Hematochezia: causes

Ong Jo Ern, Year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 22 April 2016

Massive bleeding in lower GI tract is relatively uncommon. Most cases are caused by diverticular disease or ischemic colitis, but almost any of the conditions in the list below can cause massive bleeds.

Small bleeds are common, and usually arise from haemorrhoids and anal fissures. Cancer causes small bleeds: it is only very rarely a cause of massive hemorrhage. Any of the diseases in the list below [BMJ Best Practice, 2018; Cagir, 2017] may cause small bleeds. Note that the list is incomplete!

Finally, some upper gastrointestinal lesions can also present as lower GI bleeding if the hemorrhage is massive. [Cagil, 2017].

Also see Hematochezia for how to take a history of a patient presenting with blood in the stools.

  1. Diverticular disease. Acquired lesion commonly located in the left colon; have a greater tendency to bleed in the right colon. Most common cause of lower GI bleed. More common in older population.
  2. Meckel’s diverticulum. Congenital lesion due to incomplete obliteration of vitelline duct, more common in children.
  3. Colonic angiodysplasia. Common among older people, in the right colon. Dilated tortuous submucosal vessels. Angiodysplasias are acquired arteriovenous malformations, but congenital AV malformations may also

    bleed, often massively. Congenital malformations occur more often in the small bowel [Moore, 1976].

  4. Ischemic colitis. Due to mucosal hypoxia as a result of hypoperfusion of intramural vessels of intestinal wall (in atherosclerosis/vasculitis). Intussusception may be associated with a bleed, typically small:

    this bleeding also results from ischemia to the intussusception (intussusceptum, mostly).

  5. Inflammatory bowel diseases (eg. Crohn’s Disease, Ulcerative colitis)
  6. Infectious colitis. Due to bacterial infection (enterohemorrhagic Escherichia, Salmonella, Histoplasma, CMV colitis. C difficile diarrhea is usually not bloody.). Also caused by parasitic infestations

    (Cryptosporidium, Entamoeba histolytica).

  7. Neoplastic. Colorectal carcinoma, colon polyps. Polyp bleeding is usually small, but may be massive. Cancer bleeding is almost never massive.
  8. Internal haemorrhoids and anal fissures. Hemorrhoids and fissures are the commonest causes of rectal bleeding. Bleeding is small. On rare occasions, bleeding from hemorrhoids may become large.
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How to take a history of bloating

By Eishatur Rodhiah Mamat and Ng En Yng. 2 May 2016


Bloating is a common gastrointestinal symptom experienced by patients of all ages. It can be defined as “a sense of gassiness or a sense of being distended”, although actual abdominal distension does not necessarily occur [Lacy 2011]. Previously, bloating had been used interchangeably with abdominal distension, but studies have shown that only about half of patients suffering from bloating presented with measurable distension of the abdomen. For example, patients with visceral hypersensitivity or functional gastrointestinal disease may complain of bloating without any visible distension [Lacy 2011]. As bloating is a subjective symptom, it is best to describe it in the patient’s own words, such as “too much gas”, “heavy and uncomfortable feeling” and “full belly” [Seo 2013].


A simplified, convenient way of remembering the causes of bloating or abdominal distension is the 6Fs: flatus, faeces, foetus, fat, fluid & ‘fatal growth’ (commonly a neoplasm) [Corey & Friedman 2015]. Another variant of this is the inclusion of ‘filthy’ big tumours (e.g. ovarian tumour or hydatid cyst) and phantom pregnancy [Talley & O’ Connor 2010].

  • Flatus. Flatus is increased intestinal gas. The normal small intestine contains approximately 200 mL of gas.
    • Nitrogen and oxygen are swallowed (aerophagia, results from chewing gum, gulping food, smoking or anxiety)
    • Carbon dioxide, hydrogen, and methane are produced intraluminally by bacterial fermentation (of lactose and other oligosaccharides.
    • In irritable bowel syndrome and bloating, the subjective sense of abdominal pressure is due to impaired intestinal transit of gas rather than increased gas volume. Abdominal distention is the result of a lack of coordination between diaphragmatic contraction and anterior abdominal wall relaxation, a response to an increase in intraabdominal volume loads. Occasionally, increased lumbar lordosis accounts for apparent abdominal distention.

