Large Bowel Obstruction

Large bowel obstruction

Typically causes a less severe disease than small bowel obstruction

-          Symptoms are more gradual in onset

-          There are often loud borborygmi (normal bowel sounds)

-          Rectum is usually empty, and the abdomen is non-tender

-          Pain is lower down in the abdomen

-          There may be greater distension than with small bowel obstruction

Causes

-          Colon cancer

-          Benign strictures – e.g. diverticular disease, IBD, ischaemic bowel, radiation damage

-          Sigmoid colvolvulus

-          Intersusception

-          Herniae – not as common as in small bowel obstruction

-          Psuedo-obstruction (same as paralytic ileus, except it affects the large bowel)

Presentation

-          Abdominal distension and absolute constipation

-          Vomiting – a very late sign

-          Patient may have history of history of change in bowel habit and / or rectal bleeding

-          Ask about family history – IBD and colon cancer

Closed loop obstruction

Ileo-caecal valve is competent and as a result fluids and other materials can continue to pass into the large intestine (the bowel produces up to 9L of fluid per days, so even if NBM, intestinal activity cannot be completely suppressed).  Colon distends massively (>12cm – normal <6cm), and the caecum is at risk of rupture and life-threatening faecal peritonitis.

Incompetant IC valve

The obstruction causes the small bowel to distend, and may induce vomiting

Not as urgent as closed loop obstruction, because perforation isn’t as bigger risk

Can be safely imaged with barium enema / endoscopy

Colonic stenting

Can be used in palliative care where surgery isn’t appropriate

Can also be used to buy time – ‘bridge to surgery’. The stent may allow the patient to recover enough to be fit enough for an operation.

Usuually, it is colonic cancer that is stented.

Apple core stricture - a sign of colon cancer – it is a sign on barium enema,where the lumen of the bowel looks a bit like an apple core due to the cancer causing a stricture.

Pseudo-obstruction

Similar pathogenesis to paralytic ileus

You cant exclude mechanical obstruction without colonic imaging.

Mostly the same causes as paralytic ileus, but can be affected by drug use (e.g. anti-depressants), neurological disease and pneumonia.

Notes by Tom Leach

Altered Bowel Habit

Altered bowel habit is very common and can be acute or chronic.

For further information, also see the articles diarrhoea and constipation

 
















Causes

-          Acute gastroenteritis

-          Simple constipation

-          Irritable bowel or diverticular disease

-          Colonic Malignancy

-          Inflammatory bowel disease

-          Maldigestion / malabsorption

Constipation -

There are various definitions of constipation, but these are not very useful in clinical situations.

What is important is an alteration in bowel habit. Has there been a change? What kind of change? What is the frequency and consistency of the stool?

               

-          Causes

o   Dietary / drug induced

§      Opiates and analgesics are particularly common, but there are loads more!

§      Calcium intake is also very important.

§      Cationic compounds

o   Functional – e.g. IBS

o   Mechanical obstruction – e.g. strictures

o   Metabolic /systemic disease – e.g. thyroid disease – particularly common is under active thyroid in older age.

o   Local anorectal dysmotility – Anismus

o   Neurological disorders

               

-          Prevelance of functional constipation

o   This is a condition where there is no underlying pathological condition

o   It affects 3% of the population

o   Often these people won’t go to GP, they will just go to chemist and get laxatives

-          Disease associated with chronic constipation

o   Often constipation is a consequence of lack of mobility, rather than a direct consequence of the disease itself. This is particularly common in neurological conditions, e.g. parkinsons

o   Systemic diseases such as thyroidism.

o   Ano-rectal dysmotility (aka anismus) – this is common in younger people, particularly women. They will present at the stage where they are already taking lots oflaxatives and controlling their diet (e.g. taking lots offluids and eating lots of fibre). It is caused by an in-co-ordination of muscles actions. When they try to defacate, instead of the rectal angle decreasing and straightening up, instead the angle will increase, and thus making it virtually impossible to defacate.

