Thyroid Status Examination — Written Clinical Reasoning

SAQ 1 — The Systematic Thyroid Status Examination (20 marks, 30 minutes)

Prompt: Outline your systematic approach to the thyroid short case, addressing: (a) the nine-step behind-the-patient routine; (b) the Graves eye signs and the CAS; (c) the hyperthyroid versus hypothyroid phenotypes; (d) palpating the gland from behind; (e) retrosternal extension; and (f) the three most common errors. [1]

Model Answer

(a) The nine-step examination routine (4 marks): [1]

The routine is performed from behind the seated patient, in an invariant sequence: general inspection, hands, pulse, eyes, neck inspection, neck palpation, percussion over the sternum, auscultation of the thyroid, and reflexes plus legs. [1]

At the end of the bed, I take five seconds to identify the two thyroid phenotypes — the hyperthyroid (thin, agitated, restless, heat intolerance, a stare from lid retraction) and the hypothyroid (slow, puffy-faced, dry skin, lethargic). I state my impression of the thyroid status before I touch the patient. [1]

In the hands, I assess the fine tremor (with the paper test on outstretched hands), the warm sweaty palms and palmar erythema of thyrotoxicosis (or the cold dry skin of hypothyroidism), the thyroid acropachy and onycholysis (Plummer nails) of Graves disease, and the proximal muscle wasting. [1]

At the pulse, I assess the rate and rhythm — tachycardia and atrial fibrillation in thyrotoxicosis (any new atrial fibrillation mandates thyroid function tests), bradycardia in hypothyroidism. [1]

In the eyes (examined from in front), I look for exophthalmos (from the side and with an exophthalmometer), lid retraction (Dalrymple sign), lid lag (von Graefe sign), ophthalmoplegia (the six cardinal directions of gaze and convergence), and the signs of active inflammation (chemosis, conjunctival injection, eyelid oedema) that I score with the CAS. [1]

On inspection of the neck, I note the goitre (diffuse, nodular, asymmetric), the scars, the skin changes, and the dilated veins of superior vena cava obstruction. [1]

On palpation from behind, during swallowing, I assess the size, the consistency, the nodularity, the tenderness, the mobility, whether I can get below the gland, the cervical lymph nodes, and the tracheal position. [1]

I percuss the upper sternum for the dull note of retrosternal extension. [1]

I auscultate the thyroid for a bruit (a sign of Graves disease from the hyperaemic gland). [1]

I test the reflexes (brisk in thyrotoxicosis, delayed relaxation in hypothyroidism) and examine the legs (pretibial myxoedema of Graves, proximal muscle weakness). [1]

(b) The Graves eye signs and the Clinical Activity Score (4 marks): [1]

The signs specific to Graves orbitopathy — which involve the retro-orbital tissues and do not occur in the other causes of thyrotoxicosis — are exophthalmos (proptosis), ophthalmoplegia, chemosis and conjunctival injection. The mechanism is the thyroid-stimulating hormone receptor antibodies stimulating the retro-orbital fibroblasts to produce excess glycosaminoglycans, which draw in water and swell the muscles and the fat, pushing the globe forward and restricting the extraocular movement [3].

The lid retraction (Dalrymple sign) and lid lag (von Graefe sign) occur in any cause of thyrotoxicosis from the sympathetic overdrive of Muller muscle and are NOT specific to Graves [1].

The Clinical Activity Score (CAS) is the seven-item bedside score: spontaneous retrobulbar pain, pain on eye movement, eyelid erythema, conjunctival injection, chemosis, swelling of the caruncle, and eyelid oedema — each scores one point, for a maximum of seven. A CAS of three or more out of seven indicates active disease, which predicts a response to immunosuppression with intravenous methylprednisolone. The CAS measures activity, not severity; the severity is graded separately as mild, moderate-to-severe or sight-threatening [1][2].

(c) The hyperthyroid versus hypothyroid phenotypes (3 marks): [1]

The discriminating signs: for hyperthyroid, the fine tremor, the warm sweaty palms, the tachycardia (and atrial fibrillation), the systolic hypertension with a wide pulse pressure, and the brisk reflexes. For hypothyroid, the cold dry coarse skin, the bradycardia, the delayed-relaxation (hung-up) reflexes (especially at the ankle jerks), and the periorbital oedema with loss of the outer third of the eyebrows. The Graves-specific signs (exophthalmos, ophthalmoplegia, thyroid acropachy, pretibial myxoedema, thyroid bruit) identify the cause as Graves among the causes of thyrotoxicosis [5].

