1. The most important factor in endemic goitre is dietary deficiency of iodine, Goitrogens in food. 2. Defective hormone synthesis (Dyshormonogenesis) probably accounts for many sporadic goitres.

Simple goiterThere is chronic deficiency of Thyroxine (T4) and or triiodotrynine (T3) in the body which in turn causes compensatory elevation of TSH because of the lack of necessary negative feedback. Prolonged stimulation of TSH in attempt to bring normal thyroid hormones level leads to simple goiter. Such phenomenon may occur in the following settings; physiological e.g. puberty, pregnancy, lactation Iodine deficiencyEnzymatic deficiency for example in Pendreds syndrome which is caused by peroxidase deficiency,

Classification of simple goitersimple diffuse goitersimple colloid goitersimple nodular goiter

PathophysiologyChronic absence of T4/T3 causes elevated level of TSH, which then leads to diffuse homogenous hypertrophy and hyperplasia of follicular cells and colloid (secretory follicles) in efforts to produces more thyroid hormones. This is usually a reversible change. The enlarged thyroid hyper involuted with colloid is called colloid goiter.

PathophysiologyDifferential response to TSH leads to formation of nodules within the gland. Several nodules may coalesce and lead to formation of multinodular goiter. The nodules may undergo secondary changes; central necrosis, cystic degeneration, hemorrhage, calcification and malignant changes (3%).

Clinical presentationGradual onset of painless anterior neck swelling, usually long standing in endemically iodine deficient areas. Recent onset of pain or increase in size may indicate secondary changes. The enlarged gland may also affect neighboring structures and lead to wide range of symptoms and signs.

Clinical presentation Obstruction of airwaysLaryngeal nerve compressionEsophageal obstructionNeck veins obstructionSuperior vena cava syndrome (Pembertons sign).

Investigation in simple goiterThyroid function testthyroxine (T4), tri iodothyronine (T3), thyroid stimulating hormones (TSH)thyrotropin releasing hormone (TRH). This helps to know if the thyroid gland is normally, hyper or hypo functioning.

Thyroid scan with radioactive iodine (I123 or I131)In this investigation a traceable radioactive Iodine or Technetium is injected into the blood stream, the thyroid gland concentrates radioactive iodine. The concentrated radioactive iodine can be detected by gamma camera. I123 has a shorter half life as compared to I131 and therefore preferred because it has less exposure of the patient to radiation. Thyroid scan may show hot nodules (which takes more radioactive iodine than the rest of gland) in secondary hyperthyroidism, however most simple goiters have normal uptake or Cold nodules (which does not take radioactive iodine). Cold nodules are likely to be malignant.

Antithyroid receptors antibodies This type of investigation is done in patients suspected to have stimulatory auto antibodies as is the case in Graves disease (primary hyperthyroidism).

Radiological investigations Normal AP and lateral chest X-rays may demonstrate retrosternal extension of the goiter (retrosternal shadow)

Thoracic inlet X-rays may demonstrate compression or deviation of the trachea, this important to anesthetist if surgery is contemplated (difficult intubation).

USG NECKThyroid is homogeneous & slightly hyperechoic.

The normal thyroid gland is 2 cm or less in both the transversedimension and depth, and is 4.55.5 cm in length& 0.5 mm ithmus.

A diffusely enlarged thyroid gland with an isthmus widthof 1.5 cm.

Computed tomography may be indicated if more details are needed before surgery or there is suspicion of malignancy transformation.

Fine needle aspiration cytologyTo rule out malignancy of thyroid. benign,malignant, suspicious malignant, inconclusive or inadequate aspirate. If follicular pattern is seen, lobectomy is done to exclude follicular carcinoma, because the can only be differentiated by demonstrating capsular invasion.

Treatment and prevention of simple goiterDietaryIodine supplementation in iodine deficient areas, food iodine fortification is one of the best preventive measures of goiters. Medical Thyroxin supplementation In patients with diffuse hyperplastic goiter for several months (0.1 to 0.2mg per day).

