Constipation

Xinlin Chin, year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia

Definition

According to the Rome IV criteria used to diagnose functional gastrointestinal disorders, constipation is present when the following symptoms are present for = 3 weeks [Wald, 2016]

1. At least 2 of the symptoms should be present:

  • passing stools with a frequency of less than 3 times per week
  • having difficulty in stools evacuation
  • lumpy/hard stools > 25% of the time (i.e. at least one in four, on average, visits to the toilet result in lumpy or hard stools
  • straining >25% of the time
  • sensation of incomplete evacuation >25% of the time
  • sensation of anorectal obstruction/blockage >25% of the time
  • manual maneuvers required to ease defecation (digital evacuation, support of pelvic floor) >25% of the time

2. Loose stools are hardly present if laxatives are not used.

3. There are inadequate criteria for the diagnosis of irritable bowel syndrome

Physiology

Movements of the small intestine and colon

Contractions of the small intestine may mixing and peristaltic. Mixing contractions are associated with segmentation of the bowel loops. Peristaltic contractions are sequential, and move the intestinal chyme at about 1 cm per minute: this means that it takes 3-5 hours for food to travel from the pylorus to the ileocecal valve [Hall, 2011].

Contractions of the colon are relatively sluggish. Circular constrictions similar to segmentation occur in the colon, while the propulsive movements normally result in a transit time of 8-15 hours between the ileocecal valve and the anus. This allows nearly all of the water to be absorbed. Normal stool volume is about 200 ml/day. [Hall, 2011]

Defecation

Defecation is initiated by the presence of feces in the rectum. Autonomic afferents from the rectum initiate a sympathetic or parasympathetic response. The sympathetic response constricts the internal sphincter. The parasympathetic response relaxes it and allows defecation. The urge to defecate begins when rectal pressure crosses 18 mm Hg [Ganong, 1995]. The defecation reflex consists of the occurrence of strong peristaltic waves in the descending colon and rectum, associated with a closure of the glottis and contraction of the abdominal muscles [Hall, 2011].

Nerves

The sensory innervation to the rectum is carried by autonomic afferents that travel along the pelvic splanchnic nerves to the S2-S4 spinal roots. The parasympathetic efferents, which allow defecation, travel back along the same paths. The sympathetic efferents, which prevent defecation, travel to the rectum from the lumbar splanchnic nerves and the superior and inferior hypogastric plexuses [Ferzandi, 2016].

Muscles

The muscles mainly controlling defecation are the internal sphincter [Hall, 2011], the external sphincter, and the (important) levator ani.

The internal sphincter is a thickening of the terminal end of the inner circular component of the muscular layer of the large intestine [Ferzandi, 2016]. Sympathetic stimulation constricts it, while parasympathetic stimulation relaxes it.

The external sphincter is a voluntary muscle complex that surrounds the anal canal, and is usually described as a composite of three muscles [Ferzandi, 2016]. It is supplied by a branch from S4 [Gray, 1918].

The levator ani forms the pelvic diaphragm. It is supplied by the fourth sacral nerve, and may receive branches from the pudendal nerve. It includes the puborectalis muscle [Gray, 1918], which is probably of great importance to continence. [Fraga and Luis, 2005]

Pathology

Conditions such as anatomical obstruction, slow transit constipation, pelvic floor disorders, irritable bowel syndrome, medications, metabolic, neurological and psychiatric disorders may contribute to the development of constipation.

In normal transit constipation which is a functional gastrointestinal disorder, patient complains of constipation despite no mechanical obstruction is present. In slow transit constipation, there is a decreased in number of high amplitude propagated contractions (HAPCs) post prandially, causing slow colonic transit and reduced mass movements. This causes an increase in water absorption which produces a harder and more concentrated stool which is more difficult to evacuate. Abnormally strong rectal contractions, injury to the colonic pacemaker cells and the interstitial cells of Cajal may all lead to constipation. Uncommon smooth muscle disorders such as scleroderma, amyloidosis and hollow visceral myopathy cause a myopathic process and a loss of colonic contraction.

