Lahey method of palpating the posterior surface of the thyroid gland

Andy Lau Chuen Weng, Year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

29th March 2016

The correct method of palpating, during examination of the thyroid gland, is while standing behind the patient. The examiner has an excellent feel of the anterior surface of the gland. Unfortunately, the posterior surface of the gland is not so easily felt. In 1926, Frank Lahey described a method of palpating the thyroid from the front [Lahey, 1926]. By this method, the posterior surface of the gland can also be examined.


The thyroid gland is fixed at the isthmus, which is attached to the trachea. The lateral lobes are mobile. Fingers can be inserted behind the lateral lobes when the lobes are lifted from their beds.

During regular anterior palpation, the thyroid is impalpable if the lateral lobes are small, because they sink back into the grooves beside the trachea and esophagus. Thus the Lahey method is most valuable when the thyroid enlargement is slight. Even in larger goiters, this method allows assessment of the consistency of tumors, their numbers and location, and the thickness of the lobes. It can also detect thyroid remnants left behind following an inadequate thyroidectomy (a cause of persisting hyperthyroidism).


Stand in front. Elevate the patient’s chin. This brings the trachea. Rotate the chin slightly towards the side of the lobe to be palpated to relax the sternomastoid. Place the thumb against the lower lateral portion of the thyroid cartilage and the upper trachea tracheal rings, and push the trachea laterally as far as possible, without causing choking: this will push the thyroid out. (Pushing on the trachea itself will cause choking, therefore push on the thyroid cartilage.) Insinuate the fingers of the other hand behind the sternomastoid and behind the pushed out thyroid lobe to palpate the posterior surface of the gland; at the same time use the thumb to feel the anterior. If in doubt, ask the patient to swallow (Figures).


  • Lahey FH. A method of palpating the lobes of the thyroid. JAMA 1926;86:813-814.
Lahey's Method Figure 1
Lahey's Method outlines
Posted in Uncategorized

Hypothyroidism, signs and symptoms

Ong Jo Ern, Year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

13 April 2016


Symptoms and signs of hypothyroidism vary according the severity of thyroid hormone deficiency. Nonthyroidal illnesses which coexist with hypothyroidism may alter the typical manisfestations of hypothyroidism.

In general, thyroid hormone deficiency causes a reduction in metabolic processes and matrix glycosaminoglycans accumulation in the interstitial spaces of tissue [Surks, 2016]. Other metabolic derangements include hyperlipidemia, hyponatremia, and impaired drug clearance. Hyperlipidemia occurs due to decreased lipid clearance, causing an elevation of serum free fatty acids and total and LDL cholesterol [Surks, 2016]. Hyponatremia occurs in about 10% of cases of hypothyroidism. It is seen only in severe myxedema. The cause is likely to be impaired cardiac function causing baroreceptor-mediated vasopressin secretion and total body water retention [Abuzaid and Birch, 2015].

Drug clearance is also reduced in hypothyroid patients. For instance, drug dosage must be lowered in antiepileptic, anticoagulant and opiod drugs to prevent drug toxicity [Surks, 2016].

There are marked cardiovascular derangements [Surks, 2016]. The thyroid hormone regulates genes that encode for enzymes responsible for myocardial contractility and relaxation. This, with the systemic hypometabolism, reduces heart rate and contractility which in turn lowers cardiac output. Reduced cardiac output contributes to exercise intolerance and exertional dyspnea experienced by hypothyroid patients. Patients may develop a pericardial effusion. The mechanism is probably increased systemic capillary permeability coupled with electrolyte disturbances. Tamponade may rarely occur [Patil et al, 2011].

There is a strong association with hypercholesterolemia, and a weaker but significant association with hyperhomocysteinemia [Morris et al, 2001]. Both increase the risk of cerebrovascular accidents [Morris et al, 2001; Mandava, 2015].

Although the low cardiac output can lead to hypotension, this typically occurs in cases of very severe hypothyroidism, such as myxedema coma [Wall, 2000]. More commonly, compensated hypothyroidism leads to a secondary hypertension [Stabouli et al, 2010].

The major gastrointestinal derangement is constipation. Ironically, the slow digestive transit often leads to “small intestinal bacterial overgrowth” (SIBO). SIBO is probably present in over half of all patients with hypothyoidism [Patil, 2014], and in occasional patients it may cause a chronic diarrhea.