Taking the History

-          Determine onset, evolution and related symptoms

-          If the patient seems vague, consider a diary of symptoms

-          Does the patient’s definition of constipation match your definition? Ask the patient exactly what they mean, and exactly what their symptoms are.

-          If it is long standing – why have they presented now.

-          Are there any co-factors? Psychological, stress, dietary, environmental.

 Examination

-          Signs of systemic disease? E.g. in hypothyroidism – look at facial features – coarsening official features, weight gain.

-          Any abdominal mass, or faecal loading?

-          Anal disease? Haemorrhoids or fissure? A fissure can be caused by something hard in the faeces – it causes damage to the colonic wall. Often it will just cause acute constipation

-          You should always do a rectal exam!

-          Neuromuscular disease

Investigations

-          Blood tests – TFT’s and calcium

-          Plain abdo X-ray

-          Sigmoidoscopy – this excludes a mechanical cause. You don’t need to do a full colonoscopy.

-          Do a colonic transit study. Get them to eat markers on different days, and then a weekor so later, do an x-ray. You can see how far round the markers have got! Normal transit should be less than 5 days.

Hirschprung’s disease

Common in teenagers / children (neonates). It is caused by neural disease,  and prevents peristalsis of the colon. Sometimes the section of colon is very small, and you can remove it. This disease is often not picked up quickly if the section of bowel affected is small – you might just think they have a bit of constipation.

Management

-          High fibre diet, increase fluid intake, and avoid constipating drugs

-          Identify and treat metabolic or structural diseases.

-          Consider some patients for psychological help.

Laxatives

There are loads of these on the market!!

The most common are the bulk forming. They basically perform the same role as dietary fibre. They attract fluid and form a nice bulk that can be easily passed through the colon.

-          Osmotic laxatives – these are much more aggressive at keeping fluid in the bowel. The active ingredient in many of these is movicol. Often these are dissacharides that have no enzyme in the human to break them down. They are broken down by bacteria into osmotic compounds that help hold fluid in the colon.

-          Stimulants – these should be avoided if at all possible. Senna is a common one. It is an anthraquinones. They can damage young people’s colon, but generally in adults there is no evidence they cause any damage.

-          Softeners – these make the stool more soft and sqooshy making it easier to pass.

Diarrhoea -

-          Again there are various things used to classify this, but again the most important thing is a change in bowel habit.

-          Accounts for 10% of GP visits and 1.5% of adult hospital admission.

-          Worldwide it is the second most common cause of death. Most cases are due to infection. They can be viral / bacterial / amoebic (rare) / protozoa (e.g. giardia lamblia)

-          Chronic diarrhoea – this has existed for over a month. This occurs in 5% of the population. It is common in IBS.

-          Beware particularly old people will say they have ‘bad diarrhoea’ when in actual fact they have faecal incontinence. This is a very disabling condition (socially).

Mechanisms

-          Osmotic – something is causing too much liquid to be held in the gut

-          Secretory – due to abnormal ion transfer across the gut – the small bowel secretes about a litre of fluid across the gut with each day. Normally you absorb about 4L. In cholera, you secret up to 8L a day, but still only absorb 4L

o   Deficiency of lactase – about 10% of the population are lactase deficient. As part of the weaning process, mammals normally lose lactase. If you have no lactase then you can’t break down lactose, and thus it will be broken down by gut bacteria and cause diarrhoea

-          Dysmotility – reduced or increased gut transit time.

In many cases of diarrhoea there is more than one mechanism in action. In some cases it is purely one.

Celiac ulcers and ulcerative colitis often cause diarrhoea.

C. difficile can also cause diarrhoea. It produces a toxin that will damage the membrane of the colon. It causes a condition called pseudomembranous colitis. It is common in hospital with acquired C. difficile.

Immunosupressed patients will be at more risk from diarrhoea. These patients will often be affected by viruses that don’t affect normal people.

Villous adenoma – this is a rare cause of diarrhoea. It secretes large amounts of fluid and thus causes secretory diarrhoea.