Besides, megarectum may reduce the rectal contractile forces and impair the rectal sensation which affects the initiation of a normal rectal reflex. Patients with an impaired rectal sensation require larger volumes of rectal distention to stimulate the normal urge of defecation. A large rectocele or sigmoidocele, intussuception and rectal prolapse can impede the normal stool evacuation process. Descending perineum syndrome in which the perineum descends >3cm below the ischial tuberosity during straining and a diminished rectal contraction function may also cause constipation. This syndrome can be caused by injury to the pudendal nerves which lead to prolapse of the anal canal by the anterior rectal mucosa hence affecting rectal emptying. In pelvic floor dyssnergia which is most common in women, the internal anal sphincter fails to relax properly or the external anal sphincter inappropriately contracts during defecation [Lacy and Cole, 2004].

Common causes

Primary causes

  • Normal-transit constipation (NTC). NTC is the commonest subtype of primary constipation [Basson MD, 2017]. Stools pass through the colon at a normal rate and stool frequency is normal. However, patients believe that they experience constipation due to the perception of difficult evacuation and the passage of hard stools. The patient may also experience abdominal pain and bloating [Kumar and Clark, 2017].
  • Slow-transit constipation (STC). This condition normally occurs in young women who have bowel movements of <1 per week. It starts during puberty at patients may experience symptoms such as abdominal pain, bloating, discomfort and a decreased urge to defecate [Kumar and Clark, 2017]. This condition may also occur following an abdominal or pelvic surgery [Bailey and Love’s, 2013].
  • Pelvic floor dysfunction. In normal defecation, puborectalis and the external anal sphincter relax. A paradoxical contraction, also known as pelvic floor dyssynergia or anismus, due to dysfunction of anal sphincter and pelvic floor can prevent evacuation [Basson MD, 2017; Kumar and Clark, 2017].

Secondary causes

  • Negligence of the defecation impulse. This causes dry and large piles of feces to accumulate, leading to distension of the rectum. This constant distension causes patient to become less aware of the fullness of the rectum, which eventually leads to chronic constipation [Talley and O’Connor, 2014].

  • Drugs. The following drugs are known to be associated with constipation[Talley and O’Connor, 2014; Basson MD, 2017]:
    • Antidepressants (cyclic antidepressants, Monoamine oxidase inhibitors: MAOIs)
    • Anticholinergics (benztropine, trihexyphenidyl)
    • aluminium/calcium antacids
    • calcium channel blockers
    • metals (iron, bismuth)
    • NSAIDs (ibuprofen, diclofenac)
    • opiods (codeine and morphine): common in patients who have chronic pain/cancer-related pain [Rao, 2017]
    • cholestyramine, long – term use of stimulant laxatives: This causes development of a dilated atonic laxative colon, which requires more laxatives being used due to its reduced efficacy.
    • Sympathomimetics
    • Psychotropic drugs
    • Insufficient supplementation of thyroid hormone
  • Metabolic or endocrine diseases. Metabolic and endocrine disorders associated with constipation include hypothyroidism, hypokalemia, hyperparathyroidism, hypercalcemia, diabetes mellitus, phaeochromocytoma, porphyria [Talley and O’Connor, 2014; Basson, 2017].
  • Neurological disorders. Constipation may occur in Hirschsprung’s disease, diabetic autonomic neuropathy, spinal cord injury, multiple sclerosis, stroke, Parkinson disease, head injury, cerebral vascular accident, Chagas disease, and familial dysautonomia [Talley and O’Connor, 2014; Basson MD, 2017].
  • Structural causes. Diseases causing narrowing of the bowel lumen alter the bowel habit, causing constipation, diarrhea, or alternating diarrhea and constipation [Basson MD, 2017; BMJ Best Practice, 2016] [Talley and O’Connor, 2014] [Luniss and Nugent, 2013]. Some examples include the following:
    • Carcinoma causing colonic obstruction, hence it is crucial to take note of any altered bowel habits as this can indicate malignancy
    • Stricture
    • volvulus
    • Proctitis
    • Idiopathic megarectum
    • Anal fissure and thrombosed hemorrhoids may be caused by constipation, but the pain associated with defecation may also worsen constipation.
  • Pregnancy. Hormonal changes during pregnancy may affect the motility of small and large bowels [Bianco, 2016; Talley and O’Connor, 2014]. The activity of colonic smooth muscle is mostly affected by the increased concentration of progesterone, leading to the prolongation in gastrointestinal transit time. Progesterone also inhibits the release of motilin (gastrointestinal stimulatory hormone) causing low concentration of motilin in the plasma which again prolongs the gastrointestinal transit time. Besides, during the late gestational stage, the gravid uterus may mechanically obstruct the small bowel transit.
  • Psychological. Depression, anorexia nervosa may result in constipation [[Kumar and Clark, 2017].
  • History

    The following section describes how to take a history of constipation.