Anemia is common. There are several causes. One cause is folate deficiency secondary to bacterial overgrowth [Surks, 2016]. This is typically normocytic, and normoblastic.  Pernicious anaemia (in 10% of patients) may occur secondary to gastric atrophy that is sometimes associated with antiparietal cell antibodies (chronic autoimmune thyroiditis, eg. Hashimoto Thyroiditis). Pernicious anemia is macrocytic [Surks, 2016]. Iron deficiency anaemia may occur secondary to menorrhagia [Talley and O’Connor, 2014] – this is typically microcytic.


  1. General [Talley and O’Connor, 2014; Surks 2014]. The most important symptoms of hypothyroidism are
    • cold intolerance
    • weight gain
    • lack of appetite
    • fatigability
    • The important feature is weight gain despite a decreased appetite. It is typically modest, and results from reduced metabolic rate as well as fluid retention. Morbid obesity does not occur [Surks, 2016]. Fatigability is a very common, but nonspecific feature. In contrast, the cold intolerance, weight gain, and anorexia are very suggestive for hypothyroidism.

  2. Skin
    • Decreased sweating: this occurs from reduced calorigenesis and reduced acinar gland secretion [Surks, 2016].
    • Brittle nails.
  3. Gastrointestinal. Constipation occurs as a result of decreased gut motility leading to constipation. Diarrhea may occur, from SIBO (see above) [Patil, 2014].
  4. Reproductive
    • Irregular menstruation in women
    • Either oligo- or amenorrhea or hypermenorrhea-menorrhagia which causes decreased fertility and higher risk of early abortion[Surks, 2016]
    • Hyperprolactinaemia may occur which leads to amenorrhea or galactorrhea[Surks, 2016]
    • Decreased libido, erectile dysfunction and delayed ejaculation in men[Surks, 2016]
  5. Carpal tunnel syndrome: This may develop due to the thickening of carpal tunnel in myxedema [Talley and O’Connor, 2014]. It is a common complication of hypothyroidism and is reversible with thyroid hormone therapy.
  6. Musculoskeletal symptoms are common, and include proximal muscle weakness, cramps and myalgias [Surks, 2016].
  7. Signs

    In general, hypothyroid patients present with slow mentation and speech, delayed relaxation of deep tendon reflexes, bradycardia, coarse hair and skin, puffy facies, tongue swelling and hoarseness of voice [Talley and O’Connor, 2014].

  8. Skin
    • Cool and pale skin with peripheral cyanosis due to decreased blood flow as a result of reduced cardiac output[Surks, 2016]
    • Dry and rough as a result of atrophied epidermis and hyperkeratosis of skin[Surks, 2016]
    • Skin discolouration: a yellowish tinge may occur from hypercarotenemia due to slowing down of hepatic metabolism of carotene[Talley and O’Connor, 2014]. Hyperpigmentation may occur when there is primary hypothyroidism associated with primary adrenal failure, there is high ACTH secretion causing increased level of melanocyte stimulating hormone (MSH) with deposition of pigments on skin[Surks, 2016].
    • Coarse hair with loss of hair or thinning of the outer third of the eyebrow associated with myxedema [Surks, 2016]
    • Myxedema (non-pitting edema)
    • Vitiligo and alopecia areata (spots of baldness. These are autoimmune in origin, and occur in patients who have been treated for Graves’ disease and now present with hypothyroid [Surks, 2016].
  9. Tongue swelling [Talley and O’Connor, 2014].  This occurs in severe hypothyroidism as a result of glycosaminoglycans infiltration into the ground substance of tissues including the skin and this cause excessive interstitial fluid [Talley and O’Connor, 2014].
  10. Eyes
    • Periorbital edema due to generalized non-pitting edema (myxedema)
    • Xanthelasma as a result of hypercholesterolemia as a result of decreased fat metabolism[Talley and O’Connor, 2014]
    • Graves’ ophthalmopathy. After treatment of Graves’ hyperthyroidism, the patient might develop hypothyroidism but the features of Graves’ may persist. Presenting with stare, proptosis and weakness of extraocular muscle/ ophthalmoplegia[Surks, 2016]
  11. Voice: hoarseness [Talley and O’Connor, 2014].
  12. Thyromegaly. Enlargement of the thyroid is unusual. This is because most cases of hypothyroidism are pituitary in origin. Occasionally, hypothyroidism originating in the thyroid itself (e.g. severe iodine deficiency) results in an undersecretion of thyroid hormone. This causes a compensatory oversecretion of TSH [Surks, 2016]. In cases where the thyroid tissue is still viable, goitre will develop [Talley and O’Connor, 2014].
  13. Pallor. Anemia manifests as palmar crease pallor and conjunctival pallor [Talley and O’Connor, 2014].
  14. Cardiovascular. The common sign is bradycardia [Talley and O’Connor, 2014]. Patients may develop a pericardial effusion[Surks, 2016], manifesting with pulsus paradoxus, raised jugulovenous pulse, and muffled heart sounds.
  15. Neuromuscular. Neuromuscular changes include slow mentation and speech, and delayed relaxation of deep tendon reflexes [Talley and O’Connor, 2014].


