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What is dysphagia?

Dysphagia means difficulty swallowing, and is distinct from globus (a "lump" in the throat without organic cause) and odynophagia (pain during swallowing).

Dysphagia can be caused by neuromuscular disorders, oral disease and oesophageal disorders.


What neuromuscular conditions cause dysphagia?

These can broadly be divided into (i) central, (ii) bulbar and (iii) muscular/myenteric plexus disorders.

1) Central
- CVA - extensive small vessel disease
- Parkinson's esp. PSP
- Psychiatric - globus pharyngeus

2) Bulbar palsy (lower motor neurone)
- Brainstem: synringobulbia, infarction (lateral medullary syn), MS
- MND, polio
- Peripheral autonomic neuropathy (e.g. diphtheria, GBS, Chagas' disease)

3) Muscular/ myenteric plexus
- NMJ: myasthenia, botulism
- Myopathy
- Ganglion/ peristalsis dysfunction - e.g. CREST, lower oesophageal achalasia


What oral conditions cause dysphagia?

Pharyngitis and oral ulcers cause painful swallowing (odynophagia) with secondary dysphagia.


How can oesophageal causes of dysphagia be classified?

These can be broken down into luminal, intrinsic and extrinsic causes:

1) Luminal - FB or large food bolus
2) Intrinsic
- upper - pharyngeal pouch, post-cricoid web
- middle - oesophagitis, oesophageal stricture, oesophageal carcinoma
- lower - hiatus hernia, Schatzki ring
3) Extrinsic - "BULGIN"
Bone: cervical spondylosis
U: dysphagia LUsoria, vascular compression (e.g. aberrant R subclavian artery, aortic aneurysm, mitral stenosis (enlarged left atrium)
Infection: retropharyngeal abscess
Neoplasia: pancreatic cancer


How does dysphagia present?

The presentation of dysphagia can give clues as to the underlying cause, and is different for neurological, oral and oesophageal disorders.

Neuromuscular cases tend to present with equal intolerance to solids and liquids. Nasal regurgitation, aspiration (when attempting to swallow) and other neurological signs (e.g. diplopia, ataxia).

Oral causes of dysphagia present with odynophagia.

Oesophageal causes present with difficulty swallowing solids > liquids. Aspiration that occurs is unrelated to swallowing, and patients may also complain of chest pain, dyspepsia and hiccups.


What examination findings may help confirm a neuromuscular cause of dysphagia?

Other neurological deficits - e.g. ataxia, dysarthria and Horner's syndrome


What examination findings are associated with oesophageal causes of dysphagia?

1) Hoarse voice
- Laryngitis (GORD)
- Left recurrent laryngeal nerve palsy (carcinoma, lymph nodes)

2) Respiratory symptoms
- Right middle lobe consolidation (aspiration pneumonia)
- Unilateral wheeze (main bronchus compression)


How should dysphagia be investigated?

All patients require an upper GI endoscopy unless there are compelling reasons for this not to be performed. Motility disorders (neuromuscular) may be best appreciated by undertaking fluoroscopic swallowing studies.

A full blood count should be performed.

Ambulatory oesophageal pH and manometry studies will be required to evaluate conditions such as achalasia and patients with GORD being considered for fundoplication surgery.


What is a post cricoid web?

Occurs as part of Plummer-Vinson or Paterson-brown-Kelly syndrome. Also characterised by Fe deficiency aneamia, koilonychia, glossitis and risk of squamous cell carcinoma.


How can oesophageal cancer, oesophagitis and oesophageal candidiasis be differentiated?

Oesophageal cancer = dysphagia associated with weight loss, anorexia or vomiting during eating
Past history may include Barrett's oesophagus, GORD, excessive smoking or alcohol use

Oesophagitis = may be history of heartburn
Odynophagia but no weight loss and systemically well

Oesophageal candidiasis = there may be a history of HIV or other risk factors such as steroid inhaler use


What is dyspepsia?

Dyspepsia is indigestion and causes may arise from within or outside the GIT.


Name some causes of dyspepsia

GI disorders:
Peptic ulcer disease
Acute gastritis
Colonic carcinoma
Pancreatic disease

Systemic disease:
Renal failure

Iron supplements


What are the "alarm" features of dyspepsia?

Weight loss
Palpable abdominal mass


How should patients with dyspepsia be investigated?

