Wayne’s index

by Shimin Chen, year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

2 May 2016

In the 1950s, T3 and T4 testing was still to come. The only available test was protein-bound iodine (PBI), which was fairly unreliable.

In 1960, Sir Edward Wayne described a scale named Wayne’s index to improve the accuracy of diagnosis of hyperthyroidism and also to limit the need for other diagnostic tests [Imam and Ahmad, 2016].

This index of signs and symptoms is a clinical scoring tool to evaluate the presence and degree of hyperthyroidism [M. Galia et al., 2010]. It is also useful in resource challenged regions or when thyroid function tests results are at variance with clinical suspicion. With a score ranging from +45 to -25, a score less than 11 defines “euthyroidism” while scoring above 19 suggests “toxic hyperthyroidism”.

Although this system of scoring has very little relevance today, it is a useful guide to the relative importance of clinical features in the diagnosis of hyperthyroidism.

Symptoms, in order of importance Points if present Points if absent
Heat intolerance (cold preference) 5
Heat preference -5
Appetite – increased 3
Weight – decreased -3
Excessive sweating 3
Palpitations 2
Fatigue 2
Nervousness (anxiety) 2
Dyspnoea 1
Signs, in order of importance
Hyperkinetic movements 4
Atrial fibrillation 4
Thyromegaly 3 -3
Tachycardia 3
Bruit 2 -2
Exophthalmos 2
Hot hands 2
Lid retraction 2
Lid lag 1
Wet/ moist hands 1
Tremors 1


  • Total score (Kendall-Taylor, 1972): > 19 = toxic
  • 11-19 = equivocal
  • < 11 = euthyroid


  • Galia, A., Aimee A. Andag-Silva, A., Sjoberg A. Kho, S., OL San Luis, Jr, T. and Magboo-Gaviola, M. (2010). Validation of the UST Thyroid Scoring Index Against Ultrasensitive Assays for Thyroid-Stimulating Hormone and Free Thyroxine. Phil. Journal of Internal Medicine, 48(1), p.15.
  • Imam SK, Ahmad SI (2016). Thyroid disorders: basic science and clinical practice, Springer International Publishing, Switzerland, 2016, pp.76-77.
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Approach to a patient during physical examination

FC Fong, Year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

8 March 2016

Proper conduct of a physical examination helps gather information and puts the patient at ease. This short article offers advice on how to approach a patient for a physical examination.

Making the patient comfortable

Courtesy. Be gentle and courteous [Talley and O’Connor, 2014a]. It is good practice to know the patient’s name [Das, 2013b].

Privacy during examination. Take all reasonable steps to ensure that the examination is private [Douglas et al, 2013b]. But remember that pulling the curtains around the bed obscures vision but not sound [Douglas et al, 2013a]! Make sure the patient’s position is comfortable [Talley and O’Connor, 2014a].

Adequate exposure is needed, but cover areas not being examined [Das, 2013a].

An attendant nurse must be present if a male is examining a female patient [Das, 2013a]. For examination of the genital or anal areas, ask if the patient would like a chaperone and include the chaperone’s name in the record. Unless the adult patient requests relatives to say, ask them to leave temporarily [Talley and O’Connor, 2014a].

Preventing discomfort. When palpating the abdomen, make sure hands are warm. Ask if any particular area is tender, and examine it last. Encourage the patient to breathe gently through the mouth [Talley and O’Connor, 2014b]. Position the patient comfortably supine with only one or two pillows to relax the muscles of the abdominal wall [Douglas et al, 2013c]. If necessary, ask the patient to bend knees [Talley and O’Connor, 2014b]. Ask the patient to place arms by the side, also to relax the abdominal muscles [Douglas et al, 2013c]. Observe the patient’s face for any sign of discomfort throughout the examination [Talley and O’Connor, 2014b].

Lighting and exposure

The examination is best conducted in a warm, well-lit room [Talley and O’Connor, 2014a]. Daylight is better for observing jaundice, which may be missed in artificial light [Das, 2013a].

For a complete examination, the patient should take off all clothes and be covered only by a dressing gown [Das, 2013a].

Where to stand

Stand on the right side of the bed [Talley and O’Connor, 2014a]. This is conventional, but also makes sense for right-handers. There seems to be no reason why left-handers should not stand on the patient’s left [Qayyum et al, 2009].