  •  Abuzaid AS, Birch N. The Controversies of Hyponatraemia in Hypothyroidism. Sultan Qaboos Univ Med J. 2015 May; 15(2): e207–e212.
  • Mandava P. Homocystinuria/Homocysteinemia. Medscape, updated 3 Nov 2015, accessed 13 Apr 2016,
  • Morris MS, Bostom AG, Jacques PF, Selhub J, Rosenberg IH. Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third US National Health and Nutrition Examination Survey. Atherosclerosis. 2001 Mar;155(1):195-200.
  • Patil, AD. Link between hypothyroidism and small intestinal bacterial overgrowth. Indian J Endocrinol Metab 2014;18(3):307-9.
  • Patil VC, Patil HV, Agrawal V, Patil S. Cardiac tamponade in a patient with primary hypothyroidism. Indian J Endocrinol Metab. 2011 Jul; 15(Suppl2): S144–S146.
  • Stabouli S, Papakatsika S, Kotsis V. Hypothyroidism and hypertension. Medccape, accessed 13 Apr 2016,
  • Surks M, ‘Clinical manifestations of hypothyroidism’, UpToDate, , last updated on Mar 08, 2016, accessed on Apr 02, 2016.
  • Talley NJ & O’Connor S, ‘The Endocrine Examination’, Hunter C, Clinical Examination: A systematic guide to physical examination, 7th edn, Elsevier Australia, Chatswood, 2014; pp 360-362.
  • Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician 2000 Dec 1;62(11):2485-2490.
Posted in Uncategorized

Leg swelling

Goh Su Yi, Medical student, Monash University

23 June, 2015

This post describes how to take a history of a patient who presents with a leg swelling. It is particularly directed towards patients suspected to have deep venous thrombosis.


    There are eleven questions one should ask to a patient who presents with a history of swollen legs. [Longmore et al 2014; Hall 2011a, Hall 2011b, Hall 2011c, Williams et al 2013]. These can be divided into three sets of questions: questions about the edema itself, questions about the extent/complications, and questions about the etiology.

    Questions about the edema itself

  1. Duration
  2. What is the duration of the edema? If the onset is acute (<72 hours), deep vein thrombosis should be strongly considered [Ely et al, 2005]. The 72-hour cutoff is commonly cited but arbitrary and not well supported with evidence. Deep vein thrombosis should also be considered in patients presenting after 72 hours with otherwise consistent findings.

  3. Side and site [Longmore et al 2014, Hall, 2011b, McCollum and Chetter, 2013]
  4. Edema is typically dependent (distributed by gravity), which is why legs are affected early. Ask if the edema is localized to the ankles, or if the swelling is extending above to the legs.
    Ask which leg is affected, or if both are affected. Bilateral edema implies systemic disease [Longmore et al, 2014] Deep vein thrombosis usually occurs in one lower limb. Bilateral deep vein thrombosis may also occur, however. When the swelling is bilateral, deep vein thrombosis must be differentiated from other causes of systemic edema, such as hypoproteinemia, renal failure, heart failure, and intake of drugs such as vasodilators. Unilateral edema, and swelling that is not dependent, may indicate trauma or a tumor.

  5. Pain
  6. The most common presentation of a deep vein thrombosis is pain and swelling, especially in the calf [McCollum and Chetter, 2013]. Deep vein thrombosis and reflex sympathetic dystrophy are usually painful. Chronic venous insufficiency can cause low-grade aching. Lymphedema is usually painless [Ely et al, 2005].