Patients with any of the alarm features or who are >55 with new onset dyspepsia are classed as urgent and should be referred for endoscopy.

Non urgent patients include:
- Patients with haematemesis
- Patients aged >= 55 years who've got:
treatment-resistant dyspepsia or
- upper abdominal pain with low haemoglobin levels or
- raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
- nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain


Which patients should be tested for H.pylori infection?

Young patients or patients that do not meet the referral criteria (labelled as "undiagnosed dyspepsia"). If symptoms persist after treatment they should be referred for endoscopy.

Management of these patients can be summarised at a step-wise approach
1. Review medications for possible causes of dyspepsia
2. Lifestyle advice
3. Trial of full-dose proton pump inhibitor for one month OR a 'test and treat' approach for H. pylori


What are the causes of nausea and vomiting?

This is a wide list, but a broad overview can be remembered by: too many "GIN & TONICS"
Calcium/ endocrine dysfunction


What gastrointestinal disorders can cause vomiting?

Gastro-oesophageal: reflux, ulcer, pyloric stenosis
Pancreatic, liver, gallbladder disease


What infections can cause nausea and vomiting?

GIT: gastroenteritis; hepatitis; visceral abscess
Systemic: RTI (esp. tonsillitis, otitis media); UTI; sepsis


What are the important features of a nausea and vomiting history?

The history should reveal associated abdominal pain, fever, diarrhoea, relationship to food, drugs, headache, vertigo and weight loss. Pregnancy, alcoholism and bulimia should be considered.


How is nausea and vomiting treated?

There is a whole deck on anti-emetics, but a basic way to remember is "A123":
Muscarinic (ACh) receptor antagonists
Histamine type 1 receptor antagonist
Dopamine type 2 receptor antagonist
Serotonin type 3 receptor antagonist


How do patients with upper GI bleeds present?

Patients may present with the following:
- Haematemesis and/ or malaena
- Epigastric discomfort
- Sudden collapse

Haematemesis may be red with clots when bleeding is profuse, or black (‘coffee grounds’) when less severe. Syncope may occur with rapid bleeding. Anaemia suggests chronic bleeding. Melaena is the passage of black, tarry stools containing altered blood. This is usually due to upper GI bleeding, although the ascending colon is occasionally responsible. Severe acute upper GI bleeding occasionally causes maroon or bright red stool.

The extent to which these will occur will depend upon the source. Mortality is higher in patients presenting with haematemesis than malaena alone.


What can cause oesophageal bleeding? What clinical features are associated with these?

1) Oesophagitis - small volume of fresh blood, often streaking vomit. Malaena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms.

2) Cancer - usually small volume of blood, except as pre terminal event with erosion of major vessels. Often associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent until malignancy managed.

3) Mallory -Weiss tear - typically brisk small to moderate volume of bright red blood following bout of repeated vomiting. Malaena rare. Usually ceases spontaneously

4) Varices - usually large volume of fresh blood. Swallowed blood may cause malaena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.


What gastric diseases can cause upper GI bleeding? What features are associated with each?

1) Gastric cancer - may be frank haematemesis or altered blood mixed with vomit. Usually prodromal features of dyspepsia and may have constitutional symptoms. Amount of bleeding variable but erosion of major vessel may produce considerable haemorrhage.

2) Dieulafoy Lesion - often no prodromal features prior to haematemesis and malaena, but this arteriovenous malformation may produce quite considerable haemorrhage and may be difficult to detect endoscopically

3) Diffuse erosive gastritis - usually haematemesis and epigastric discomfort. Usually there is an underlying cause such as recent NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise

4) Gastric ulcer (MCC) - small low volume bleeds more common so would tend to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis


What is the most common cause of duodenal bleeding?

Most common cause of major haemorrhage is a posteriorly sited duodenal ulcer. However, ulcers at any site in the duodenum may present with haematemesis, malaena and epigastric discomfort. The pain of duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours after eating. Peri ampullary tumours may bleed but these are rare. In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of major haemorrhage associated with high mortality.


Summarise the causes of haematemesis?