Hand hygiene

Always wash your hands before and after examining patients [Talley and O’Connor, 2014a]. Proper hand hygiene can reduce the nosocomial infection rate by as much as 40% [Kampf et al, 2009].


  • Das S. A manual on clinical surgery. 10th ed. Kolkata; 2013a. pg 4.
  • Das S. A manual on clinical surgery. 10th ed. Kolkata; 2013b. pg 1.
  • Douglas G, Nicol F, Robertson C, editors. Macleod’s clinical examination. 13th ed. Edinburgh; 2013a. pg 42.
  • Douglas G, Nicol F, Robertson C, editors. Macleod’s clinical examination. 13th ed. Edinburgh; 2013b. pg 2.
  • Douglas G, Nicol F, Robertson C, editors. Macleod’s clinical examination. 13th ed. Edinburgh; 2013c. pg 180-181.
  • Kampf G, Löffler H, Gastmeier P. Hand hygiene for the prevention of nosocomial infections. Dtsch Arztebl Int. 2009 Oct;106(40):649-55.
  • Talley NJ, O’Connor S. Clinical examination: a systematic guide to physical diagnosis. 7th ed. New South Wales; Churchill Livingstone; 2014a. pg 28-29.
  • Qayyum MA, Sabri AA, Aslam F. Medical Aspects Taken for Granted. Mcgill J Med 2007;10(1):47-9
  • Talley NJ, O’Connor S. Clinical examination: a systematic guide to physical diagnosis. 7th ed. New South Wales; Churchill Livingstone; 2014b. pg 197.
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Berry’s sign, in thyromegaly

Eishatur Rodhiah Mamat and Edward Tan Hong Swo, Year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

22 April 2016

Berry’s sign is named after a British surgeon, Sir James Berry, who was the first to describe it.

Berry’s sign is the absence of carotid pulsation on palpation [Heston and Wahl, 2010]. The absence of carotid pulsation in a patient presenting with a thyroid swelling suggests malignancy.

Eliciting the sign

Ask the patient to extend the neck (best if the patient is sitting, as a proper extension is difficult with the patient lying down). Palpate the carotid is at the level of upper border of thyroid cartilage just anterior to the sternocleidomastoid [Saha, 2013]. (It’s safer not to palpate both sides simultaneously. Pressure on the carotid can slow the heart, and bilateral pressure can cause dangerous slowing [McConachie, 1987].) The carotid pulse of both sides of the neck should be palpated separately to avoid imposing discomfort on the patient.[Saha 2013].

An enlarged thyroid (in goiters) may displace the carotid artery posteriorly. The absence of carotid pulsation upon palpation is a positive Berry’s sign [Babu 2013].


Berry’s sign indicates the presence of infiltration of the carotid sheath by a malignant thyroid swelling [Saha 2013]. As the carotid is encased by the malignant tumour, its pulsation will be masked. A benign thyroid enlargement usually does not infiltrate the carotid sheath [Heston and Wahl, 2010]. Therefore, Berry’s sign is useful in differentiating between a malignant and a benign thyromegaly.


  • Babu RD. Clinical surgery pearls. 2nd ed. New Delhi: Jaypee Brothers Medical Publishers Ltd; 2013, p25.
  • Heston TF, Wahl RL. Molecular imaging in thyroid cancer. Cancer Imaging [Internet]. 2010 [cited 2016 Mar 30];10(1):1-7. Available from doi: 10.1102/1470-7330.2010.0002.
  • McConachie I. Value of pre-operative carotid sinus massage. Anaesthesia 1987;42:636-8
  • Saha ML. Bedside clinics in surgery.2nd ed. New Delhi: Jaypee Brothers Medical Publishers Ltd; 2013, p249.
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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
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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, http://emedicine.medscape.com/article/1952251-overview#a1.
  • 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, http://www.medscape.com/viewarticle/733788.
  • Surks M, ‘Clinical manifestations of hypothyroidism’, UpToDate, http://www.uptodate.com.ezproxy.lib.monash.edu.au/contents/clinical-manifestations-of-hypothyroidism?source=machineLearning&search=clinical+features+of+hypothyroidism&selectedTitle=1~150&sectionRank=1&anchor=H2#H2 , 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.
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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, http://www.uptodate.com/contents/chronic-venous-disease-beyond-the-basics.
  • Chaar CIO. Phlegmasia Alba and Cerulea Dolens. Medscape, http://emedicine.medscape.com/article/461809-overview#a4, 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
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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.
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