  7. Alleviating and exacerbating factors
  8. Ask if the edema improves on lying down. Dependent edema improves during the night, because the fluid moves to the new dependent area, causing a sacral padding. For the same reason the edema is worst in the evenings as prolonged standing or walking results in increasing swelling of the legs.[Longmore, 2014] Venous edema is more likely than lymphedema to improve overnight [Ely et al, 2005].

    Questions about the extent or the complications of the edema

  9. Skin changes [Alguire and Mathes 2015]
  10. Ask about skin changes like irritation, redness, itching, oozing of the skin. Ask about breaks in continuity of skin (ulcers).
    Pooling of blood in the legs often causes the skin to become irritated and inflamed. This can cause redness, itching, dryness, oozing fluid, scaling, open sores from scratching, and crusting or scabbing. Some people develop an area of intensely painful skin that turns red or brown, and is hard, and scar-like. This usually develops after many years of venous disease but can occur suddenly.

    Open, non-healing sores caused by chronic venous disease often begin as small sores but can expand to become quite large, usually painful, tender to touch, shallow, have a red appearance at the bottom, and may ooze or drain small to large amounts of fluid.

    Questions about conditions that may have caused the edema

  11. Trauma
  12. Ask about trauma. Inflammation following trauma is characterised by vasodilation of local blood vessels, increased permeability of the capillaries allowing leaking of large quantities of fluid into the interstitial spaces. [Hall 2011b]

  13. Pregnancy
  14. In women of childbearing age, ask about pregnancy. During pregnancy, various hormones can result in development in edema. [Hall 2011c, Alguire and Mathes, 2015]. Pregnancy can be associated with pedal edema, if a patient has pre-eclampsia. Further, pregnancy predisposes to deep venous thrombosis, causing “phlegmasia alba dolens” or, worse, “phlegmasia cerulaea dolens”.

  15. Periods of immobility
  16. Ask about recent periods of immobility. Immobility is a risk factor of thromboembolism [McCollum and Chetter, 2013].

  17. Tumours and irradiation
  18. Ask about a history of pelvic/abdominal neoplasm or radiation. These can predispose to venous thrombosis [Ely et al, 2005].

  19. Drugs
  20. Ask about a history of drug intake [Talley and O’Connor, 2010; Yaqoob 2012]. Estrogen has a weak aldosterone-like effect, and causes a mild salt retention. This is typically associated with a weight gain in pre-menstrual phase. Mineralocorticoids like aldosterone cause sodium retention, and liquorice has aldosterone-like actions. Calcium channel blockers like dihydropyridine (nifedipine) cause an increased capillary pressure due to relaxation of pre-capillary arterioles. This can result in an edema. Prednisone and anti-inflammatory drugs are also common causes of leg edema. [Ely et al, 2005].

  21. Systems review for heart, liver, kidney, or sleep disorders
    • Ask about

    • history of heart, liver, kidney disease. These can cause edema. Is there a history consistent with sleep apnea? Sleep apnea can cause pulmonary hypertension, which is a common cause of leg edema. Features that may suggest sleep apnea include snoring or apnea noted by the partner, daytime somnolence, or a neck circumference greater than 17 inches [Ely et al, 2005].
    • edema elsewhere. [Longmore et al 2014] Swollen legs may suggest heart, kidney, or liver failure. However, edema can occur nearly anywhere. The more common sites are: legs (common in heart disease), abdomen (common in liver disease), around the eyes (common in kidney disease).
    • shortness of breath. Edema in the chest (pulmonary edema and pleural effusion) may occur in heart disease, and presents with shortness of breath


