Thyroid Status Examination — Clinical Case

DCE Short Case

Patient brief (provided to trainee)

Patient: Mrs Susan Chen, 48 years old, primary school teacher. [1]

Presenting complaint: Three months of palpitations, heat intolerance, a tremor, and a 6-kilogram weight loss despite an increased appetite. Her general practitioner noted an irregular pulse and referred her for an endocrinology assessment. [1]

Past history: No significant past medical history. No medications. No family history of thyroid disease, though her mother has type 1 diabetes. [1]

Examination findings (trainee elicits): [1]

General inspection: The patient is thin and restless, fidgeting on the examination couch, with a visible diffuse neck swelling and a prominent stare. She is dressed lightly despite the air-conditioned room. [1]

Hands: A fine, rapid tremor of the outstretched fingers, amplified when a sheet of paper is placed on the dorsum of the hands. The palms are warm, moist and sweaty, with palmar erythema. No thyroid acropachy. No onycholysis. [1]

Pulse: 112 beats per minute, irregularly irregular (confirmed on ECG as atrial fibrillation). [1]

Eyes (from in front): Bilateral exophthalmos — the sclera is visible above the iris on straight-ahead gaze. Lid retraction (the Dalrymple sign) — the upper lid does not cover the upper limbus. Lid lag (the von Graefe sign) — the upper lid lags behind the downward movement of the globe. Impaired upgaze and impaired convergence on testing the six cardinal directions of gaze. Conjunctival injection and chemosis of both eyes. [1]

Neck inspection: A diffuse, symmetric swelling in the anterior triangle, moving on swallowing. No scar. No skin change. No dilated veins. [1]

Neck palpation (from behind, during swallowing): A smooth, diffuse, symmetric enlargement of the thyroid gland, with a soft, fleshy consistency. No nodularity. No tenderness. The gland is mobile on swallowing. The trainee can get below the lower pole of each lobe. No cervical lymphadenopathy. The trachea is central. [1]

Percussion: Resonant over the upper sternum — no retrosternal extension. [1]

Auscultation: A soft, continuous bruit over the thyroid gland. [1]

Reflexes: Brisk at the biceps, triceps, supinator and knees. [1]

Legs: Raised, firm, non-pitting, waxy plaques on the anterior shins bilaterally, consistent with pretibial myxoedema. [1]

Trainee presentation (model answer)

"Mrs Chen is a 48-year-old primary school teacher who presents with three months of palpitations, heat intolerance, a tremor, and weight loss despite an increased appetite. [1]

On general inspection, she is thin and restless, with a visible diffuse neck swelling and a prominent stare. [1]

In the hands, there is a fine tremor of the outstretched fingers, warm sweaty palms, and palmar erythema. [1]

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

On examination of the eyes from in front, there is bilateral exophthalmos with scleral show, lid retraction (the Dalrymple sign), and lid lag on downward gaze (the von Graefe sign). There is impaired upgaze and impaired convergence, consistent with ophthalmoplegia from Graves orbitopathy. There is conjunctival injection and chemosis. The Clinical Activity Score is 4 out of 7, indicating active Graves orbitopathy. [1]

On examination of the neck from behind, there is a smooth, diffuse, symmetric enlargement of the thyroid gland, with a soft consistency, no nodularity, no tenderness, and the gland is mobile on swallowing. I can get below the gland. The trachea is central, and there is no cervical lymphadenopathy. Percussion over the sternum is resonant. On auscultation, there is a soft bruit over the gland. [1]

The reflexes are brisk. On the shins, there are raised, firm, waxy plaques consistent with pretibial myxoedema. [1]

In summary, this patient is clinically hyperthyroid, with the findings of Graves disease — the diffuse goitre with a bruit, the Graves orbitopathy with active disease, and the pretibial myxoedema. She has atrial fibrillation as the cardiovascular complication of the thyrotoxic state. [1]

My plan is to measure the blood pressure for a wide pulse pressure, measure the height and weight, check the thyroid function tests — I expect a suppressed TSH with an elevated free T4 and free T3 — and the TSH receptor antibodies, which I expect to be positive. I would also refer to ophthalmology for a formal assessment of the optic nerve function and the cornea, given the active orbitopathy [1][2]."

Examiner probing questions and model answers

Q1: "How did you arrive at the diagnosis of Graves disease from the bedside findings?" [1]

"The diagnosis rests on the Graves-specific signs, which do not occur in the other causes of thyrotoxicosis. Graves disease is the only cause of thyrotoxicosis that produces orbitopathy, so the bilateral exophthalmos, the ophthalmoplegia (impaired upgaze and convergence), the chemosis and the conjunctival injection make the diagnosis. The other Graves-specific findings in this patient are the pretibial myxoedema and the thyroid bruit (from the hyperaemic vascular gland stimulated by the thyroid-stimulating immunoglobulins). The lid retraction and the lid lag are supportive but not specific — they occur in any cause of thyrotoxicosis from the sympathetic overdrive. The laboratory confirmation is the TSH receptor antibody, which is positive in Graves disease and negative in toxic multinodular goitre and toxic adenoma [3][5]."