    1. Frequency of bowel movement
    2. Infrequent bowel movements define constipation, therefore this question should be asked first.

    3. Duration
    4. This can help to differentiate a congenital or acquired cause in adolescents and young children. It is less likely for young patients and elderly patients (> 50 years old) having symptoms for at least 2 years and have had done a recent screening colonoscopy to develop neoplastic obstruction [Basson, 2017].

    5. Onset
    6. The nature of onset provides etiological information. Intestinal obstruction, ileus due to other medical illness and Ogilvie syndrome may present as acute constipation [Basson, 2017]

    7. Stool
    8. Color. Black stools occur due to upper GI bleed, ingestion of large doses of iron or bismuth [Das, 2013b]. Blood mixed with feces occurs if it originates from bowel higher than sigmoid colon, where stools is still soft [Das 2013c]. Whitish/ clay colored stool indicates biliary obstruction [Das , 2013b].

      Character. Hard, dry stools occur when defecation is delayed. The colon absorbs all the water, leaving behind stools that are difficult to pass. The presence of hard stools is a defining factor in constipation. Most causes of constipation can cause hard stool. Importantly, difficult-to-pass hard stool is a risk factor for anal disorders like fissures and hemorrhoids [Lunniss and Nugent, 2013]. A growth in the lower part of rectum and anal canal may change the shape of the stools causing it to be pipestem or tape-like [Das, 2013c].

      Blood or mucus. Both cancer and hemorrhoids can cause bright red rectal bleeding. Patients with hemorrhoids may also present with rectosigmoid cancer. Patients who age more than 50 and have a family history of colorectal disease should be screened for colorectal cancer. [Basson, 2017b] Children who have intestinal obstruction symptoms with passage of blood and mucus per anum may have acute intussuception [Das, 2013a].

      Change in bowel habit. This may indicate development of a malignancy as colonic obstruction due to carcinoma can cause constipation [Talley and O’Connor, 2014]. Patients with colorectal carcinoma may present with increasing constipation, or alternating diarrhea and constipation, according to the site of the lesion. [Das, 2013b] In ulcerative rectal carcinoma, there is an overnight accumulation of blood, mucus, pus and feces causing patient to have an urgent call to pass stools upon waking. This condition is also known as ‘spurious morning diarrhoea’ [Das, 2013c].

    9. Abdominal features
    10. Abdominal pain. An annular lesion high in the rectum can obstruct the bowel lumen and cause lower abdominal colic [Das, 2013c] .

      Pain during defecation. This suggests the presence of fissure or tenesmus due to a rectal tumor. If there is no pain but patient could not pass out soft stools, this means that there is obstruction of the rectal outlet [Basson, 2017] .

      Flatus. Absolute constipation (inability to pass feces and flatus) is usually associated with intestinal obstruction and peritonitis [Das, 2013a] .

      Straining on passing stool. Disorders of the pelvic floor muscles, nerves or anorectal disease can cause difficulty in evacuation [[Talley and O’Connor, 2014] .

      Tenesmus. Tenesmus is the painful straining to empty the bowel without any result. It can be due to a proliferative growth at the ampulla of the rectum. [Das 2013c] Patients with pelvic abscess or pelvic appendicitis may present with ‘tenesmus’ with the passage of blood and mucus due to irritation of the rectum [Das, 2013a] .

      Sensation of rectal fullness. This may be caused by a proliferative growth in the ampulla of rectum causing patient to feel that he has not completely emptied his bowel after defecation [Das, 2013c]. Patients who feel there may be a blockage at the anus area when they try to pass stool may have disorders of the pelvic floor muscles, nerves or anorectal disease [Talley and O’Connor, 2014].