  • Alguire P, Mathes B. Patient information: chronic venous disease (beyond the basics), viewed 21 April 2015,
  • Chaar CIO. Phlegmasia Alba and Cerulea Dolens. Medscape,, Updated 12 Oct 2015, accessed 30 Mar 2016.
  • Ely J, Osheroff J, Chambliss L, Ebell M 2005, “Approach to leg edema of unclear etiology”, Journal of the American Board of Family Medicine, vol.19, no.2, pp. 148-160.
  • Hall J. Pregnancy and lactation. In: Guyton and Hall Textbook of Medical Physiology, 12th edition, Saunders Elsevier, Philadelphia 2011c, p1003-17
  • Hall JE. The body fluid compartments: extracellular and intracellular fluids: Edema. In: Guyton and Hall Textbook of Medical Physiology, 12th edition, Saunders Elsevier, Philadelphia 2011a, p285-301
  • Hall J. Resistance of the body to infection: Leukocytes, granulocytes and monocyte-macrophage system and inflammation. In: Guyton and Hall Textbook of Medical Physiology, 12th edition, Saunders Elsevier, Philadelphia 2011b, p423-32
  • Longmore M, Wilkinson I, Baldwin A, Wallin E. Swollen legs. In: Oxford Handbook Of Clinical Medicine, 9th edition, Oxford University Press, United States, 2014, p 580-581
  • McCollum P, Chetter I. Venous disorders. In: Williams N, Bulstrode C, O’Connel P (editors). Bailey and Love’s Short Practice Surgery, 26th edition, Boca Raton, 2013, p 901-922
  • Talley N, O’Connor S. The cardiovascular system. In: Clinical Examination: A Systematic Guide to Physical Diagnosis, 6th edition, Churchill Livingstone, Australia, 2010, p 35-105
  • Yaqoob MM. Distribution and composition of body water. In Kumar P, Clark M (editors) Kumar and Clark’s Clinical Medicine, 8th edition, Saunders Elsevier, Spain) 2012, p637-668
Posted in Uncategorized

Kocher’s test for stridor in a goiter

by Tan Yan Wei, year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

26 March 2016


A large thyroid gland presses on the trachea. This pressure may decalcify the tracheal cartilage (tracheomalacia), and produce some degree of narrowing [Dandekar et al, 2016]. This can cause difficulties during intubation for surgery, as well as after surgery [Agarwal et al, 2007]. Although pre-operative compression testing does not appear to reliably predict tracheomalacia [Agarwal et al, 2007], it can be a useful guide to increased awareness.

Kocher’s test is done during examination of the thyroid to rule out trachea narrowing (scabbard trachea). [Bhat, 2013] A “scabbard” trachea is a deformity of the trachea caused by flattening and approximation of the lateral wall, producing stenosis. It is called scabbard trachea because the trachea looks, radiologically, like a scabbard: the sheath of a sword.


The test is started by asking the patient to extend the neck, followed by asking the patient to take heavy deep breaths through the mouth continuously. After that, the examining physician compresses the swelling from the sides. The test is positive if there is the presence of stridor when the lateral lobes are pushed posteromedially with fingers [Bhat, 2013]. An 11-12 minute procedure of the examination can be viewed at .

Significance/ Implication

The positive Kocher’s test is normally seen in scabbard trachea, which may occur in a large multinodular goiter or carcinoma of the thyroid.

When there is a long standing thyroid enlargement, the constant pressure of the thyroid gland on the trachea causes weakened tracheal rings. When the thyroid is being compressed during this test, the weakened trachea narrows, and this presents as stridor during compression of the thyroid (positive Kocher’s test). Due to the weakened tracheal ring, the patency of the trachea is mainly maintain by thyroid. This is important because after thyroidectomy, there is no support to trachea and so it may collapse, causing respiratory embarrassment. For this condition, temporary tracheostomy need to be done for 2-3 weeks. After 2-3 weeks, the trachea will regain its strength.

Tracheomalacia causing stridor is a rare complication after thyroid surgery [Lacoste et al, 1993; Findlay et al, 2011]. Nevertheless, it does occur, and may be commoner in countries where large endemic goiters are common [Agarwal et al, 2007; Abdel Rahim et al, 1999]. It may take the treating team by surprise and cause life-threatening respiratory distress [Tripathi and Kumari, 2008; Lee et al, 2011]. Surgeons should, therefore, be aware of the possibility of tracheomalacia when operating on large goiters. As regards the Kocher test, studies ([Agarwal et al, 2007, and others]) indicate that this test is only moderately reliable. A more reliable indicator of the need for tracheostomy may be the assessment of the tracheal cartilage at the time of surgery. The test is, of course, uncomfortable for the patient, and it can be debated whether it should be performed at all.

There are three interesting asides. One: Kocher’s sign (also known as Ramsay’s sign) is different fro the Kocher’s test described here. The sign refers to a retraction of the upper eyelid in Graves’ disease. Two: There is also a “Kocher’s testicular sign”! Three: Finally, did Kocher really describe the Kocher test? Plenty of books call it the Kocher test, but no book is able to provide an authentic reference.