Traveller’s diarrhoea

-          Up to 50% of travellers experience this.

-          Symptoms tend to last 3-4 days.

-          Most common causing agent is E. Coli. (40%)

-          Specific pathogen is identified 50-80% of the time.

Dysmotility related diarrhoea

-          Increased intestinal transit time – can be caused by small bowel overgrowth (found in diabetes and scleroderma)

-          Reduced intestinal transit time

Fictitious diarrhoea

It is not that rare. In this condition, these people will take laxatives to cause diarrhoea, and then deny they eve take them. If you have done loads of tests, and can’t find anything wrong, it is worthwhile doing a ‘laxative screen’ – test the patient’s urine and stools for laxatives.

It occurs in 4-15% of patients with chronic diarrhoea. It may account for up to 1/3 of patients referred to GI specialist for diarrhoea.

The psychology is poorly understood. There are two main groups of people who present with it.

Appendicits

This is the most common indication for abdominal surgery in children.

Appendicitis is acute inflammation of the appendix

Epidemiology

-          About 5% of the population will have appendicitis at some point

-          Most commonly occurs in the 2^nd and 3^rd decades, but can occur at any age

-          Appendicitis in pregnancy

o   Occurs in 1/1000 pregnancies

§ This is not more common than the general population, however, it carries a greater risk of mortality

§ Risk of mortality is greatest after 20 weeks gestation

§ Perforation occurs in 15-20% of cases

·         Fetal mortality without perforation – 1.5%

·         Fetal mortality with perforation – 20-30%

§ As pregnancy advances, the position of the appendix changes, thus pain is usually poorly localised, and signs of peritonitis are usually less obvious

§ If appendicitis is suspected in pregnancy is should be investigated quickly with laparotomy by an experienced surgeon

Pathology

Results from obstruction of the appendical lumen. Typically from lymphoid tissue hyperplasia, but also sometimes from faeces, foreign body or worms.

-          Once obstructed, there can be:

o   Bacterial overgrowth

o   Distension

o   Ischaemia

o   Inflammation

-          If untreated, there may be:

o   Necrosis

o   Perforation

§ Sometimes, this is contained by the greater omentum, in which case, and appendical abscess may form

o   Gangrene

Clinical features

-          Pain – typically episgastric or periumbilical, before localising to the RLQ

§ Pain migration occurs due to the different innervations of the layers. The viscera (i.e. the appendix tissue itself) is innervated by the splanchnic nerves, which are poorly localising, and localise to the centre of the abdomen. Once the peritoneum becomes involved, different nerve pathways are activated, and the pain can be more closely localised. These differences are due to the different embryological derivations of the layers of the gut.

o   Peritonitis if present– classic peritonitis pain of wasboard rigidity – as the pain is exacerbated by the slightest movement (e.g. rolling, coughing, even breathing)

o   Rebound tenderness at McBurney’s point – press at this point does not elicit pain, but relieve the pressure (the ‘rebound’) elicits pain (or elicits more pain than the initial pressing)

§ Mcburney’s Point –2/3’s of the way along an imaginary line from the umbilicus to the anterior superior iliac spine on the right hand side

o   Rovsing’s Sign – pain felt in the LRQ when the LLQ is palpated

o   Psoas sign –increased pain during passive extension of the right hip

o   Obturator sign –pain felt on passive internal rotation of the flexed hip

-          Nausea

-          Vomiting

-          Anorexia

-          Low grade fever

-          The above classical symptoms only appear in <50% of patients. There are lots of other presentations!

o   Pain is less likely to be localised in children

o   Bowel movements – often less frequent, or absent especially if peritonitis is present

o   Urine dipstick – may show WBCs and/or RBCs

Diagnosis

-          If classical signs / symptoms are present, then diagnosis if often clinical

o   Delaying diagnosis in these patients can be life-threatening – delaying treatment increases the risk of perforation and peritonitis

o   The Alvarado Score is a way of scoring suspected appendicitis clinically to identify those who may need surgery. BUT in trials, it has proved no more effective than good clinical judgement. However, it may still be useful when making assessment