  • Fat. Abdominal fat causes:
    • poor diet (imbalance between caloric intake and energy expenditure)
    • sedentary lifestyle
    • manifestation of certain diseases (Cushing’s syndrome)
    • associated with an increased risk of insulin resistance and cardiovascular disease.
  • Fluid. The accumulation of fluid within the abdominal cavity (ascites) often results in abdominal distention. Causes include:
    • liver cirrhosis (84% of ascites)
    • cardiac ascites
    • peritoneal carconomatosis
    • mixed ascites (from cirrhosis and 2nd disease)
    • massive hepatic metastasis (less common)
    • infection (less common, such as TB, Chlamydia infection)
    • pancreatitis (less common)
    • nephrotic syndrome (less common)
    • hypothyroidism (rare)
    • familial Mediterranean fever (rare)
  • Fetus. Typically, an increase in abdominal size is first noted at 12–14 weeks of gestation, when the uterus moves from the pelvis into the abdomen. Abdominal distention may be seen before this point as a result of fluid retention and relaxation of the abdominal muscles.
  • Feces. In severe constipation or intestinal obstruction, increased stool in the colon causes increased abdominal girth. These conditions are often accompanied by abdominal discomfort or pain, nausea, and vomiting and can be diagnosed by imaging studies.
  • Fatal Growth. An abdominal mass can result in abdominal swelling. Examples include enlarged organs (hepatomegaly, splenomegaly, bladder distention), abdominal aortic aneurysm, malignancies, abscesses, or cysts that grow to sizes.


The table provides an outline of the questions to ask in patients experiencing bloating and their significance.

Feature/characteristic Feature variant What it may indicate
Onset [Bickley 2013] After meal




Drinking milk




Gastroparesis, ileus, anti-cholinergic drugs, gastric outlet obstruction


Lactose intolerance


Bowel obstruction, malignancy


Progression Severity increases


Ascites (due to heart failure, liver cirrhosis etc), pregnancy, malignancy


Associated symptoms [Seo 2013; Talley & O’Connor 2010; Modi & Clearfield 2013] Weight loss




Nausea or vomiting




Increased belching or flatulence










Inability to pass flatus




Shortness of breath

Malignancy, diseases causing malabsorption, eating disorders


Bowel obstruction, gastric outlet obstruction, pregnancy


Bowel obstruction, small intestinal bacterial overgrowth, gut flora disturbances, aerophagia


Inflammatory bowel disease, irritable bowel syndrome, gastroenteritis


Inflammatory bowel disease, impaired evacuation, bowel obstruction, ileus



Heart failure, liver cirrhosis




  • Bickley LS, Szilagyi PG, Bates B. Bates’ Guide to Physical Examination and History Taking. 10th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2009.
  • Corey KE, Friedman LS. Abdominal Swelling and Ascites. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e. New York, NY: McGraw-Hill; 2015.http://accessmedicine.mhmedical.com.ezproxy.lib.monash.edu.au/content.aspx?bookid=1130&Sectionid=79726411. Accessed Apr 27, 2016.
  • Lacy BE, Gabbard SL, Crowell MD. Pathophysiology, Evaluation, and Treatment of Bloating: Hope, Hype, or Hot Air? Gastroenterology & Hepatology. 2011;7(11):729-739.
  • Seo AY, Kim N, Oh DH. Abdominal Bloating: Pathophysiology and Treatment. J Neurogastroenterol Motil 2013;19:433-453. http://dx.doi.org/10.5056/jnm.2013.19.4.433
  • Talley NJ, O’Connor S. Clinical Examination.A systematic guide to physical diagnosis. 6th edition, Churchill Livingstone, 2010
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Daryl Tan Shuang Shuang and Cheang Hoi Lim, Year 3, Jeffrey Cheah School of Medicine and Health Sciences
30 June 2018


The hypothalamus contains feeding and satiety centres.

The satiety center, which inhibits appetite even in the presence of food, is located in the ventromedial nucleus of the hypothalamus and a feeding center is located in the lateral hypothalamic area (LHA). Information feeds into these centers from the arcuate nucleus of the hypothalamus. The arcuate nucleus has various neurons that project onto the satiety feeding centers.hypothalamus

  • Lowering of appetite: Anorexigenic neurons release pro-opiomelanocortin (POMC) and cause decreased appetite.
  • Orexigenic neurons release neuropeptide Y (NPY) and agouti-related protein (AGRP) and cause increased appetite.