Q2: "What is the significance of the CAS of 4 out of 7, and how does it influence the management of the orbitopathy?" [1]

"A CAS of three or more out of seven indicates active Graves orbitopathy, which predicts a response to immunosuppression. This patient has a CAS of 4 out of 7 — the pain on eye movement, the conjunctival injection, the chemosis, and the eyelid oedema — so her orbitopathy is active. According to the 2021 EUGOGO guideline, for active moderate-to-severe Graves orbitopathy, the first-line treatment is a combination of intravenous methylprednisolone (a cumulative dose of 4.5 g in 12 weekly infusions) and mycophenolate sodium. Before initiating the treatment, I would exclude the sight-threatening complications — the optic nerve compression and the corneal exposure — by checking the visual acuity, the colour vision (red desaturation), the visual fields, and the pupillary reflexes. If there is any sign of optic nerve compromise, the management escalates to high-dose intravenous glucocorticoids and urgent orbital decompression [1][2]."

Q3: "Why does this patient have a thyroid bruit, and what would its absence suggest?" [1]

"The thyroid bruit reflects the increased vascularity of the Graves gland — the thyroid-stimulating immunoglobulins act on the TSH receptors of the follicular cells and stimulate both hormone synthesis and blood flow, so the gland becomes hyperaemic and the increased flow produces the bruit. The bruit does not occur in toxic multinodular goitre or toxic adenoma, which are autonomous (they produce hormone independently of the TSH receptor) but not as vascular. So the bruit is a discriminating sign for Graves among the causes of thyrotoxicosis. Its absence in a thyrotoxic patient would point me toward toxic multinodular goitre or toxic adenoma (if there is a palpable nodule) or thyroiditis (if the gland is tender or normal and the thyrotoxicosis is transient)." [1]

Q4: "What is the mechanism of the pretibial myxoedema, and how does it relate to the other Graves manifestations?" [1]

"Pretibial myxoedema, or thyroid dermopathy, is the deposition of glycosaminoglycans (hyaluronic acid) in the dermis of the shins, producing the raised, firm, non-pitting, waxy plaques. The mechanism is the thyroid-stimulating hormone receptor antibodies stimulating the skin fibroblasts to produce excess glycosaminoglycans — the same autoimmune mechanism that operates in the orbit in Graves orbitopathy, where the antibodies stimulate the retro-orbital fibroblasts. Pretibial myxoedema is specific to Graves disease and is almost always associated with orbitopathy. It completes the triad of exophthalmos, myxoedema (dermopathy) and osteoarthropathy (thyroid acropachy) that defines severe Graves autoimmune disease. The treatment of the dermopathy is topical corticosteroids under occlusion, though many lesions are mild and require no treatment [3][4]."

Q5: "This patient has atrial fibrillation. How do you manage it alongside the Graves disease?" [1]

"The atrial fibrillation is a cardiovascular complication of the thyrotoxic state. I manage it with two arms: rate control and the treatment of the underlying cause. For the rate control, I use a beta-blocker — propranolol is preferred because it controls the adrenergic symptoms (the tremor, the anxiety, the tachycardia) and, at higher doses, it inhibits the peripheral conversion of T4 to T3. For the underlying cause, I treat the Graves disease with a thionamide (carbimazole), because up to two-thirds of thyrotoxic atrial fibrillation reverts to sinus rhythm once the patient is rendered euthyroid. I also assess the thromboembolic risk with the CHA2DS2-VASc score — thyrotoxic atrial fibrillation carries a higher risk of stroke than non-thyrotoxic atrial fibrillation, so I would consider anticoagulation, particularly in older patients or those with other stroke risk factors. I would not attempt electrical or pharmacological cardioversion until the patient is euthyroid, because the recurrence rate is high while the thyroid state remains uncontrolled [5]."

Q6: "What are the treatment options for the Graves disease itself, and how do you counsel the patient?" [1]

"The three definitive options are the antithyroid drugs (carbimazole or propylthiouracil), the radioactive iodine, and the surgery (subtotal or total thyroidectomy). The choice depends on the patient's age, the goitre size, the presence and activity of the orbitopathy, the desire for pregnancy, and the patient's preference. The antithyroid drugs are the first-line treatment in most patients in Australia and New Zealand — a 12 to 18 month course of carbimazole achieves a remission in approximately 40 to 50 per cent of patients. The radioactive iodine is an effective definitive treatment but can worsen the Graves orbitopathy (it releases thyroid antigens and stimulates the autoimmune response), so it is used with caution in a patient with active orbitopathy, and it is preceded by a course of glucocorticoids to protect the eyes. The surgery is reserved for the large goitre, the patient who declines or fails the other options, or the patient with a suspicion of malignancy. I would counsel the patient about the advantages and disadvantages of each option, the need for shared decision-making, and the importance of the long-term follow-up, because all three options carry a risk of hypothyroidism requiring lifelong thyroxine replacement [5]."