§ Alvarado score more accurate in Men and Children

Alvarado Score

Criteria	Score	Criteria	Score
Pain migration	1	Nausea / Vomiting	1
Anorexia	1	RLQ Tenderness	2
Rebound tenderness	1	Temp >37.3	1
WCC > 10x109 / L	2	Neutrophil Count >75%	1

-          <4 – appendicitis unlikely

-          5-6 – observe

-          >7 - operate

Investigations

In atypical and non-urgent presentations, laparotomy can be avoided, and other
investigations instead performed.

-Contrast CT – is useful, but can take time to organise. Good sensitivity and
specificity, and able to diagnose other differentials

-USS – can
identify appendicitis, but not good at identifying other causes

-Laparatomy – don’t be afraid to perform a diagnostic laparotomy if necessary

Management

-APPEDICECTOMY! – don’t be afraid to treat quickly. Delaying
treatment increases mortality. The negative appendicectomy rate is
about 10%

oContraindicated in IBD involving the caecum. Also may
be unsuitable in very elderly or severely ill patients.

§In patients who can’t undergo surgery, IV antibiotics
are beneficial. They are not curative, but reduce
mortality by 50% and thus buy some time.

Complications

-Perforation
± peritonitis

-Abscess formation 

Notes by Tom Leach

Clostridium Difficile Infection

Clostridium Difficile is carried in the normal gut fauna of the large intestine in about 5% of the population.

-          It can be spread by the faecal-oral route, and by person-person contact – hence the importance of hand-washing between patients on the ward!

-          It is also present in soil, water and in pets

Generally, becomes problematic after taking antibiotics and is a very common hospital acquired infection.

-          in some instances it can be acquired and become symptomatic in the abscence of antibiotic use, but this is rare

Pathology

Taking certain antibiotics (e.g. clindamycin, penicillins (amoxicillin, ampicillin) and 3^rd generation cephalosporins are most commonly implcaited, although loads of others are involved! IV antibiotics present a greater risk than oral) kills off other normal gut bacteria, leaving the way clear for C. Difficile to reproduced unchecked, as it is no longer in competition with other bacteria for resources. This overgrowth of C difficile can cause diarrhoea, and on colonoscopy, the appearance of pseudomembranous colitis (yellow plaques that can be easily dislodged).

-          The symptoms of c diff infection are a result of the toxins produced by the bacteria and not directly of the bacteria itself

Investigations

-          Stool sample for enterotoxins produced by c difficile

o   Sensitivity + Specificy both 95% - HOWEVER – there are examples of patient deaths from c diff in cases of negative test results, so always consult the micobiologist

Signs and Symptoms

-          Usually occurs approx 5-10 days after antibiotic use but can be anywhere from 1 day to 2 months

-          Diarrhoea ± blood

-          Abdominal discomfort / pain

-          Nausea and vomiting is rare

-          Sepsis (rare)

-          Acute abdomen (rarer)

Treatment

-          Metronidazole – 400mg/8h PO for 8-10 days

o   Vancomycin is often second line, but more expensive

-          It is also often wise to inform the GP of the infection, so that if the need arises to prescribe antibiotics in the future, the GP is able to prescribe metronidazole simultaneously to avoid a recurrence of pseudomembranous colitis.

Notes by Tom Leach

Colorectal Cancer

This article refers to cancer of the large bowel.

Interestingly, the small bowel is a very rare site for carcinoma, despite the fact it has the highest cell turnover of anywhere in the body, and has a very large surface area.

Colorectal Cancer -epidemiology

-          Second most common cancer in the Western World (behind lung cancer)

-          50% of cases will result in death

-          Relatively rare in Africa, Asia and South America

-          Peak incidence in the 7^th decade

Etiology

-          Family history.