  • Abdel Rahim AA, Ahmed ME, Hassan MA. Respiratory complications after thyroidectomy and the need for tracheostomy in patients with a large goitre. Br J Surg 1999; 86: 88-90.
  • Agarwal A, Mishra AK, Gupta SK, Arshad F, Agarwal A, Tripathi M, Singh PK. High Incidence of Tracheomalacia in Longstanding Goiters: Experience from an Endemic Goiter Region. World J Surg 2007;31:832-7
  • Bhat MS, Chapter 6 Thyroid, Jaypee Brothers Medical Publisher (P) Ltd, India, 2013, pg 526
  • Dandekar M, Kannan S, D’Cruz A. The thyroid and parathyroids. In: Lumley JSP, D’Cruz AK, Hoballah JJ, Scott-Connor CEH (editors) In: Hamilton Bailey’s Demonstrations of Physical Signs in Clinical Surgery, 19th edition. CRC Press, Boca Raton, 2016, p410.
  • Findlay JM, Sadler GP, Bridge H, Mihai R. Post-thyroidectomy tracheomalacia: minimal risk despite significant tracheal compression.Br J Anaesth. 2011;106(6):903-6. doi: 10.1093/bja/aer062.
  • Lacoste L, Gineste D, Karayan J, et al. Airway complications in thyroid surgery. Ann Otol Rhinol Laryngol 1993; 102: 441-6.
  • Lee C, Cooper RM, Goldstein D. Management of a patient with tracheomalacia and supraglottic obstruction after thyroid surgery. Canadian Journal of Anesthesia 2011, 58:1029.
  • Tripathi D, Kumari I. Tracheomalacia: A Rare Complication After Thyroi dectomy. Indian J Anaesth [serial online] 2008 [cited 2016 Mar 28];52:328-30. Available from:
Posted in Uncategorized

The thyroid gland: history and examination

By Vinod Ramachandran

Year 3, Monash University Malaysia

23 Mar 2016


This article is titled “History and examination of the thyroid gland”. It has a definite focus towards a patient with a thyromegaly, but it can also be considered a guide to the history and presentation of a patient with a swelling in the neck.


    Demographic details

  1. Age
  2. Simple goiter; girls approaching puberty and pregnancy; multinodular, solitary nodular goiters and colloidal goiters; women in their 20s and 30s; Papillary carcinoma; young girls; follicular carcinoma; middle aged women; Anaplastic carcinoma; old age; Hashimoto’s disease; middle aged women

  3. Sex
  4. Majority of thyroid disorders are seen in women. Thyrotoxicosis is much commoner in females than in males; Thyroid carcinomas occur three times more often in females

  5. Occupation
  6. Thyrotoxicosis may appear in individuals working under stress & strain

  7. Residence
  8. Endemic goiter due to iodine deficiency. Certain areas known to have low iodine content in the water and food


  9. Swelling
  10. How to take a history of swelling is described in the presentation titled “Mass, history and examination”. The same questions should be asked, including onset, duration, rate of growth, and appearance of symptoms such as pain. Does it cause symptoms that relate to pressure effects on nearby structures? A swelling that appears after trauma may be a hematoma, not a thyroid swelling. Benign swellings grow slowly; malignant swellings (like an anaplastic cancer of the thyroid) usually grow faster. Note that papillary cancers of the thyroid usually grow slowly. Goitres are painless, unless the patient has thyroiditis. Anaplastic carcinomas infiltrate surrounding structures and often cause pain.

    Special features of neck swellings

  11. Adjacent structures: trachea, esophagus, recurrent laryngeal nerves
  12. Ask about the effect of the swelling on the

    a. trachea, causing breathing difficulty and stridor.

    b. esophagus, causing dysphagia.

    c. recurrent laryngeal nerve, causing hoarseness.

    The thyroid may also press on the carotid, but that will be evaluated during examination.

  13. Hyperthyroidism and hypothyroidism
  14. In a patient with a neck swelling that may be the thyroid gland, look for symptoms of hyperthyroidism and hypothyroidism

    Hyperthyroidism: Heat intolerance, raised appetite, weight loss, sweating, palpitations, tiredness, agitation/nervousness, dyspnea; also diarrhea, menstrual changes (commonly amenorrhea), insomnia

    Hypothyroidism: Weight gain, loss of appetite, constipation, cold intolerance, hoarseness of voice, decreased hearing, hair loss, dry skin, hand pain (carpal tunnel syndrome), angina pectoris, intellectual/ motor slowing (excessive sleeping), muscle cramps, (commonly menorrhagia)

    Past, treatment, family, and dietary history

  15. Medications
  16. Ask about treatment the patient has taken, and its effects on the swelling. Drugs (some may be goitrogenic)

  17. Family history
  18. Some thyroid disorders have a familial predilection.

  19. Dietary history
  20. Dietary habits are important as vegetables of the brassica family (cabbage, kale, rape) are goitrogens. If there is insufficient iodine in the diet, an iodine-deficiency goiter may develop.