Surgery indications

In patients with obstructive symptoms, When malignancy is suspected clinically or after FNAC, Hyper functioning nodules For cosmetic reasons

Hypothyroidism is a condition characterized by abnormally low thyroid hormone production. Because thyroid hormone affects growth, development, and many cellular processes, inadequate thyroid hormone has widespread consequences for the body.HYPOTHYROIDSM

Medications and food (GOITROGENS) Pituitary or hypothalamic disease Severe iodine deficiency Thyroid destruction (from radioactive iodine or surgery) Hashimoto's thyroiditis Lymphocytic thyroiditis (which may occur after hyperthyroidism)Aetiology

DRUGSAnti-thyroidCough medicinesSulfonamidesLithiumPhenylbutazonePASiodineOral hypoglycemic agents

GOITROGENS

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FOODSoybeansMilletCassavaCabbageExcess iodine or lithium ingestion, which decrease release of thyroid hormone

GOITROGENS

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Goitrogens(cassava, lima beans, maize, bamboo shoots, and sweet potatoes)

In this condition, the thyroid gland is usually enlarged (goiter) and has a decreased ability to make thyroid hormones. Hashimoto's is an autoimmune disease in which the body's immune system inappropriately attacks the thyroid tissue. Hashimoto's is 5 to 10 times more common in women than in menHashimoto's thyroiditis

Increased antibodies to the enzyme, thyroid peroxidase (anti-TPO antibodies). Patient with Hashimoto's thyroiditis has one or more other autoimmune diseases such as diabetes or pernicious anemiaHashimoto's can be identified by detecting anti-TPO antibodies in the bloodHashimoto's thyroiditis

The likelihood of this depends on a number of factors including the dose of iodine given, along with the size and the activity of the thyroid gland. If there is no significant activity of the thyroid gland six months after the radioactive iodine treatment, it is usually assumed that the thyroid will no longer function adequately. The result is hypothyroidism. Similarly, removal of the thyroid gland during surgery will be followed by hypothyroidism.Thyroid destruction secondary to radioactive iodine or surgery

If for some reason the pituitary gland or the hypothalamus are unable to signal the thyroid and instruct it to produce thyroid hormones, a decreased level of circulating T4 and T3 may result, even if the thyroid gland itself is normal. If this defect is caused by pituitary disease, the condition is called "secondary hypothyroidism." If the defect is due to hypothalamic disease, it is called "tertiary hypothyroidism."Pituitary or Hypothalamic disease

A pituitary injury may result after brain surgery or if there has been a decrease of blood supply to the area. In these cases of pituitary injury, the TSH that is produced by the pituitary gland is deficient and blood levels of TSH are low. Hypothyroidism results because the thyroid gland is no longer stimulated by the pituitary TSH. This form of hypothyroidism can, therefore, be distinguished from hypothyroidism that is caused by thyroid gland disease, in which the TSH level becomes elevated as the pituitary gland attempts to encourage thyroid hormone production by stimulating the thyroid gland with more TSH.Pituitary injury

In areas of the world where there is an iodine deficiency in the diet, severe hypothyroidism can be seen in 5% to 15% of the population. Severe iodine deficiency:

The symptoms of hypothyroidism are often subtle. They are not specific (which means they can mimic the symptoms of many other conditions) and are often attributed to aging. Patients with mild hypothyroidism may have no signs or symptoms. The symptoms generally become more obvious as the condition worsens and the majority of these complaints are related to a metabolic slowing of the body. Symptoms of hypothyroidsm

FatigueDepressionModest weight gainCold intoleranceExcessive sleepinessDry, coarse hairConstipationDry skinMuscle crampsIncreased cholesterol levelsDecreased concentrationVague aches and painsSwelling of the legsCommon symptoms

As the disease becomes more severe, there may be puffiness around the eyes, a slowing of the heart rate, a drop in body temperature, and heart failure. In its most profound form, severe hypothyroidism may lead to a life-threatening coma (myxedema coma). In a severely hypothyroid individual, a myxedema coma tends to be triggered by severe illness, surgery, stress, or traumatic injury.