-          Age

-          Diet rich in fat and meat, and low in fibre – associated with a Western Lifestyle

-          IBD – due to high cell trunover

-          Diabetes

-          Atherosclerotic disease

-          Age and family history are the two best predictors for colorectal cancer

Benign Disease

This is characterised by the presence of adenomas. An adenoma is a benign epithelial neoplasm, with the potential to become malignant.

Clinical features and diagnosis

-          Often asymptomatic, usually only found incidentally

-          Rectal bleeding (rare)

-          Hypokalaemia (very rare)

Management

-          Endoscopic mucosal resection (EMR) – removal of polyps by colonoscopy. Upon discover of one or more polyps, colonoscopy, and subsequent EMR is advisable, whereby all visible lesions should be removed. This should be followed by lifelong surveillance (every 3-5 years up to the age of 75) to check for the development of more polyps and / or colorectal cancer.

-          50% of patients will develop further polyps.

Pathology: Adenoma to Carcinoma

-          A minimum of three separate genetic defects have to occur:

§      Onocgene activation (k-ras, c-myc)

·         associated with small adenomas becoming big adenomas.

§      Loss / mutation of tumour suppressor genes

§      Loss / suppression of genes involved with DNA repair path ways.

·         E.g., genes involved in the inhibition of apoptosis may become over-expressed

-          It will take 8-10 on average for an adenoma to become a carcinoma.

-          The mutations can occur in any order!

-          Many of the genes associated with colorectal cancer are found in two specific locations: 5q & 18q - . Loss of herterzygositiy (LOH) in these regions is common during the formation of colorectal cancer, and some recognised genetic defects (e.g. FAP) are caused by LOH in these regions.

-          Over 90% of colorectal carcinomas show 2 or more of the above mutations, 40% show three or more. It is the number of mutations, and not the order that affects the development of cancer.

Malignant Disease

General Presentation

-          Iron Deficiency Anaemia

-          Weight loss

-          Malaise

-          Vague abdominal pain

-          Faecal occult blood loss

-          Palpable mass (e.g. in right iliac fossa, left flank etc)

-          Obstruction

-          Altered bowel habit

-          Tenesmus (desire to defecate)

-          Rectal bleeding

-          Anal and perianal pain

-          Faecal incontinence

-          Recurrent UTI – due to fistulation to the bladder

-          Sister Mary Joseph Nodule – this is a lymph node that can be felt at the umbilicus and is a sign of metastatic spread

-          Ascites – high in protein – due to local peritoneal cavity spread

Red flag symptoms: - patients with the following should be sent for 2 week referral immediately:

-          Palpable rectal mass (any age)

-          Iron deficiency anaemia in men of any age

-          Iron deficiency anaemia in non-menstruating women of any age

-          Rectal bleeding and change of bowel habit for more than six weeks in patients over 40

-          Rectal bleeding for 6 weeks or more in anybody over 50

-          Anybody with a palpable rectal mass

Spread

-          Usually occurs locally through the bowel wall, and to local lymph nodes

-          Spread to the liver is relatively common

Investigations

-          Faecal Occult blood

o   Guaiac test – for Hb breakdown products. 98% specific, but only 40-80% sensitive

o   Antibody test – uses antibodies that bind to human blood to test for the presence of blood.

-          Routine biochemisty – U+E’s, FBC, LFT’s, CRP, ESR

-          Colonoscopy – Investigation of choice!

-          Barium enema – in cases where colonoscopy cannot be performed

-          USS/CT – can asses bowel wall thickness as well as looking for metastatic spread

Staging

Both Duke’s scale, and TNM are used, with a move towards TNM is recent years

The traditional Duke’s system works as follows:

-          Stage A – the tumour is confined to the mucosa – 5- year survival rate is 90%

-          Stage B – the tumour has spread through all the layers of the mucosa to the serosa. There are no lymph nodes metastasis. The 5-year survival rate is 60%

-          Stage C – the same as stage B, but there is lymph node involvement. Survival is about 30%. 

o   C1 – there is local lymph node involvement

o   C2 – there is distant lymph node involvement

o   C2 caries a worse prognosis than C1

-          Stage D – this category was not originally included, but later added to refer to disease with wide spread metastatic involvement.