    General physical examination

  21. Body habit
  22. Patients with thyrotoxicosis are usually thin and underweight. Patients with hypothyroidism are usually obese and overweight. In case of carcinoma of thyroid; signs of anaemia and cachexia may be present, especially with anaplastic cancers. Patients with early papillary cancer are usually well-preserved.

  23. Alertness and motor activity
  24. Patients with thyrotoxicosis may show hyperkinetic movements. Voice changes may occur with hypothyroidism, and with thyroid cancers.

  25. Hands
  26. Patients who are hyperthyroid may show features such as fine tremors, onycholysis, palmar erythema, warm and sweaty palms, and clubbing. Xanthomas, cool and dry palms, and cyanosis suggest hypothyroidism.

  27. Vital signs
  28. Pulse and blood pressure: Tachycardia and other arrhythmias occur in hyperthyroidism, while bradycardia and hypotension indicate hypothyroidism.

  29. Eyes
  30. The eye signs of hyperthyroidism include exophthalmos, chemosis, conjunctival injection, corneal ulceration, opthalmoplegia, lid-lag, lid retraction, and others. The eye signs of hypothyroidism include periorbital edema, loss of outer third of eyebrows, and xanthelasmas near the eyes.

  31. Face
  32. Patients with hypothyroidism may have dry skin and hair, and yellow discoloration of the face and palms due to hypercarotenemia that results from slowing down of hepatic metabolism of carotene.



  33. Mass
  34. Inspect the swelling as for a mass. Note the location, size, shape, surface, edges, margins, overlying skin, pulsatility, and adjacent structures (particularly the trachea). Dilated veins may indicate compression of the superior vena cava.

  35. Four special features of neck swellings
  36. Inspect the swelling for:

    a. Look for movement with swallowing. You may need to ask the patient to swallow some water.

    b. Thyroglossal cysts (but usually not the thyroid glands) move with protrusion of the tongue.

    c. Look at the adjacent structures, especially the trachea.

    d. Look for pressure on the thoracic inlet (Pemberton’s test).


    Palpate from behind.

  37. Mass
  38. Palpate the swelling as for a mass. Note the tenderness, temperature, location, size, shape, surface, margins, edges, fixity, consistency, and thrill. Consider fluctuation and transillumination. Tenderness indicates thyrotoxicosis. A raised temperature indicates inflammation: thyrotoxicosis, or an abscess. Thrills occur in thyrotoxicosis. Be sure to check if you can get below the gland.

    The “Lahey’s test” is a palpation of the thyroid from the front. Its objective is to feel the posterior part of the gland.

  39. Three special features of neck swellings
  40. Inspect the swelling for:

    a. Examine the trachea.

    b. Perform Kocher’s test.

    c. Feel the carotid (Berry’s sign).


  41. Percuss the swelling for one special feature of a neck swelling
  42. Although most swellings do not need percussion, there are some exceptions (e.g. a suspected kidney mass). In neck swellings, one should percuss the upper sternum for a possible retrosternal extension of the goiter.


  43. Auscult the swelling, as any other mass. Look for a bruit. Toxic thyroids may produce bruits. Carotid body tumors of the neck (which are, of course, not related to thyroids) also produce bruits.
  44. Nodes

  45. Cervical lymph nodes
  46. Always examine the cervical nodes.

    Examination for thyroid function

  47. Hyperthyroidism
  48. Evaluate the patient for hyperthyroidism. The commonest features of hormonal dysfunction are in the eyes, which have already been examined during general physical examination. Other general features of hyperthyroidism include pretibial myxedema.

  49. Hypothyroidism
  50. Evaluate the patient for hypothyroidism .

    Examination of other systems

  51. Neurological examination
  52. Patients with hyperthyroidism may have neurological changes such as anxiety, proximal muscle weakness, and increased tendon reflexes. Patients with hypothyroidism may have changes such as mental dullness (even coma), hearing loss, and decreased tendon reflexes.