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A diagnosis of hypothyroidism can be suspected in patients with fatigue, cold intolerance, constipation, and dry, flaky skin. A blood test is needed to confirm the diagnosis.When hypothyroidism is present, the blood levels of thyroid hormones can be measured directly and are usually decreased. However, in early hypothyroidism, the level of thyroid hormones (T3 and T4) may be normal.Diagnosis of hypothyroidism

Thyroid stimulating hormone (TSH) assays are the most sensitive screening tool for primary hypothyroidism.The generally accepted reference range for normal serum TSH is 0.40 4.2 mlU/L.If the levels are above the reference range then the next step is to measure free Thyroxine (T4).Patients with primary hypothyroidism usually have elevated TSH levels and decreased free hormone levels.In patients with hypothalamic or pituitary dysfunction, TSH levels do not increase in appropriate relation to the low free T4 levels

Treatment of hypothyroidism requires life-long levothyroxine (T4) therapy.This is a more stable form of thyroid hormone and requires once a day dosing, whereas T3 is much shorter-acting and needs to be taken multiple times a day. Synthetic T4 is readily and steadily converted to T3 naturally in the bloodstream, 100 to 150 micrograms per dayTreatment of hypothyroidism

Cretinism Hypothyroidism developing in infancy/early childhood Severe mental retardation occurs in iodine deficient areas of world (i.e., Himalayas, inland China, Africa) May also be sporadic, owing to enzyme deficiencies thyroid hormone synthesis

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Cretinism

Clinical features: Impaired skeletal development Impaired CNS development Inadequate maternal thyroid hormone prior to fetal thyroid gland formation SEVERE mental retardation Normal brain development if maternal thyroid deficiency occurs after fetal thyroid gland development

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Toxic goiter, thyrotoxicosis or hyperthyroidismHyperthyroidism is a condition in which an overactive thyroid gland is producing an excessive amount of thyroid hormones that circulate in the blood. Thyrotoxicosis is a toxic condition that is caused by an excess of thyroid hormones from any cause. Thyrotoxicosis can be caused by an excessive intake of thyroid hormone or by overproduction of thyroid hormones by the thyroid gland. Hyperthyroidism can be primary or secondary depending on the etiology.

Causes of hyperthyroidism Graves' Disease Functioning adenoma ("hot nodule") and toxic multinodular goiter (TMNG) Excessive intake of thyroid hormones Abnormal secretion of TSH Thyroiditis (inflammation of the thyroid gland) Excessive iodine intake

Primary hyperthyroidismGraves disease Gravess disease is an autoimmune disease of the thyroid gland, in which there is a circulating autoantibody which resembles TSH. The autoantibody binds to and stimulates G-protein coupled thyrotropin receptors on thyroid gland leading to thyroid hormone release and hyperplasia.

Primary hyperthyroidismGraves disease These antibodies include thyroid stimulating immunoglobulin (TSI antibodies), thyroid peroxidase antibodies (TPO), and TSH receptor antibodies

Primary hyperthyroidismGraves disease Graves' disease is hereditary and is up to five times more common among women than menFemale: male ratio is 9:1Graves disease tends to affect young than older womenIt causes about two third of all cases of hyperthyroidismThese antibodies also react with retrobulbar auto antigens to cause periorbital edema and protrusion of eye ball (exophthalmos).

The triggers for Grave's disease include:stress, smoking, radiation to the neck, medications,Infectious organisms such as viruses.

In patients with secondary hyperthyroidism, there is a pre existing thyroid pathology for example goiter or inflammatory condition which leads to excess production of thyroid hormones or there is an extra thyroid source of hormone production. Secondary hyperthyroidism has high predilection to involve cardiovascular systemSecondary hyperthyroidism

In this form of secondary hyperthyroidism, there is hypersecreting toxic nodule in the background of multinodular goiter (Plummers disease); This tends to occur in iodine deficient areas (endemic goiters).

Multinodular goiter

This form of secondary hyperthyroidism is characterized by presence of benign glandular nodule in the thyroid gland, usually follicular which secrets excess hormones.

Toxic adenoma

In this form of secondary hyperthyroidism, there is a hormone producing tumor elsewhere in the body. For example metastatic follicular thyroid carcinoma, choriocarcinoma which produces -hCG whose alpha chain resembles TSH and thyroid tissue containing teratoma. The excess thyroid hormones lead to clinical features typical of hyperthyroidism.

Ectopic thyroid hormone

In this form, excess hormone has been introduced into the body. An example is what is called thyrotoxicosis factitious which is due to excess intake of thyroxine hormone and Jod-Basedow which is caused by excessive intake of iodine in endemic goiter.Exogenous causes

This is another cause of excess thyroid hormone production; an adenoma in the pituitary gland (which normally controls the thyroid gland) produces TSH which in turn leads to excess T4 and T3.