Treatment

-          80% of patients will have surgery

-          Resection is the treatment of choice for Dukes A-C

-          Radio and chemotherapies may be used as adjuvants in Dukes B-C, and as palliative treatments in Dukes D

-          Surgery

o   You should remove 2cm either side of the tumour (5cm in all directions in the rectum)

o   Can be a laparotomy or laparoscopy

o   Anastomosis is usually, although not always made afterwards

Genetic Disorders associated with Colorectal Cancer

Familial Adenomatous Polyposis (FAP)

-          Accounts for 1% of cases, prevalence is 1 in 10 000

-          Autosomal dominant

-          Patients inherited a ‘bad copy’ of the APC gene on chromosome 5. They have one remaining ‘good copy’ of the gene, which is still liable to mutation, and when it does, polyposis results

-          90% of these patients will develop bowel cancer

Hereditary non-polyposis colorectal cancer (HNPCC)

-          Autosomal dominant

-          Average onset of cancer is in the mid-forties

-          Despite the name, polyps are often still present

-          Also increase the risk of cancer in the small bowel, stomach, and other regions

Constipation

Introduction

Constipation is a symptom and not a condition.

It is most common in women and the elderly. Often it is more like a perception that a real entity.

It can be affected by psychological factors. For example, it is possible to override the body’s autonomic responses subconsciously and thus exert a higher form of control over them and change the body’s reaction to certain situations. This is more common in women than men, and can often have a social aspect; e.g. women are embarrassed to go for a poo at work, or whilst out of the house. Some people argue that it is because we are conditioned from childhood that pooing is something dirty that we do in private and no-one else has to know about it. This may happen in constipation, but the process can be reversed if people ‘learn’ how to let their natural responses take over.

-          Constipation patients can be given ‘lessons’ on how to poo. At first many patients are wary of this technique and sceptical. It may take several lessons before they relax and settle down and understand what it is for, but it is possible to ‘learn’ how to poo normally again.

Constipation is defined clinically as a ‘change’ from your normal bowel habit. Normal can be anywhere from 3 times a day to 1-2 times a week. The important this is what is normal for you. When constipation is present there will usually be some degree of straining, perhaps a feeling of incomplete evacuation and lumpy or hard stools.

 

What causes constipation

There are many, many causes, important ones include:

-          Lack of fibre & fluid intake

-          Lack of physical activity

-          Irritable bowel syndrome

-          Drugs – particularly opiates, but also iron supplements, anti cholinergics, calcium antagonists and aluminium containing ant-acids.

-          Neurological causes – e.g. MS, parkinson’s, a CVA, spinal chord lesions

-          Metabolic causes – pregnancy, diabetes, hypercalcaemia, hypothyroidism

-          Depression – possibly linked to general decreased activity of the nervous system and less 5-HT.

-          Hirschprung’s disease

-          Colonic carcinoma

-          Diverticular disease

-          Obstruction

-          Crohn’s

-          Fissures

-          Haemorrhoids

-          Pregnancy – it has been shown that progesterone reduces colonic muscles tone, thus leading to constipation. This also sometimes has an effect during a woman’s menstrual cycle – if a woman is constipated, the symptoms may be worse during the luteal phase of her cycle.

-          Diabetes, hyperthyroisim and hypercalcaemia can all lead to altered motility.

Pathology

The role of the colon is to absorb water and electrolytes, and move faeces along to the rectum. About 2L of fluid pass into the large bowel each day. Stimulation of peristalsis is mostly by short chain fatty acids which are produced by the break down dietary fibre by floral bacteria in the ascending colon. It is also stimulated by release of serotonin (5-HT) by local neurones in response to colonic distension.

Normal colonic transit time is 8-24 hours, with on average 250g of stool production each day.