      Use of pharmacologic or physical method to help stools pass. Ask the patient if he or she needs the help of a finger to press around the anus or vaginal region to facilitate the passage of stools? [Talley and O’Connor, 2014] This can indicate chronic laxative abuse or colonic obstruction. [Basson, 2017]

    11. Systemic features
    12. Weight loss.Ask about weight loss [Das, 2013b]. Gastrointestinal tract malignancies present with marked and progressive weight loss.

    13. Past medical history
    14. Fissures and internal piles are associated with habitual constipation. [Talley and O Connor, 2014]. Patients having hemorrhoids may deny that they were previously treated for constipation or are currently being treated for constipation [Basson, 2017b]. Hypothyroid patients can present with slow transit time and reduced motility. Diabetes is associated with chronic dysmotility. Besides, panhypopituitarism, pheochromocytoma, or multiple endocrine neoplasia 2B increase the risk of having constipation. Central nervous disorders (Parkinson’s, multiple sclerosis, spinal injury or tumors, stroke, CNS syphilis) can also cause constipation [Basson, 2017b].

    15. Family history
    16. Polyposis is a hereditary disease. Patients who have piles, fissures, prolapse and rectal carcinoma may have a positive family history [Das, 2013c] .

    17. Drugs
    18. Ask if patients take the following drugs as they can cause constipation. Codeine, antidepressants, antacids: reduce bowel motility [Basson, 2017]. Chronic laxative abuse contributes to constipation [Basson, 2017b]

    19. Personal history
    20. Ask about the following:

      Change in diet. Too little fibre or water may cause an acute onset of constipation [Basson, 2017b].

      Amount and types of fluid consumed daily. Milk causes constipation in certain individuals. The diuretic effects of coffee, tea and alcohol reduce the amount of water available in the colon, leading to constipation [Basson, 2017]

      Exercise. Exercise stimulates bowel motility [Basson, 2017].

    21. Psychosocial issues
    22. In some situations, there may be a need to ask about social isolation, dependency, poor nutrition, reduced mobility may cause constipation [Rao, 2017]. Patients who have chronic constipation, especially when associated with anismus (failure of normal relaxation of pelvic floor muscles during defecation), may have a history of being sexually abused [Basson, 2017b].

    Examination

    1. Abdominal examination
    2. Inspect for any scars of previous surgery which might have affected the nerves supplying the colonic and pelvic floor function such as the autonomic nervous system and pudendal nerve. Inspect for distension. [Lacy and Cole, 2004]

      Palpate for masses, and to determine if there is a significant amount of stool in the colon: Examine for abdominal distention or masses, which may indicate the presence of colonic stools or tumors. Large abdominal wall hernias such as ventral hernias interrupts the generation of intra-abdominal pressure needed to initiate defecation.[Lacy and Cole, 2004]

      Auscult for bowel sounds. Complete absence of sounds for 4 minutes indicates paralytic ileus [Talley and O’Connor, 2014b]. Loud, high-pitched, tinkling quality (due to presence of air and liquid) indicates obstructed bowel [Talley and O’Connor, 2014b]

    3. Rectal examination
    4. Inspect for fissures, haemorrhoids, masses, evidence of previous surgery can cause difficult defecation [Lacy and Cole, 2004]. Excoriation of perianal skin indicates fecal soiling which may occur in elderly patient with fecal impaction and overflow incontinence [Lacy and Cole, 2004]. Inspect to check for the presence of internal rectal prolapse. Distinguish a true full-thickness rectal prolapse from a mucosal prolapse, which is unlikely to cause constipation (instruct the patient to bear down as if to have a bowel movement) [Basson MD, 2017]. During straining, patients with descending perineum syndrome show abnormal perineal descent of > 3cm (Normal: 1-3 cm). Check presence of rectocele: this is usually at the anterior rectal wall [Basson MD, 2017].