TSH producing pituitary adenoma

Post viral thyroiditis with transient self limiting thyrotoxicosis (Subacute de Quervain thyroiditis); this form of hyperthyroidism is usually painful and may be associated with other systemic symptoms. Radiation induced thyroiditis with release of preformed thyroid hormones is commonly seen in patients undergoing neck radiation

Other causes

Inflammation of the thyroid gland may occur after a viral illness (Subacute thyroiditis). This condition is associated with a fever and a sore throat that is often painful on swallowing. The thyroid gland is also tender to touch. There may be generalized neck aches and pains. Inflammation of the gland with an accumulation of white blood cells known as lymphocytes (lymphocytic thyroiditis) may also occur.Thyroiditis

Central nervous systemCentral nervous system features are very common in patients with primary thyrotoxicosis. tremors which can be observed on the tongue and fingers, nervousness, emotional liability (patients become irritated easily), they may also be lethargic or agitated and usually they have warm and moist hands.

Clinical features of hyperthyroidism

Increased metabolic rate

weight loss, heat intolerance,excessive sweating, and tiredness cause by muscle weakness as a result of proteolysis.

Cardiovascular; very common in patients with secondary hyperthyroidism. They include awareness of heart beats (palpitation) due to tonic and chronic effect of excess thyroid hormones, irregular heartbeats (arrhythmia), sleeping tachycardia, high output heart failure and thyroid bruit due to excess blood flow to the gland.

Gastro intestinal tract (GIT);loss of body weight despite having good or increased appetite, and increase bowel motions (diarrhea).

Genital urinary tract (GUT)

irregular menstruation, amenorrhea, loss of libido and erectile dysfunctions

Ophthalmological featuresEye symptoms as is the case for central nervous system are common in Graves disease. Eye protrusion or exophthalmos can be true when it is caused by retrobulbar cellular infiltration and mucopolysaccharide depositions or false exophthalmos when it is caused by elevation of superior eye rid due to hyper activity of levator pulpebral superioris muscle or Muller muscle. The later is caused by increased sympathetic tone.

True exophthalmos : actual protrusion of the eyeballs.It is an autoimmune diseaseInfiltration of retro bulbar tissue with inflammatory cells & accumulation of inflammatory fluids.

Probably due to cross- reaction of thyroid antigen & eye (Schwartz )

C.T showing infiltration of Retro bulbar spaces

True exophthalmos

B. Certain eye signs :1. Stellwag's sign : Staring look with infrequent blinking.

2.Dalrymple's sign : rim of sclera is seen between cornea and the upper lid.3.Von Graef's sign : Lagging of the upper eye lid4.Joffroy's sign :

Loss of forehead corrugation when looking up 5. Moebius' sign : Lack of convergence (due to ocular myopathy )

Exophthalmos can lead to exposure conjunctivitis, keratitis (corneal ulceration) and perforation. Ophthalmoplegia or eye paralysis can be caused by cellular infiltration. Ophthalmoplegia can be bilateral or unilateral and can be associated with diplopia (double vision).

Graves OpthalmopathyClass 0 No symptoms or signs Class I Only signs, no symptoms (eg, lid retraction, stare, lid lag) Class II Soft tissue involvement Class III Proptosis Class IV Extraocular muscle involvement Class V Corneal involvement Class VI Sight loss (optic nerve involvement)

Clinical featuresPrimary Hyperthyroidism (Graves)Secondary Hyperthyroidism (Plumer)AgeYoung ageElderlyOnsetAbruptGradualCourseRemissions & exacerbationsSteady courseNervous symptoms++++Metabolic manifestations++++Eye signs+++FALSECV manifestations++++Thyroid glandDiffuseNodular

A rare presentation of thyrotoxicosis, there is extreme signs of thyrotoxicosis associated with severe metabolic disturbances. It occurs in patient with hyperthyroidism who has not been well prepared (hyperthyroidism is not controlled) before surgery. It may also occur in patients with major stress eg major trauma and infection. Clinical features includes; hyper-thermia, tachycardia, irritability, profuse sweating and diarrhea.