This can best be remembered as "VINTAGE":
Inflammation (e.g. oesophagitis or peptic ulcer)
Neoplasia (e.g. oesophageal or gastric)
- 1) Mallory-Weiss tear
- 2) Surgery, ERCP, aorto-duodenal fistula
- 3) Hypovolaemic shock: ischaemic, stress ulcer in stomach
Angiodysplasia + other vascular abnormalities
- angiodysplasia (dilated vessel complexes in clusters)
- hereditary haemorrhagic telangiectasia (dilated vessels ALL over bowel wall)
- others (e.g. Dieulafoy lesion, PAN)
Generalised bleeding disorder


Outline the management of upper GI bleed? When should patients undergo endoscopy?

1) IV access
2) Clinical assessment - risk of complications related to circulatory status, liver disease, and comorbidity (i.e. cardiorespiratory, cerebrovascular or renal disease that increases the hazards of endoscopy and surgery)
3) Bloods - cross match blood, check FBC, LFTs, U+E and Clotting (as a minimum)
4) Resuscitation - oxygen is given to patients in shock. IV crystalloid infusion restores BP, and blood transfusion is indicated if there is shock and active bleeding. Antibiotics are given in chronic liver
5) Endoscopy - ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper GI endoscopy within 24 hours of admission. In those who are unstable this should occur immediately after resuscitation or in tandem with it
6) Monitoring - hourly pulse, BP and urine output should be monitored


What are the indications for surgery in patients with upper GI bleeding?

Patients > 60 years
Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known cardiovascular disease with poor response to hypotension


How should oesophageal varices be managed?

Patients with suspected varices should receive terlipressin prior to endoscopy.

Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be done with care; gastric balloon should be inflated first and oesophageal balloon second. Remember the balloon with need deflating after 12 hours (ideally sooner) to prevent necrosis. Portal pressure should be lowered by combination of medical therapy +/- TIPSS.

Identifiable bleeding points should receive combination therapy of injection of adrenaline and either a thermal or mechanical treatment. All who have received intervention should receive a continuous infusion of a proton pump inhibitor (IV omeprazole for 72 hours) to reduce the re-bleeding rate.


What is the Blatchford score?

The need for admission and timing of endoscopic intervention may be predicted by using the Blatchford score. This considers a patients Hb, serum urea, pulse rate and blood pressure. Those patients with a score of 0 are low risk, all others are considered high risk and require admission and endoscopy.


Should patients with GI bleeding receive PPI prior to endoscopy?

The requirement for pre endoscopic proton pump inhibition is contentious. In the UK the National Institute of Clinical Excellence guidelines suggest the pre endoscopic PPI therapy is unnecessary. Whilst it is accepted that such treatment has no impact on mortality or morbidity a Cochrane review of this practice in 2007 did suggest that it reduced the stigmata or recent haemorrhage at endoscopy. As a result many will still administer PPI to patients prior to endoscopic intervention.


What is the Rockall score?

Following endoscopy it is important to calculate the Rockall score for patients to determine their risk of rebleeding and mortality. A score of 3 or less is associated with a rebleeding rate of 4% and a very low risk of mortality and identifies a group of patients suitable for early discharge.


Lower gastrointestinal bleeding occurs due to haemorrhage from the small bowel, colon or anal canal. How does colonic bleeding present?

This typically presents as bright red or dark red blood per rectum. Colonic bleeding rarely presents as malaena type stool, this is because blood in the colon has a powerful laxative effect and is rarely retained long enough for transformation to occur and because the digestive enzymes present in the small bowel are not present in the colon. Up to 15% of patients presenting with haemochezia will have an upper gastrointestinal source of haemorrhage.

As a general rule right sided bleeds tend to present with darker coloured blood than left sided bleeds. Haemorrhoidal bleeding typically presents as bright red rectal bleeding that occurs post defecation either onto toilet paper or into the toilet pan. It is very unusual for haemorrhoids alone to cause any degree of haemodynamic compromise.


What are the causes of lower GI bleeding?

Remember these by using "DRIPPING TAPS"

Diverticulae (e.g. colonic, Meckel's, jejunal)
Polpys - both benign and neoplastic
Inflammation (e.g. ulcerative colitis - blood diarrhoea)
Neoplasia (e.g. carcinoma, lymphoma)
Gastric upper bowel bleeding (bloody if rapid transit)

Trauma (e.g. surgery, radiation colitis)
Arterial/ Angiodysplasia/ AVM)
Pseudomembranous colitis
Systemic (e.g. coagulopathy, amyloid)


What are the different presentations of bleeding diverticulae?