Types on constipation

Constipation can be broadly divided into 3 categories:

-          Normal transit constipation (59%) – in this type of constipation, stools travel through the colon at the normal rate. Patients also have normal stool frequency, but they believe they are constipated – this is probably because they have difficulty with the act of actually passing a stool. Patients often claim abdominal pain and bloating.

o   This condition can be assessed by ingestion of radio markers – various shapes that are ingested on different days to identify how long it takes a shape to travel through the colon. This type of test helps distinguish slow transit from normal transit constipation

-          Slow transit constipation (13%) – this often occurs in young women, and will result in defecation of less than once a week. The condition often starts at puberty and symptoms involves abdominal pain, bloating, and infrequent urge to defecate. The diagnosis can be difficult as it is similar to that of constipation due to IBS. Some patients with this condition has impaired bowel emptying, and some have impaired stimulation of colonic motility. Some patents will also have co-existing disorders of the small intestine that may be consistent with a diagnosis of chronic idiopathic pseudo-obstruction.  

-          Defacatory disorders (25%)- this is often caused by improper relaxation of pubrectalis, external anal sphincter and other associated muscles of defecation. It is a bit of a paradox, because through straining too hard, people can prevent these muscles from relaxing. It is especially common in women and may actually be a learned response. Often an anterior rectocele may form. This is where there is a weakness in the rectal/vaginal septum, and a protuberance of the rectum may form If this protuberance has a diameter of >3cm, then faeces can get stuck in it.

In other patients, the mucosa of the anterior wall of the rectum prolapses downwards during straining, preventing proper emptying of the rectum. In some patients, the rectum may become overly sensitive to the presence of small volumes of faces in the rectum, and as a result the patient will pass small volume stools frequently, an often have a sensation of incomplete evacuation.

o   Defecation disorders can be diagnosed by using imaging of the rectum during defecation.

Investigations

-          You may want to perform a vaginal and rectal examination if you suspect that the constipation is caused by a pelvic floor defect (can happen in childbirth, trauma or in serious colonic disease). An easy way to rule this out is to see if the perineum descends on straining. If it does not, then it is a pelvic floor dysfunction.

-          Radio opaque markers (as seen above)

Examination is perhaps more important than investigation. Some important things to look out for are:

-          Check the perineum and do a PR. You might find impaired sensation or disorders of the rectal floor. You may also feel a rectal mass, or a prolapsed, and it is very important when you do a PR that you ask the patient to squeeze your finger to test anal sphincter function.

Here we can see various radio-opaque shapes ingested on 3 separate days. The imaging is always done 120 hours after ingestion of the first set of shapes, and thus from this we can see that all the shapes are still present, and are spread along the colon, thus confirming a diagnosis of sever slow transit constipation.

Treatment

It is very important that the underlying condition is treated as the main priority. Education is also an important factor – patients should be educated on patterns of normal bowel movement, and reassured, that even 1-2 times a week is normal for some people. Those who are obese and lead a sedentary lifestyle should be encouraged to lose weight.

Most people will respond to increased dietary fibre and fluid intake, and if necessary, laxatives. You don’t need to PR every patient! This is more likely after first line treatments have failed, or in especially risky patients – i.e. they have a short history and also experience rectal bleeding – and as such you are very suspicious of rectal carcinoma. – in such cases you should always refer the patient for a barium enema and / or colonoscopy.

It is extremely important not to become reliant on laxatives. They can permanently alter the functioning of the bowel.

-          Normal and slow transit constipation – the first line treatment of this should be an increase of fibre and fluid intake in the diet. You should try to increase fibre through dietary means rather than with fibre supplements – as the supplements can affect the way floral bacteria operate thus not producing the desired effect. Patients should be encouraged to drink 6-8 glasses of water daily, and to eat 20-30g of fibre every day. This approach does not help in all cases.