Thyroid storm (thyrotoxic crisis)

Medical treatmentSymptomatic treatmentAntithyroid treatmentTreatment of thyrotoxicosis

Medications which either target the thyroid hormones or symptoms. Indications include; primary thyrotoxicosis in small gland, primary thyrotoxicosis in young age, pre-operative preparation, post-operative recurrence and patients refusal of surgery.

Medical treatment

This targets central nervous system and cardiovascular symptoms. Beta adrenergic blockers are the mainstay of symptomatic therapy for thyrotoxicosis.Propranolol in range of 40mg twice or thrice a day has been used with greatest success due to additional benefit of inhibition of peripheral conversion of T4 to T3 Symptomatic treatment

Fevers are treated with cooling measures and antipyretics.Intravenous glucocorticoids are indicated if adrenal insufficiency is suspected.Aggressive hydration of up to 3 5 L/d of crystalloid compensates for potentially profound GI and insensible losses.Charcoal hemoperfusion has been shown to be effective in treatment of iatrogenic or intentional ingestion of excessive doses of levothyroxine

These drugs either blocks iodine binding to tyrosine and decrease antibody titers (Carbimazole) or block iodine binding and prevent conversion of T4 to T3 (propylthiouracil). Antithyroid treatment

Antithyroid drugsInhibitors of hormone synthesis 1.Propylthiouracil (PTU) 2.Methimazole (Tapazole)Blockade of hormone releaseLopanoic acidSaturated solution of potassium iodideLugol solution

The drug of choiceRecommended as DOC for women who are pregnant or breastfeeding.Dosage:HYPERTHYROIDSM: 300 450 mg/day 8 hrly initially (may require up to 600 900 mg/day)Maintenance: 100 150 mg/day 8hrlyPropylthiouracil (PTU)

THYROTOXIC CRISES:Initial 200 300 mg PO q4 6hr initially on day 1 (may require 800 1200mg/day),Then reduce graduallySome practitioners propose an initial dose of 600 1000mg with gradual dose reduction after initial response.Maintenance: 100 150mg/day PO divided q8 12hrGRAVES DISEASE:50 150mg PO initiallyMaintenance: 50mg PO q8 12hr for up to 12 18 months, then taper and discontinue if TSH is normal

All patients must be euthyroid before embarking in surgery, ECG, CXR, and Echocardiogram must be done to rule out arrhythmia and heart failure. Thoracic inlet X-ray in huge goiters to rule tracheal deviation and compression as discussed above. Lugols iodine reduces risk of hemorrhage.

Surgical treatment

Graves disease in young, large gland or in patients with exophthalmos, multi-nodular or solitary nodule, unresponsive, poor compliance to medical treatment and when there is contraindication to drug e.g. hypersensitivity.Indications for surgical intervention

Subtotal thyroidectomy; leaves about 8-10 gram of thyroid tissue, either 4-5gram on each side or 8-10 gram on one side. Near total thyroidectomy removes nearly all thyroid tissue leaving only about 4gm thyroid tissue; Lobectomy removes the entire lobe one side with isthmusectomy eg in solitary toxic nodule;Partial thyroidectomy; bilateral partial lobectomy eg in multinodular toxic goiter involving both lobes.Types of surgery

Hemorrhage Primary is a type of bleeding which occur during surgery due to arterial or venous cut, Reactionary bleeding occurs when a patients blood pressure comes to normal after waning of hypotensive anesthetic drugs or due to pain and Secondary bleeding which occurs 7 days to 2 weeks after surgery, usually due to infection of wound.

Complication of thyroid surgery

Respiratory obstructionApart from hematoma formation, the following can also cause airway obstruction post thyroidectomy period; traumatic laryngeal oedema, bilateral recurrent laryngeal nerve injury leading to vocal cords paralysis, especially in patients with huge thyroid complicated by difficult surgery, tracheomalacia occurs in patients with huge goiters or those with retrosternal extension.

Recurrent laryngeal nerve injuryRecurrent laryngeal nerve injury can be unilateral leading to hoarseness of voice & dyspnea on exertion, bilateral incomplete in which the patient can present with stridor (due to irritation of adductor fibers)bilateral complete with voice loss (aphonia).

Superior laryngeal nerve damage Superior laryngeal nerve injury may also occur in difficult surgery, loss of function of this nerve leads to loss of high pitched voice (cricopharyngius paralysis).