Colonic diverticular disease: this is the most common cause. Patients present with profuse, red or maroon diarrhoea and shock. Bleeding almost always stops spontaneously, but if not, the diseased segment is located by angiography or colonoscopy and resected.

Illeal (e.g. Meckel's diverticulum): presents with childhood bleeding

Jejunal: bleeding usually presents with malabsorption + vitamin B12 deficiency due to bacterial overgrowth


What infections can cause lower GI bleeding?

1) Bacterial: Salmonella, Campylobacter, E.coli, pseudomembranous colitis, TB

2) Other: HIV, CMV, Candida

3) Parasites: amoebic dysentry, hookworm (melaena)


How are patients with lower GI bleeds managed?

Prompt correction of any haemodynamic compromise is required. Unlike upper gastrointestinal bleeding the first line management is usually supportive. This is because in the acute setting endoscopy is rarely helpful.

When haemorrhoidal bleeding is suspected a proctosigmoidoscopy is reasonable as attempts at full colonoscopy are usually time consuming and often futile.

In the unstable patient the usual procedure would be an angiogram (either CT or percutaneous), when these are performed during a period of haemodynamic instability they may show a bleeding point and may be the only way of identifying a patch of angiodysplasia.

In others who are more stable the standard procedure would be a colonoscopy in the elective setting. In patients undergoing angiography attempts can be made to address the lesion in question such as coiling. Otherwise surgery will be necessary.

In patients with ulcerative colitis who have significant haemorrhage the standard approach would be a sub total colectomy, particularly if medical management has already been tried and is not effective.


How should obscure major GI bleeding be investigated?

If upper endoscopy and colonoscopy are inconclusive, mesenteric angiography usually identifies the site and embolisation can be used to stop the bleeding. If angiography is negative, double balloon enteroscopy or wireless capsule endoscopy can be employed to identify a bleeding source in the small intestine. When all else fails, laparotomy with on-table endoscopy is indicated.


What is occult GI bleeding?

Occult bleeding (no visible blood) may reach 200 mL/day, cause iron deficiency anaemia and signify serious disease. The most important cause is colorectal cancer, which may have no GI symp- toms. GI investigations should be considered in any patient with unexplained iron deficiency anaemia. A negative faecal occult blood (FOB) test does not exclude important GI disease. FOB is now only used in population screening for bowel cancer.


What is the WHO definition of diarrhoea?

Diarrhoea: > 3 loose or watery stool per day or >250g stool per day
Acute diarrhoea < 14 days
Chronic diarrhoea > 14 days


What are the 3 most common types of diarrhoea?

1) Invasive
2) Secretory
3) Osmotic


What is invasive diarrhoea?

Pathogens invade enterocytes causing low volume diarrhoea, which contains blood and leukocytes (i.e. dysentery).

It is caused by Shigella spp, Campylobacter, Salmonella and Entamoeba histolytica


What screening tests should be performed for invasive diarrhoea?

Faecal smear for leukocytes - positive in most cases
Order stool culture, stool for O&P (ova and parasites) and stool antigen


What is secretory diarrhoea?

Loss of isotonic fluid causing high volume diarrhoea.
Mechanisms include:
- laxatives
- enterotoxins stimulate Cl- channels regulated by cAMP and cGMP
- serotonin increases bowel motility

There is no inflammation in the bowel mucosa.
Diarrhoea persists with fasting.


What causes secretory diarrhoea?

1) Laxatives - esp. phenolphthalein containing, e.g. senna, bisacodyl
- danger of melanosis coli (black bowel syndrome)

2) Infection (toxin mediated):
i) Food poisoning (toxin or organism pre formed within food)
- toxin mediated: staph aureus, Clostridium perfringens
ii) Gastroenteritis (i.e. organism colonizes and multiplies within bowel)
- toxin mediated: cholera, enterotoxigenic E.coli

3) Increased serotonin: carcinoid syndrome


What screening tests should be performed for cases of secretory diarrhoea?

Faecal smear for leukocytes - negative in most cases
Increased 5-HIAA: carcinoid syndrome
Stool osmotic gap <50mOsm/kg


What is osmotic diarrhoea?

Osmotically active substance is drawing hypotonic solution out of the bowel, causing high volume diarrhoea but no inflammation in the bowel mucosa.


What causes osmotic diarrhoea?