POMC and AGRP/NPY neurons appear to be the major targets for several hormones that regulate appetite, including leptin, insulin, GLP-1, cholecystokinin (CCK) andghrelin. [Costanzo, 2014]


  • Palatability of food. Palatability is controlled by cranial nerves (CN1, 7, 9) The feeling of satiety is mediated by autonomic sensory nerves innervating the proximal GI and is contained in the afferent arm of CN 10. Neurotransmitters and hormones stimulate or inhibit control of appetite by signaling molecules in the brain [Williams G. et al.,2000]
  • Adaptive response. The adaptive response allows an organism to mobilize energy reserves to sustain increased metabolism required to wage immune response & heal injuries [Soeters PB et al.,2009] or repair the destruction from rapidly dividing malignant cells. [Argiles JM et al., 1997]
  • Secondary nutrition impact symptoms. These are a consequence of chronic fatigue or nausea, altered taste, depression, pain, xerostomia, disorders of GI motility including gastroparesis and constipation. [Del Fabbro et al., 2011]
  • Depression, food aversions & medications including amphetamines, antibiotics, opioids, antihistamine, digoxin, ranolazine. [Wiffen et al., 2014]
  • Increased symptoms of anorexia in ESRD may be mediated by sex hormones. [Carrero et al., 2007]
  • Aging. Food intake gradually diminishes in response to decreased energy needs due to reduced physical activity & decreased resting energy expenditure. Changes in taste and smell lead to a decreased desire to eat [Heckel et al., 2015]
  • “Failure to thrive (FTT) syndrome. This is a syndrome of weight loss, decreased appetite, poor nutrition & inactivity accompanied by dehydration, depressive symptoms, impaired immune function, and low cholesterol [Sarkisian et al., 1996]. Frailty is a mid-point between independence & pre-death [Hamerman, 1999]


  • Appetite is a desire for food, often of a particular type,and is useful in helping to choose the quality of the food to be eaten. [Costanzo, 2014]
  • Anorexia is either loss of appetite or reduced caloric intake. [Bruera, 1997]
  • According to the DSM-IV-TR criteria, anorexia nervosa (AN) is characterized by a refusal to maintain a minimally normal body weight, an intense fear of gaining weight or becoming fat, and a disturbance in the experience of body shape or weight. [Boeren, 2013]


  1. Duration.
  2. a. Chronic
    i. Very common in patients with advanced cancer & other chronic diseases such as CKD – affects 30-40% of adult patients on maintenance hemodialysis and is associated with increased rates of hospitalization, poor quality of life and increased mortality. [Kalanter-Zadeh et al., 2004]
    ii. Advanced illnesses such as heart failure, cancer, CKD, chronic liver disease, COPD. Chronic illness affecting any organ system. [Soeters et al., 2009]
    b. Acute
    i. Exercise. Only high intensity exercise induces a suppression of hunger. This appetite suppression is short-lived and recovery is rapid. Hunger tends to return to near control levels within 15 minutes. This recovery period is extended slightly but not significantly by doubling the duration of high-intensity exercise. [King et al., 1994]
    ii. Development of acute phase response (APR) during infections, e.g. cholecystitis, cholangitis, appendicitis, UTI [Kanra et al., 2006]

  3. Normal eating habits.
  4. a. Patients with anorexia nervosa commonly restrict their diet to vegetables, fruit, and diet products, and often skip meals altogether. They develop mealtime rituals, such as cutting food into tiny pieces, patting liquid off with napkins, or picking food apart. [Am Fam Physician, 2015]

  5. Weight loss.
  6. a. Even a 5% weight loss, combined with cognitive concerns, may produce a group with a clinically significant eating disorder
    b. Atypical anorexia nervosa (AAN) was observed in both healthy weight and overweight/obese adults, highlighting the importance of screening for restrictive eating disorders at all weights [Forney et al., 2017]

  7. Inability to eat, or secondary nutrition impact symptoms (S-NIS)
  8. a. Rule out symptoms that may be related to the underlying illness, symptoms and syndromes that may contribute to reduced caloric intake
    b. In particular, pain, xerostomia, nausea, constipation, and depression are frequent in patients with a chronic illness and may result in decreased caloric intake if not adequately treated.
    c. Most common S-NIS due to cancer are early satiety, constipation, nausea/vomiting, and depressed mood. [Del Fabbro et al., 2011]