      Palpate for neurological defects: stroke the perianal skin: there is a neurological defect if the reflex contraction of the external anal sphincter is absent [Lacy and Cole, 2004]. Ask patient to voluntarily contract external anal sphincter to assess the strength of external anal sphincter and puborectalis muscle [Lacy and Cole, 2004]. Assess the tone of internal anal sphincter. Patients who have pelvic floor dyssynergia may present with elevated tone and incomplete relaxation of the anal sphincter. [Lacy and Cole, 2004]. A rectal prolapse can be identified during straining when a fold of tissue strikes the examiner’s finger or when tissue is pushed out through the anus [Lacy and Cole, 2004]

    5. Pelvic examination
    6. An internal prolapse or rectocele may be present hence it is important to palpate the woman’s posterior vaginal wall while patient is resting or straining to defecate. [Basson MD, 2017]

    7. Neurological examination
    8. Parkinson’s disease, brain or spinal cord injury, peripheral neuropathy and multiple sclerosis can cause constipation [Basson MD, 2017].

    9. Endocrine system examination
    10. Constipation is also associated with hypothyroidism, hypopituitarism, and diabetes mellitus [Basson MD, 2017]

    References

    • Basson MD. Constipation Clinical Presentation. Medscape [updated 2017 Mar 28, cited 2017 August 3] http://emedicine.medscape.com/article/184704-overview.
    • Bianco A. Maternal gastrointestinal tract adaptation to pregnancy. UpToDate [updated 2016 Mar 14, cited 2017 Sep 6].
    • BMJ Best Practice. Constipation; [updated 2016 Jan 25, cited 2017 August 1].
    • Das S.(a) A manual on clinical surgery. 10th ed. Kolkata; 2013. pg 454.
    • Das S.(b) A manual on clinical surgery. 10th ed. Kolkata; 2013. pg 484.
    • Das S.(c) A manual on clinical surgery. 10th ed. Kolkata; 2013. pg 540.
    • Ferzandi TA. Fecal incontinence. http://emedicine.medscape.com/article/268674-overview#a11, last updated May 5, 2016, accessed 9 October 2017.
    • Fraga F, Luis X. Fisiopatologia anorectal. Tesis Doctorals en Xarxa, 2005. http://www.tdx.cat/handle/10803/4459;jsessionid=A1B50CC62926CAADBD1B94F5A5781D36, accessed 9 October 2017.
    • Ganong WF. Review of Medical Physiology. 17th edition. Prentice-Hall International, 1995, p469.
    • Gray, H. The anatomy of the human body: The Muscles and Fasciæ of the Pelvis, http://www.bartleby.com/107/119.html and The Muscles and Fasciæ of the Perineum, http://www.bartleby.com/107/120.html, accessed 9 October 2017.
    • Hall JE. Guyton and Hall Textbook of Medical Physiology. 12th edition. Saunders Elsevier, Philadelphia, 2011, p770-2.
    • Kumar P, Clark M, editors. Gastrointestinal Disease, In: Clinical Medicine, 9th edition, Elsevier, 2017, pages 415-417.
    • Lacy B.E., Cole M.S., ‘Constipation in the Older Adult’, Clinical Geriatrics 2004, vol.12, pp. 44-54.
    • Lunniss P, Nugent K. The anus and anal canal. In Williams NS, Bulstrode CJK, O’Connell, PR (editors) Bailey and Love’s Short practice of surgery, 26th edition, CRC Press, Taylor and Francis Group, 2013 P1236-67.
    • McMortensen NJ, Ashraf S. The small and large intestines. In Williams N.S., Bulstrode CJK, O’Connell PR (editors) Bailey & Love’s Short Practice of Surgery, Hodder Arnold, 26th ed, 2013, p 1177-1179.
    • Rao SSC. Constipation in the older adult. UpToDate [updated 2017 Jul 05, cited 2017 August 1].
    • Talley NJ, O’Connor S. The Gastrointestinal System, In: The gastrointestinal history: Constipation, 7th edition, Elsevier, New South Wales, 2014, pages 177-207.
    • Wald A. Etiology and evaluation of chronic constipation in adults. UpToDate [updated 2016 May 12, cited 2017 August 2]
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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

References

  • 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].

References

  • 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].

Significance/Implication

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.

    References

  • 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.

Anatomy

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).

Method

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).

References

  • 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

Physiology

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.

    Symptoms

  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].

References

  •  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.

    History

    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

References

  • 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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