1) Malabsorption
- disaccharidase deficiency
- giardiasis
- ANY cause of malabsorption

2) haemorrhage into bowel
3) Ingestion of poorly absorbable solutes (e.g. magnesium sulfate laxatives)


What screening tests are useful for osmotic diarrhoea?

Faecal smear for leukocytes - negative
Stool osmotic gap >100mOsm/kg


What is the stool osmotic gap?

300 mOsm/kg (value used to represent normal POsm)
Osmotic gap <50 mOsm/kg from POsm is a secretory diarrhea.
- Indicates that diarrheal fuid POsm approximates normal POsm
Osmotic gap >100 mOsm/kg from POsm is an osmotic diarrhea.
- Indicates a hypotonic loss of stool due to presence of osmotically active substances


Summarise the main causes of diarrhoea

Think of "SOILINGS"

Secretory - as well as infection and toxic, there are also systemic causes (e.g. thyrotoxicosis, hypoadrenalism)
Inflammation or Ischaemia (e.g. UC, vasculitis)
Laxatives and other drugs - e.g. erythromycin, prokinetics
Irritable bowel syndrome
Neuropathy - autonomic, e.g. diabetes
Structural - e.g. rectal adenomas, neoplasia, diverticular disease
Special - e.g. alcohol, overflow (faecal impaction)


What is the most common cause of chronic or relapsing diarrhoea?

The most common cause is irritable bowel syndrome, in which diarrhoea is most severe before and after breakfast and rarely occurs at night. At other times the patient is constipated. The stool often contains mucus but never blood, and 24-hr stool volume is <200 g. Chronic diarrhoea can also be due to inflammatory or neoplastic disease of the colon or small bowel, or to malabsorption. Negative investigations suggest irritable bowel syndrome.


What is the Rome criteria?

Criteria useful for diagnosing IBS. Includes:
1) Abdo-rectal pain: relieved by defacation, radiates to thighs + back, bloating
2) Stool frequency: >3x/day or <3/week
3) Stool form: hard pellets, watery, mucus

Exclusion criteria: onset > 40 years, bloody stool, weight loss + normal sigmoidoscopy


What is malabsorption?

Chronic diarrhoea with increased faecal excretion of fats (steatorrhoea).
Concurrent deficiencies in fat soluble vitamins, minerals, carbohydrates, and proteins may also occur.

Clinically, chronic diarrhoea and weight loss in a patient with a normal diet suggests malabsorption.


What are the clinical features of malabsorption?

Bulky, pale, offensive stools that float (statorrhoea) signify fat malabsorption.
Abdominal distension, borborygmi, cramps and undigested food in the stool may be present.
Malaise, lethargy, peripheral neuropathy and symptoms related to vitamin or mineral deficiencies may occur.


What causes malabsorption?

Malabsorption results from abnormalities of the three components of normal digestion:
1) Intraluminal maldigestion due to deficiency of bile or pancreatic enzymes
2) Mucosal malabsorption from small bowel resection or damage to the small intestinal epithelium
3) ‘Post-mucosal’ lymphatic obstruction preventing the uptake of absorbed lipids into lymphatic vessels


What can cause pancreatic deficiency and lead to malabsorption?

Pancreatic insufficiency is most commonly caused by chronic pancreatitis (most commonly due to alcohol in adults and cystic fibrosis in children).

Dietary triglyceride is digested by pancreatic lipase, which is deficient in chronic pancreatitis. Fats are undigested producing fatty stool.

Maldigestion of proteins is also present. Due to reduced pancreatic trypsin.
Carbohydrate absorption is NOT affected because amylase is present in the salivary glands and disaccharidases are present in the brush border of intestinal epithelium.


What causes bile acid/ salt deficiency?

1) Inadequate synthesis of bile acids from cholesterol (cirrhosis)
2) Intrahepatic/ extrahepatic blockage of bile - e.g. PBC, stone in common bile duct
3) Bacterial overgrowth in small bowel with destruction of bile salts/ acids - e.g. small bowel diverticula, autonomic neuropathy
4) Excess binding of bile salts
5) Terminal ileal disease - prevents recycling of bile acids, e.g. Crohns disease, or resection


What are the consequences of bile acid/salt deficiency?

Bile salts/ acids produce micelles to enhance reabsorption of fats by the small intestinal villi. Micelles contain MGs, FAs and fat soluble vitamins. Note that ALL fat soluble vitamins (i.e. A, D, E and K) are packaged into micelles so any disease producing maldigestion of fats also produces deficiencies of all the fat soluble vitamins.


