Thyroid Status Examination — Viva

Short Case Viva Defence

Examiner instruction

"Please examine this patient's thyroid status. Present your findings and offer a differential diagnosis." [1]

Candidate's model examination and presentation

"Before I begin, I would like to introduce myself, explain the examination to the patient, and obtain consent. I would ensure the patient is comfortable, sitting upright on the edge of the bed, with the neck exposed from the clavicles to the jaw." [1]

General inspection: "On general inspection, this thin, restless woman has a visible diffuse neck swelling and a staring appearance, consistent with the hyperthyroid phenotype. She is fidgeting and moving her hands." [1]

Hands: "In the hands, there is a fine tremor of the outstretched fingers — I have placed a sheet of paper on the dorsum of the hands to amplify it, and the paper is trembling. The palms are warm and sweaty, with palmar erythema. There is no thyroid acropachy and no onycholysis." [1]

Pulse: "The pulse is 112 beats per minute and irregularly irregular, consistent with atrial fibrillation." [1]

Eyes (from in front): "On examination of the eyes, there is bilateral exophthalmos — the sclera is visible above the iris when the patient looks straight ahead, and there is a prominent stare. There is lid retraction, the Dalrymple sign — the upper lid does not cover the upper limbus. There is lid lag, the von Graefe sign — the upper lid lags behind the downward movement of the globe as the patient follows my finger from above to below. On testing the eye movements, there is impaired upgaze and impaired convergence, consistent with ophthalmoplegia from Graves orbitopathy — the inferior rectus and the medial rectus are the most commonly affected muscles. There is conjunctival injection and chemosis. The Clinical Activity Score is 4 out of 7 — the patient has pain on eye movement, conjunctival injection, chemosis, and eyelid oedema — indicating active Graves orbitopathy." [1]

Neck inspection: "On inspection of the neck, there is a diffuse, symmetric swelling in the anterior triangle, moving on swallowing. There is no scar, no skin change, and no dilated vein." [1]

Neck palpation (from behind): "I am now examining the thyroid from behind. I have asked the patient to flex the neck slightly to relax the sternocleidomastoid. I have placed my fingertips over the gland — the isthmus across the trachea and the two lobes on either side. I have given the patient a sip of water and I am palpating as she swallows. The gland is smoothly and diffusely enlarged, with a soft, fleshy consistency. There is no nodularity, no tenderness, and the gland is mobile on swallowing. I can get below the lower pole of each lobe, so there is no retrosternal extension. There is no cervical lymphadenopathy. The trachea is central." [1]

Percussion: "Percussion over the upper sternum is resonant — there is no retrosternal extension." [1]

Auscultation: "On auscultation of the thyroid, with the patient holding the breath, there is a soft, continuous bruit over the gland, consistent with the increased vascularity of Graves disease." [1]

Reflexes: "The reflexes are brisk." [1]

Legs: "On the shins, there are raised, firm, non-pitting, waxy plaques, consistent with pretibial myxoedema." [1]

Summary: "In summary, this patient is clinically hyperthyroid, with the findings of Graves disease — the diffuse goitre with a bruit, the Graves orbitopathy with a CAS of 4 out of 7, and the pretibial myxoedema. She has atrial fibrillation as the cardiovascular complication of the thyrotoxic state. I would like to measure the blood pressure for a wide pulse pressure, measure the height and weight, and check the thyroid function tests — I expect a suppressed TSH with an elevated free T4 and free T3, and positive TSH receptor antibodies." [1]

Examiner probing questions and model answers

Q1: "You scored the CAS at 4 out of 7. Walk me through the seven items and what a score of 3 or more means clinically." [1]

"The seven items of the Clinical Activity Score are: spontaneous retrobulbar pain, pain on eye movement, eyelid erythema, conjunctival injection, chemosis, swelling of the caruncle, and eyelid oedema or fullness — each scores one point, for a maximum of seven. This patient has pain on eye movement, conjunctival injection, chemosis, and eyelid oedema, giving a CAS of 4 out of 7. A CAS of three or more out of seven indicates active Graves orbitopathy, which predicts a response to immunosuppression with intravenous methylprednisolone. The CAS measures activity — the inflammatory component of the disease — not severity. The severity is graded separately as mild, moderate-to-severe, or sight-threatening, based on the degree of proptosis, the presence of diplopia, and the optic nerve function. So this patient has active, moderate-to-severe Graves orbitopathy, and I would refer to ophthalmology for a formal assessment and the initiation of immunosuppression [1][2]."