-          Laxatives –use of these should be restricted to very severe cases. There are different types that act in different ways

o   Osmotic laxatives –these draw fluid out of the interstitia and into the colonic lumen. A common example is magnesium sulphate (5-10g), taken usually at breakfast time, it will work within 2-4 hours.

o   Stimulatory laxatives –these work by stimulating the colonic mucosa to contract more often, thus, churning up the stool and moving it along the bowel quicker. Some may also increase intestinal secretion.

o   Enema –this may be performed in the elderly and infirm, and those with neurological disorders.

Diverticulitis

What is diverticular disease?

It is an acquired condition, in which there are small out-pouchings of the mucosa of the large intestine, known as diverticulae.

Definitions:

Diverticulosis – the presence of diverticulae in the large intestine

Diverticular Disease – the presence of symptoms resulting from the existence of diverticulae in the large intestine

(Acute) diverticulitis – ongoing inflammation of one or more diverticulae

Epidemiology

-          Primarily a disease of the elderly, very uncommon in those under 40

-          50% of the over 70’s have diverticulae

-          Most commonly occurs in the sigmoid colon

-          75-90% of cases of diverticulosis are asymptomatic

-          Diverticular disease is present in 10-25% of cases, and of these, about 20% will develop acute diverticulitis at some stage.

-          Slightly more common in females

-          Associated with a western lifestyle

Aetiology

-          Lack of fibre in the diet (particularly in processed foods)

Pathology

It is thought that in the presence of a lack of fibre, the muscles of the colon must work harder to move faeces along. This causes very high pressures in the colon, and as a result, some parts of the mucosa will form out-pouchings.

-          This can occur, because the muscle coverage along the outside of the colon (the taeniae coli) do not entirely encircle the whole of the intestine, but instead are present in bands. The herniation of the mucosa occurs inbetween these bands.

-          There may also be muscle changes, whereby the taeniae coli become thickened and fibrosed, pre-disposing the formation of diverticulae

 

Clinical features

-          Up to 95% symptomless

-          Diverticular disease can cause erratic bowel habits (constipation or diarrhoea) and left iliac fossa pain, which may or may not be colicky

-           Complications of diverticular disease:

o   Acute diverticulitis

§    Left iliac fossa pain

§    Malaise / fever

§    Palpable mass

§    Abdominal distension

§    Tachycardia

§    These symptoms are similar to appendicitis, but usually occur on the left hand side.

§    This inflammation will often spontaneously resolve, but in some cases it can progress to:

·         Fistulation

·         Abscess

·         Peritonitis

·         Perforation

·         Haemorrhage

·         In some cases, acute diverticulitis can be life threatening (e.g. in cases of perforation)

o   Perforation

o   Large bowel obstruction

o   Fistula (to bladder)

o   Fistula to small intestine

o   Lower GI bleed

Investigations

-          Clinical Examination – the sigmoid colon may be palpable

-          Barium Enema – the investigation of choice, but should not be used if there are active complications.

-          Ultrasound – can asses bowel wall thickness, and rule out other differentials

-          Sigmoidoscopy – if other investigations have been inconclusive

-          Diverticular disease is notorious for concealing colon carcinoma

Investigations for Acute Diverticulitis

-          CRP and ESR – usually raised

-          Ultrasound / CT – can show wall thickening, diverticulae, and also abscess or perforation

Treatment for Acute Diverticulitis

-          Antibiotics (usually metronidazole)

-          Fluids

-          Analgesia – but be careful! You don’t want to give a constipating analgesic (i.e. many opioids, particularly morphine as this also raises intra-luminal pressure)

Often patients can be managed at home, but in severe cases, hospitalisation may be required, in which case fluids may be given IV

Long term management of Diverticular Disease

-          Asymptomatic disease – no direct treatment – recommend high fibre diet and high fluid intake

-          Symptomatic disease –

o   Analgesics – again, avoid opioids

o   Laxatives, if necessary – but avoid stimulant laxatives

o   Anticholinergics – may be useful in patients with over-active sigmoid colon

o   Surgery – to resect the sigmoid colon – in severe cases