What small bowel diseases cause malabsorption?

1) Damage to villi (coeliac disease)
- villi increase absorptive surface of the small intestine
- required to absorb micelles into enterocytes
- loss of villi lead to loss of micelles in stools

2) Apoprotein B48 in enterocytes is important in resynthesizing TGs and packaging them into chylomicrons
- loss of enterocytes and/or deficiency of apoB48 diminishes formation of chylomicrons

3) ApoB48 also important for transporting chylomicrons into lymphatics
- deficiency of apoB48 or lymphatic blockage in the intestinal cells (Whipple's disease) decreases chylomicron transportation in the blood


How should malabsorption be investigated?

First enquire about symptoms of steatorrhoea. If present do preliminary bloods for U&Es, immunoglobulins, Ca++, Mg++, FBC, clotting, albumin, folate, B12, coeliac antibodies.

Second investigate small intestine:
- duodenal biopsy
- barium studies
- faecal calprotectin

If these are NORMAL, investigate the pancreas:
- pancreatic function tests - faecal elastase
- ultrasound scan

If these are NORMAL, consider bile salt malabsorption
- SeHCAT scan*
- serum 7 alpha hydroxycholestenone

*nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT


What is considered significant weight loss?

Unplanned weight loss of >3 kg over 6 months is significant. Pathological weight loss can be caused by psychiatric illness, systemic disease, GI causes or advanced disease of any specific organ system.


What features in the history can point to the underlying cause of weight loss?

1) Physiological - obvious from the history, but can be more difficult in older age

2) Psychiatric illness - features of anorexia nervosa, bulimia and affective disorders; alcoholic patients lose weight through self neglect and poor diet

3) Systemic diseases - chronic infections lead to weight loss and a history of recent travel, fever, night sweats, rigors, productive cough and dysuria must be sought. Sexual history is important. Weight loss is a late feature of disseminated malignancy

4) GI disease - dysphagia and gastric outlet obstruction cause defective intake. Malignancy may cause weight loss by mechanical obstruction, anorexia, or systemic effects. Malabsorption from pancreas or small bowel causes profound weight loss and nutritional deficiences. Crohn's and UC cause anorexia, fear of eating and loss of protein, blood and nutrients from the gut


How should weight loss be investigated?

Urinalysis for glucose, protein and blood
Bloods - LFTs, random blood glucose, and TFTs, ESR
Bone marrow aspirate or liver biopsy to identify cryptic miliary TB when there is strong clinical suspicion


What is constipation?

This is infrequent passage of hard stools, often with straining, a sensation of incomplete evacuation and peri-anal or abdominal discomfort. It may be the end result of many disorders.


What can cause constipation?

- lack of dietary fibre
- altered motility - e.g. irritable bowel syndrome
- structural - e.g. colonic carcinoma, diverticular disease, Hirschsprungs disease
- obstructed defacation - e.g. anal fissure, Crohn's disease

Non GI:
- drugs - e.g. opiates, anticholinergics
- neurological - e.g. MS, paraplegia
- metabolic/ endocrine - e.g. hypercalcaemia, hypothyroidism


Which patients should be investigated for constipation?

In the absence of a history suggesting a specific cause it is not necessary to investigate every person with constipation. Most respond to dietary fibre supplementation and the judicious use of laxatives. Middle-aged or elderly patients with a short history or worrying symptoms (rectal bleeding, pain or weight loss) must be investigated promptly, by either barium enema or colonoscopy. Others should be investigated as follows:
- initially DRE, proctoscopy, sigmoidoscopy, routine biochemistry to include Ca++ and TFTs
- if normal, 1 month trial of supplementary fibre and/or laxatives
- if symptoms persist, examination of the colon by barium enema or colonoscopy to look for structural disease


What are the four types of abdominal pain?

1) Visceral - usually midline, due to stretching or torsion of a viscus, poorly localised

2) Parietal - usually sharp, lateralised and localised due to peritoneal irritation

3) Referred - e.g. gallbladder pain referred to back or shoulder


What causes acute abdominal pain?

One of the most common ways to think about the potential causes is the location of the pain. Sometimes patients present with generalised pain but probably the most common present is pain in a particular region of the abdomen. Some conditions characteristically cause central pain before localising to a particular area. A good example is appendicitis, which typically presents with central abdominal pain before localising to the right iliac fossa.