  9. Etiology and risk factors.
  10. a. Gender: Anorexia nervosa is more common among females than males. Girls or women are more likely than boys or men to report weight dissatisfaction, dieting for weight control and use of purging. [Striegel-Moore et al., 2009]
    b. Psychological changes: Look for obsessive/ perfectionist traits or fear of gaining weight: these may indicate anorexia nervosa. Maladaptive perfectionism may be more strongly associated with cognitively versus behaviorally-oriented eating disorder symptoms. [Jason et al., 2016]. Fear of failure motivate the behavioral components of perfectionism that aims on reassurance seeking. [Hassan et al., 2015] The patient may be frequently starving but in denial [Lynn et al., 2012]. Depression is often associated with loss or deterioration of social networks, and is a common psychological problem in the elderly and a significant cause of loss of appetite. [Lorenzo et al., 2003]
    c. Endocrine dysfunction. Hypogonadism is especially common in men with cancer. It may go undetected and contribute to loss of appetite or decreased lean body mass. [Dev et al., 2014]. Explore hypothyroidism.
    d. Ask about misuse of laxatives, diuretics or enemas. Self-induced purging may be aided by the misuse of laxatives. The ICD 10 criteria (WHO, 1992) stress the importance of purging behaviour on the grounds that vomiting and laxative misuse are considered pathological behaviours in our society in comparison to dieting and exercise. Constipation is extremely common, mainly due to dehydration; steatorrhoea and protein losing gastroenteropathy have also been reported secondary to laxative abuse. [British Psychological Society, 2004]
    e. Amenorrhea: this may occur due to hypothalamic dysfunction, low fat stores, malnutrition [Am Fam Physician, 2015]
    f. Jaundice and tea-colored urine. Anorexia, nausea, emesis, or weight loss appearing within 2 weeks prior to onset of jaundice suggests hepatitis or biliary obstruction secondary to gallstones. The same symptoms occurring continuously for more than 2 weeks prior to the appearance of jaundice suggest a malignant biliary obstruction, chronic hepatitis, or toxin exposure (especially alcohol). Recurrent brief episodes of anorexia, nausea, or emesis extending over months to years, especially when accompanied by right upper quadrant abdominal pain, implicate gallstones. [Stillman, 1990]
    g. Medications. Medications that may influence appetite include anti-convulsants, anti-depressants, levodopa, digoxin, metformin, and thyroid medications [Lynn et al., 2012]
    h. Fever. Patients may have sickness-associated anorexia, appetite being suppressed by inflammation [Gautron and Laye, 2009]. Anorexia Nervosa patients with a bacterial infection showed a reduced fever response, were often difficult to diagnose because of fewer signs and symptoms, and infection became more frequent with increasing patient age. [Brown et al., 2005]