(d) Palpating the gland from behind (3 marks): [1]

I stand behind the seated patient, with the neck slightly flexed to relax the sternocleidomastoid. I place both hands around the neck with the fingertips over the gland — the isthmus across the trachea below the cricoid, and the two lobes on either side. I give the patient a sip of water and ask them to swallow as I palpate. The gland moves up on swallowing, which allows me to feel the lower border, 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, the mobility, and whether I can get below the gland. The behind-the-patient approach is used because 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. [1]

(e) Retrosternal extension (3 marks): [1]

The signs of retrosternal extension are: (1) I cannot get my fingers below the lower pole of the gland — the gland extends below the clavicle into the mediastinum; (2) the percussion note over the upper sternum is dull, where it should be resonant over the air-filled trachea; and (3) the Pemberton sign — the patient develops facial plethora and distended neck veins on raising both arms above the head, because the clavicles compress the retrosternal goitre against the great veins at the thoracic inlet. A retrosternal goitre can compress the trachea (stridor), the oesophagus (dysphagia) and the great veins (superior vena cava obstruction), so I confirm with a CT of the neck and chest. [1]

(f) The three most common errors (3 marks): [1]

1. The position error — palpating from the front. The thyroid examination is performed from behind the seated patient. The candidate who stands in front and palpates with the thumbs has demonstrated a fundamental technique error. [1]

2. The thyroid status versus the gland error. The instruction to examine the thyroid status means I must assess both the patient's thyroid status (the hands, the pulse, the eyes, the reflexes, the skin) and the gland. The candidate who examines only the neck has done half the examination. [1]

3. The omitted closure error. The candidate who presents the findings and stops has not closed the examination. The closure must include measuring the blood pressure (for the wide pulse pressure of thyrotoxicosis), measuring the height and weight, and ordering the thyroid function tests with the appropriate antibodies and imaging. [1]

SAQ 2 — Interpreting a Complex Thyroid Short Case (10 marks)

Prompt: A 48-year-old woman is examined in the DCE short case. Findings: thin and agitated at rest with a visible diffuse neck swelling; fine tremor of the outstretched hands; pulse 112 beats per minute and irregularly irregular; bilateral exophthalmos with scleral show, lid retraction and lid lag; impaired upgaze and impaired convergence with chemosis and conjunctival injection; a smooth diffuse symmetric goitre with a bruit, mobile on swallowing, and you can get below it; brisk reflexes; and raised firm waxy plaques on the shins. (a) Interpret the constellation of findings and give the primary diagnosis. (b) What is the CAS and what does it indicate? (c) What are the sight-threatening complications you must check for? (d) What investigations would you order? [1]

Model Answer

(a) Primary diagnosis (3 marks): [1]

The constellation of the thin agitated phenotype, the fine tremor, the atrial fibrillation, the smooth diffuse goitre with a bruit, the brisk reflexes, and the Graves-specific signs (bilateral exophthalmos, ophthalmoplegia with impaired upgaze and convergence, chemosis, pretibial myxoedema) is consistent with Graves disease with active Graves orbitopathy. The diagnosis is clinically secure from the eye signs and the dermopathy, because these do not occur in the other causes of thyrotoxicosis. The bruit reflects the hyperaemic vascular gland of Graves. The atrial fibrillation is the cardiovascular complication of the thyrotoxic state [5].

(b) The CAS (2 marks): [1]

The patient has pain on eye movement (I would confirm by history), conjunctival injection, chemosis, and eyelid oedema (I would assess the fullness) — giving a CAS of at least 3 to 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. I would score the full seven items at the bedside and state the total [1][2].

(c) The sight-threatening complications (2 marks): [1]

The two sight-threatening complications are optic nerve compression (the swollen extraocular muscles compress the optic nerve at the orbital apex, producing reduced visual acuity, impaired colour vision with red desaturation, a relative afferent pupillary defect, and visual field defects) and corneal exposure (the severe proptosis and the lid retraction prevent eyelid closure — lagophthalmos — leading to exposure keratopathy). 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, and the pupillary reflexes. Any abnormality is a sight-threatening emergency requiring urgent ophthalmology referral [1].

(d) Investigations (3 marks): [1]

I would measure the blood pressure (I expect a systolic hypertension with a wide pulse pressure from the increased stroke volume and the reduced systemic vascular resistance of the thyrotoxic state), measure the height and weight (to document the weight loss and to dose the antithyroid drugs), and order the thyroid function tests — I expect a suppressed TSH with an elevated free T4 and free T3. I would also order the TSH receptor antibodies (also called thyroid-stimulating immunoglobulins), which I expect to be positive and which confirm Graves disease. For the orbitopathy, I would refer to ophthalmology for a formal assessment of the optic nerve function and the cornea, and I would consider an MRI of the orbits if there is any concern about optic nerve compression. I would cross-link the management of the Graves disease (the antithyroid drugs, the radioactive iodine, and the surgery) to the dedicated thyroid-disorders topic, which carries the drug doses and the long-term follow-up [5].