RUQ - cholecystitis, cholangitis
Epigastric - pancreatitis, peptic ulcer, gastritis
Loin - renal colic, pyelonephritis
Central - AAA, mesenteric ischaemia, small bowel obstruction
Suprapubic - UTI, cystitis, retention, gynaecological pain
RIF - Appendicitis, ectopic pregnancy


How do patients with an acute abdomen present?

This depends on the underlying cause. Acute abdominal pain is usually the result of one of 3 pathological processes:
1) Inflammation (e.g. appendicitis, pancreatitis, diverticulitis) - diffuse pain develops gradually over hours. If the parietal peritoneum is involved, pain becomes localised. Movement exacerbates it; rigidity and guarding occur

2) Perforation (e.g. peptic ulcer, ovarian cyst, diverticular disease) - pain starts abruptly, is severe and leads to generalised peritonitis

3) Obstruction (e.g. intestinal, biliary or ureteric) - pain is colicky with spasms causing the patient to writhe around. If it does not dissappear between spasms, this suggests complicating inflammation


Where is the pain of biliary colic?

Caused by a gallstone getting lodged in the bile duct.
Classically provoked by eating a fatty meal.
In contrast to acute cholecystitis no fever and inflammatory markers are normal.


What is acute cholecystitis?

Inflammation/infection of the gallbladder secondary to impacted gallstones.
Murphy's sign positive (arrest of inspiration on palpation of the RUQ).
Fever and raised inflammatory markers.


What is ascending cholangitis? Where does the pain localise?

Ascending cholangitis is a bacterial infection of the biliary tree. The most common predisposing factor is gallstones.

Charcot's triad of right upper quadrant pain, fever and jaundice occurs in about 20-50% of patients.


What are the features of acute pancreatitis?

Pain often in the epigastric region sometimes radiating to the back.
Usually due to alcohol or gallstones.

Pain is often very severe. Examination may reveal tenderness, ileus and low-grade fever


What are the features of peptic ulcer disease?

Pain is in the epigastrium.
There may be a history of NSAID use or alcohol excess.
Duodenal ulcers: more common than gastric ulcers, epigastric pain relieved by eating.
Gastric ulcers: epigastric pain worsened by eating.
Features of upper gastrointestinal haemorrhage may be seen (haematemesis, melena etc).


What are the classical features of appendicitis?

Pain initial in the central abdomen before localising to the right iliac fossa (RIF).

Anorexia is common. Tachycardia, low-grade pyrexia, tenderness in RIF

Rovsing's sign: more pain in RIF than LIF when palpating LIF.


What is acute diverticulitis?

Infection of existing large bowel diverticula.
Colicky pain typically in the LLQ.
Diarrhoea, sometimes bloody.
Fever, raised inflammatory markers and white cells.


What are the features of bowel obstruction?

History of malignancy (intraluminal obstruction)/previous operations (adhesions).
Vomiting. Not opened bowels recently.
'Tinkling' bowel sounds.


Where is the pain associated with renal colic located?

Loin pain radiating to groin.
Pain is often severe but intermittent. Patient's are characteristically restless.
Visible or non-visible haematuria may be present.


What are the features of acute pyelonephritis?

Loin pain + fever + rigors


Where is the pain of urinary retention?

Suprapubic region.
Caused by obstruction to the bladder outflow.

Much more common in men, who often have a history of benign prostatic hyperplasia.


How does ectopic pregnancy present?

Typically presents with pain in the right or left iliac fossa and a history of amenorrhoea for the past 6-9 weeks. Vaginal bleeding may be present.


How does mesenteric ischaemia present?

Patients often have a history of atrial fibrillation or other cardiovascular disease.

Diarrhoea, rectal bleeding may be seen.

A metabolic acidosis is often seen (due to 'dying' tissue).
Central abdominal pain.


How should chronic abdominal pain be investigated?

A detailed history, including fever, weight loss and mood, is essential. If abdominal and rectal examination is normal, a careful search should be made for disease affecting the vertebral column, spinal cord, lungs and cardiovascular system.
The choice of investigations depends on the history and examination.

E.g. pain provoked by food in the presence of widespread atherosclerosis is likely to be mesenteric ischaemia and is best investigated using mesenteric anrgiography

Decks in Year 4 - SPM Class (129):