    1. Costanzo, Linda S. Physiology. Fifth edition. Philadelphia, PA: Saunders/Elsevier, 2014; pp 337-8.
    2. Williams G, Harrold JA, Cutler DJ. The hypothalamus and the regulation of energy homeostasis: lifting the lid on a black box. Proc Nutr Soc. 2000 Aug;59(3):385-96.
    3. Soeters PB, Grimble RF. Dangers, and benefits of the cytokine mediated response to injury and infection. Clin Nutr. 2009 Dec;28(6):583-96.
    4. Argilés JM, Alvarez B, López-Soriano FJ. The metabolic basis of cancer cachexia. Med Res Rev. 1997 Sep;17(5):477-98.
    5. Del Fabbro E, Hui D, Dalal S, Dev R, Nooruddin ZI, Noorhuddin Z, Bruera E. Clinical outcomes and contributors to weight loss in a cancer cachexia clinic. J Palliat Med. 2011 Sep;14(9):1004-8.
    6. Wiffen PJ, Derry S, Moore RA. Impact of morphine, fentanyl, oxycodone or codeine on patient consciousness, appetite and thirst when used to treat cancer pain. Cochrane Database Syst Rev. 2014
    7. Carrero JJ, Qureshi AR, Axelsson J, Avesani CM, Suliman ME, Kato S, Bárány P, Snaedal-Jonsdottir S, Alvestrand A, Heimbürger O, Lindholm B, Stenvinkel P. Comparison of nutritional and inflammatory markers in dialysis patients with reduced appetite. Am J Clin Nutr. 2007 Mar;85(3):695-701.
    8. Heckel M, Stiel S, Ostgathe C. Smell and taste in palliative care: a systematic analysis of literature. Eur Arch Otorhinolaryngol. 2015;272(2):279.
    9. Sarkisian CA, Lachs MS. “Failure to thrive” in older adults.Ann Intern Med. 1996;124(12):1072.
    10. Hamerman D. Toward an understanding of frailty. Ann Intern Med. 1999;130(11):945.
    11. Bruera E. ABC of palliative care. Anorexia, cachexia, and nutrition. BMJ. 1997;315(7117):1219.
    12. Boeren A. Perfectionism in anorexia nervosa: a literature review.Bachelorthesis Psychology and Health, Tilburg University, 2013 July, available at http://arno.uvt.nl/show.cgi?fid=131260.
    13. Kalantar-Zadeh K, Block G, McAllister CJ, Humphreys MH, Kopple JD. Appetite and inflammation, nutrition, anemia, and clinical outcome in hemodialysis patients. Am J Clin Nutr. 2004 Aug;80(2):299-307.
    14. Soeters PB, Grimble RF. Dangers, and benefits of the cytokine mediated response to injury and infection. Clin Nutr. 2009 Dec;28(6):583-96.
    15. N.A. King, V.J. Burley, J.E. Blundell. Exercise-induced suppression of appetite: effects on food intake and implications for energy balance. Eur J Clin Nutr. 1994 Oct;48(10):715-24.
    16. Kanra GY, Ozen H, Kara A. Infection and anorexia. Turk J Pediatr. 2006 Oct-Dec;48(4):279-87.
    17. Am Fam Physician. Initial Evaluation, Diagnosis and Treatment of Anorexia Nervosa and Bulimia Nervosa. 2015 Jan; 91(1): 46-52.
    18. Forney KJ, Brown TA, Holland-Carter LA, Kennedy GA, Keel PK. Defining “significant weight loss” in atypical anorexia nervosa. Int J Eat Disord. 2017 Aug;50(8):952-962.
    19. Striegel-Moore RH, Rosselli F, Perrin N, et al. Gender Difference in the Prevalence of Eating Disorder Symptoms. The International journal of eating disorders. 2009;42(5):471-474.
    20. Jason M. Lavender, Tyler B. Mason, Linsey M. Utzinger, Stephen A. Wonderlich, Ross D. Crosby, Scott G. Engel, James E. Mitchell, Daniel Le Grange, Scott J. Crow, and Carol B. Examining Affect and Perfectionism in Relation toEating Disorder Symptoms among Women with Anorexia Nervosa. Peterson Psychiatry Res. 2016 Jul 30; 241: 267–272.
    21. Hassan Y., Ali M. Comparison of Perfectionism and Related Positive-Negative Dimension in People With High Traits on Obsessive Compulsive and Eating Disorder Characteristics. J Psychiatry Behav Sci. 2015 Sep;9(3):e264.
    22. Lynn S. Bickley, Peter G. Szilagyi. Bates’ Guide to Physical Examination and History Taking 11th Edition. 2012 Nov; 4: 136.
    23. Lorenzo M. Donini, Claudia Savina, Carlo Cannella. Eating Habits and Appetite Control in the Elderly: The Anorexia of Aging. 2003 March; 15(1): 73-87.
    24. Dev R, Hui D, Del Fabbro E, Delgado-Guay MO, Sobti N, Dalal S, Bruera E. Association between hypogonadism, symptom burden, and survival in male patients with advanced cancer. Cancer. 2014 May;120(10):1586-93.
    25. National Collaborating Centre for Mental Health (UK). Eating Disorders: Core Interventions in the Treatment and Management of Anorexia Nervosa, Bulimia Nervosa and Related Eating Disorders. Leicester (UK): British Psychological Society (UK); 2004. (NICE Clinical Guidelines, No. 9.) 2, Eating disorders. Available from: https://www.ncbi.nlm.nih.gov/books/NBK49318/
    26. Stillman AE. Jaundice. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 87. Available from: https://www.ncbi.nlm.nih.gov/books/NBK413/
    27. Lynn S. Bickley, Peter G. Szilagyi. Bates’ Guide to Physical Examination and History Taking 11th Edition.2012 Nov; 4: 108.
    28. Gautron, L., & Layé, S.. Neurobiology of Inflammation-Associated Anorexia. Frontiers in Neuroscience, 2009; 3, 59. http://doi.org/10.3389/neuro.23.003.2009
    29. Brown RF, Bartrop R, Beumont P, Birmingham CL. Bacterial infections in anorexia nervosa: delayed recognition increases complications. Int J Eat Disord. 2005 Apr;37 3):261-5.
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Xinlin Chin, year 3, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia


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


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 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].


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].


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]


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].


    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]


    • 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]
Posted in Uncategorized

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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