Q2: "What are the sight-threatening complications that you must exclude at the bedside?" [1]

"The two sight-threatening complications are optic nerve compression and corneal exposure. Optic nerve compression occurs when the swollen extraocular muscles compress the optic nerve at the orbital apex — the signs are reduced visual acuity, impaired colour vision (red desaturation — the patient reports that a red target appears washed out or darker in the affected eye), a relative afferent pupillary defect on the swinging torch test, and visual field defects. Corneal exposure occurs from the severe proptosis and the lid retraction, which prevent eyelid closure — lagophthalmos — leading to exposure keratopathy and corneal ulceration. At the bedside, I check the visual acuity with a Snellen chart, the colour vision with an Ishihara plate or a red target, the visual fields by confrontation, the pupillary reflexes, and the cornea with fluorescein staining if a slit lamp is available. Any abnormality is a sight-threatening emergency requiring urgent ophthalmology referral and high-dose intravenous glucocorticoids or urgent orbital decompression [1]."

Q3: "How do you distinguish Graves disease from toxic multinodular goitre at the bedside?" [1]

"The clinical distinction rests on the Graves-specific signs. Graves disease is the only cause of thyrotoxicosis that produces orbitopathy, so the presence of exophthalmos, ophthalmoplegia, chemosis or conjunctival injection makes the diagnosis. The other Graves-specific findings are the pretibial myxoedema, the thyroid acropachy, and the thyroid bruit (from the hyperaemic vascular gland). Toxic multinodular goitre, by contrast, produces a multinodular, asymmetric, lumpy goitre without eye signs, without pretibial myxoedema, and without a bruit. The bruit is a discriminating single sign because the Graves gland is hyperaemic from the thyroid-stimulating immunoglobulins acting on the TSH receptors, whereas the toxic multinodular goitre is autonomous but not as vascular. The laboratory confirmation is the TSH receptor antibody, which is positive in Graves and negative in toxic multinodular goitre [5]."

Q4: "Why do you palpate the thyroid from behind, and what are you feeling for?" [1]

"I palpate from behind because the thyroid sits deep to the strap muscles and the sternocleidomastoid, and the fingertips from behind can feel the gland between the trachea and the muscle, whereas the thumb approach from the front compresses the gland against the trachea and gives a less reliable assessment of the consistency and the nodularity. I am feeling for five things: the size (enlarged, normal or absent), the consistency (smooth and soft for Graves, firm and granular for Hashimoto, hard and irregular for malignancy, tender and warm for subacute thyroiditis), the nodularity (diffuse, multinodular, solitary), the mobility (mobile on swallowing versus fixed by malignancy), and whether I can get below the lower pole — if I cannot, the gland has retrosternal extension and I must percuss the sternum and image the chest. I palpate the cervical lymph nodes and the tracheal position at the same time." [1]

Q5: "What does a thyroid bruit mean, and how do you distinguish it from a carotid bruit?" [1]

"A thyroid bruit is a soft, continuous, systolic or to-and-fro murmur heard over the thyroid gland, caused by the increased vascularity of Graves disease — the gland is hyperaemic from the thyroid-stimulating immunoglobulins acting on the TSH receptors of the follicular cells. A thyroid bruit does not occur in toxic multinodular goitre or toxic adenoma, so it is a discriminating sign for Graves among the causes of thyrotoxicosis. I distinguish it from a carotid bruit by the location — the thyroid bruit is over the gland, central over the trachea, while the carotid bruit is over the carotid bifurcation, lateral in the anterior triangle, and it radiates toward the angle of the jaw. I also distinguish it from a venous hum, which is abolished by gentle compression of the jugular vein." [1]

Q6: "This patient has atrial fibrillation. How does this change your management?" [1]

"The atrial fibrillation is a cardiovascular complication of the thyrotoxic state — approximately 10 to 15 per cent of thyrotoxic patients develop atrial fibrillation, rising to 20 to 25 per cent in older patients. The management has two arms. First, I control the ventricular rate with a beta-blocker (propranolol is preferred because it also controls the adrenergic symptoms and inhibits the peripheral conversion of T4 to T3). Second, I treat the underlying thyrotoxicosis with a thionamide (carbimazole), because the atrial fibrillation will often revert to sinus rhythm once the patient is rendered euthyroid — up to two-thirds of thyrotoxic atrial fibrillation reverts spontaneously with the restoration of the euthyroid state. I also consider anticoagulation, because thyrotoxic atrial fibrillation carries a higher risk of thromboembolism than non-thyrotoxic atrial fibrillation, particularly in older patients — I would assess the stroke risk with the CHA2DS2-VASc score and the bleeding risk with the HAS-BLED score. I would not attempt cardioversion until the patient is euthyroid, because the thyrotoxic atrial fibrillation has a high recurrence rate before the thyroid state is controlled [5]."