Thyroid insufficiency Thyroid insufficiency following thyroidectomy may occur 2 to 5 years later, it may occurs as high as 20 to 45% in patients who have undergone total thyroidectomy

Parathyroid insufficiencyHypoparathyroidism occurs when both parathyroid glands are accidentally traumatized, devascularized or damaged. If seen after removal, the glands must be reimplanted on deltoid muscles or sternocleidomastoid muscles. The incidence of hypoparthyroidisim occurs in less than 0.5% of all patients underwent thyroidectomy.Parathyroid hormone is responsible for calcium homeostasis (increases GIT calcium reabsorbtion, resorbs bone, reduces renal calcium excretion and enhances phosphorus renal excretion). In absence causes hypocalcaemia.

Keloid scar and hypertrophic scarsKeloid and hypertrophic scars are late complication of thyroidectomy, occurring several years after surgery. The two can be differentiated because the former forms mass which crosses an incision line and the later does usually cross the incision line.

Hematoma and bleeding This is one of the most common complications in thyroid surgery. When suspected, reopen the wound immediately and ligate any bleeding vessel (wound exploration and bleeder ligation). Such treatment should start at bed side if bleeding is severe or when hematoma is obstructive. Give IV fluids using large bore canula and transfuse if necessary.

Management of some important post operative complications

Respiratory obstruction and recurrent laryngeal nerve damageIntubate the patient immediately if obstruction is severe, or perform cricothyroidotomy if intubation is not convenient. Ventilate or give high flow oxygen 8 L/second and make sure an intravenous line is established with crystalloids.

Hypoparathyroidism Symptoms and signs of hypocalcaemia include circumoral paresthesias, mental status changes, tetany, carpopedal spasm, laryngospasm, seizures, QT prolongation on ECG, and cardiac arrest. In such condition, a patient is given IV 10mls of 10% Calcium Gluconate over 10 minutes, or calcium carbonate 2.5g to 5g orally.

Thyroid stormSupportive measures which includes IV fluids ice packs and antipyretics, oxygen mask 8litres per second, and sedatatives. Specific treatment include giving propranolol 1mg IV as drip repeated if needed, oral Carbimazole or propylthiouracil and Digoxin if heart failure is diagnosed.

Retrosternal goiter

What is Retrosternal goitera goitre with a portion of its mass located in the mediastinum

Why Primary intra-thoracic goitres arise from aberrant thyroid tissue which is ectopically located in the mediastinum, receive their blood supply from mediastinal vessels and are not connected to the cervical thyroid. They are rare, representing less than 1% of all RGsSecondary RGs develop from the thyroid located in its normal cervical site. Downward migration of the thyroid into the mediastinum is facilitated by negative intra-thoracic pressure, gravity, traction forces during swallowing and the presence of anatomical barriers preventing the enlargement in other directions (thyroid cartilage, vertebral bodies, strap muscles, especially in patients with a short, large neck). These secondary RGs are, characteristically, in continuity with the cervical portion of the gland and receive their blood supply, depending on cervical vessels, almost always through branches of the inferior thyroid artery.

Types Plunging goiter : rise with deglutition and then descent again through the thoracic inlet Mediastinal goiter : lie wholly in the chest but are connected with the thyroid and supplied by thyroid vessels through narrow band Intrathracic goiter : lie wholly in the chest but completely separated from the gland supplied by mediastinal vessels

How Short-necked individualsUsually after middle ageIntrathracic goiter more common in men

Symptoms May remain symptomless for years Dyspnea due to displacing and compressing on the trachea The Dyspnea aggravated by any posture that reduces the thoracic inlet as lying down or flexion the neck The patient prefer to spend the night in a chairSome time they miss diagnosed as asthmaticSometimes there is dysphagia

Signs Inspection

SignsPalpation : thyroid gland enlarged

Signs Percussion of the sternum may reveal retrosternal dullness

Investigations X-ray

Investigations

X-ray

Investigations CT

Investigations CT

Investigations CT

Investigations Tc99m

Investigations Fiberscope

Treatment Thyroidectomy is the only line of treatment Mostly via cervical approach , rarely a median sternotmy is required Devascularization is done via the neck from which the retrosternal portion derived its blood supply Special care should be exerted to avoid injury of the recurrent laryngeal nerves during the delivery of retrosternal goter

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