  53. Examination of the rest of the body
  54. The other systems: cardiovascular, respiratory, and others should be examined for completeness.


  • Talley NJ, O’Connor S. The thyroid. In: Clinical Examintion, a Systematic Guide to Physical Diagnosis. 7th edition, Australia: Elsevier; 2014, p355-61.
  • Das S. A Manual on Clinical Surgery. 10 ed. Kolkata: Somen Das; 2013.
Posted in Uncategorized

Striae distensae (stretch marks)

Jery Park, Year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

6 Mar 2016

Striae distensae are a common scarring on the skin. They can be erythematous, violaceous or hyperpigmented linear striations.

There are 2 main types:

  1. Striae rubra
  2. Striae alba

Striae rubra presents in striae distensae before progressing to striae alba in the course of 6 to 10 months.

Common causes are: pregnancy, rapid weight gain or loss, rapid growth, bodybuilding exercise and medications(particularly topical and systemic corticosteroids).

Striae distensae are commonly found on abdomen, breasts, medial upper arms, hips, lower back and thighs.

What to look for in a patient with striae

Characteristic Variants Clinical implications
Color Red (erythematous) or violet (violaceous): “striae rubra” During pregnancy, rapid weight gain or loss, rapid growth, bodybuilding exercise and medications (particularly topical and systemic corticosteroids)
White: “striae alba” Past pregnancy
Location Lateral borders of hips, and over the back at the upper sacral region only Puberty striae in boys
Over the hips posteriorly and laterally, extending to the posterolateral thighs Puberty striae in girls
Chest, and back in the area between the scapulae and the sacral bones Bodybuilders, striae related to lifting or stretching
Breasts, entire anterolateral abdomen mostly below the umbilicus Pregnancy
Intertriginous areas* Striae distensae secondary to topical corticosteroid use
Particularly prominent and widely distributed Cushing’s syndrome

*Intertriginous: where two skin areas may touch or rub together,eg axilla

Posted in Uncategorized

Dilated abdominal veins, examination of

Gerald Tan, Year three, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

Last updated 26 Feb 2016

What to look for in a patient who has dilated abdominal veins

Characteristic Sign Differential diagnosis
Location Periumbilical Caput medusae
Over costal margin Congenital (no clinical revelance)
Flow (below umbilicus, obstruct from 2 points to determine) Towards legs Caput medusae due to portal hypertension
Towards head Obstructed inferior vena cava


Caput medusae: There exist anastomoses from the superficial epigastric veins to the portal vein via the paraumbilical veins. These veins carry oxygenated blood from the mother to the foetus and usually close after birth. In portal hypertension, the veins re-canalise and cause a caput medusae. The flow goes down because the blood is trying to go to the great saphenous vein from the superficial epigastric veins .

Dilated veins in IVC obstruction:  Deoxygenated blood cannot be returned normally to the heart. The abdominal veins stagnate and build pressure, overcoming the normal valves. Blood from the great saphenous vein can backflow into the superficial epigastric veins which anastomose with the lateral thoracic vein, which is a tributary of the axillary vein. The flow goes up because the blood is trying to go to the SVC due to IVC obstruction [Snell].


In the picture above, note the dilated veins over the chest and abdomen. This patient had a superior mediastinal tumor occluding the superior vena cava (see the CT scan below).


This CT scan slice is taken just before the tracheal bifurcation. You can see the trachea (on the patient’s right), and the esophagus (to the left of the trachea). Above the trachea is the arch of the aorta, opacified by contrast. The superior vena cava is not visible, since it has been flattened by the tumor.


  • Browse NL, Black J, Burnand KG, Thomas WEG. The abdominal wall, herniae and the umbilicus. In: Browse’s Introduction to the Symptoms and Signs of Surgical Disease, 4th Edition, Taylor & Francis Group, UK, 2005. Page: 385.
  • Snell RS. The Abdomen. In: Clinical Anatomy by Regions, 9th edition, Lippincott Williams & Wilkins, Maryland. Pages: 96, 98, 126, 195.
  • Talley NJ, O’Connor S. The gastrointestinal examination. In: Clinical Examination, 7th Edition, Elsevier Australia, New South Wales, 2014. Pages: 196, 197.
Posted in Uncategorized