Causes:

 Haemorrhoids Distal to Ligament of

 Polyps - Adenomas - Cancer (anywhere in the GIT)
 Diverticuli (colonic / oesophageal) Treitz
 Ulcerative Colitis & Crohn’s Disease (IBD)
 Fissures (tears)
 Colitis
Ischaemia Management:
Infectious
Non-infectious  Resus
 Enteritis A B C D - appropriate resus related to amount of bleeding
Ishaemic Mucosa most affected Admit the patient
- Sloughing out after ischaemia Monitor for ongoing bleeding while investigations are being done
- Bleeding when sloughing of many layers
May be d/t incarceration  Investigate
Infectious - Enteritis (viral)
- Amoebiasis (parasite) Bloods
- Candida (fungi)  FBC
- Bacterial  CRP / ESR / WCC
Non-infectious - IBD
 INR / PTT
- Radiation damage
 U&E - raised urea & Creatinine = upper GI bleed (blood digested)
- Chemical erosions (caustic ingestion)
 Trauma
Scopes
Foreign body might cause damage in the lumen
External trauma usually doesn’t present with GI Bleeding
 Colonoscopy
- see entire colon
 Angiodysplasia
- biopsy
AV malformations
- stent
AbN dilated vessels
- control bleeding
Slow bleeding
 Sigmoidoscopy if that is all that is available
 Coagulopathy
INR too high
 G-Scope if Upper GI bleed suspected
Various causes
Radiology
 Drugs
Warfarin
 Barium meal & follow-through
- double balloon endoscopy also an alternative
Other blood thinning
- capsule endoscopy
NSAID-ulcers presenting with lower GI melina stools
- isotope scan - can’t locate the problem but can confirm a bleed
 Extra-GI Bleeding
Aorta
 CT / MRI (see tumours)
Haemobilia  U/S (helps to distinguish tumours vs. cysts
Aorto-enteric fistulae  Angio
- Diagnose problem
- Treat the bleeding (possible permanently)

 Treat the cause (if not done during Dx)

Hernia: Protrusion of bowel loop through abdominal wall.

Complications of Hernias
 Strangulation
 Incarsiration
 Perforation
 Obstruction  inflammation  adhesions

Obstruction: Protrusion of bowel loop through abdominal wall. Lactic Acidosis DDx: Buffers:
 Implies that the full lumen of a bowel loop herniates (not a Richter’s hernia)  Ischaemia  Resp system (early)
 Blood supply may be cut off  ARVs  Albumin (intermediate)
 Sx of obstruction present  Metformin  Hb (intermediate)
Lactic acidosis  Liver Disease  Renal (late)
Peritonism (on palpation: rigidity, rebound tenderness, percussion tenderness)
Perforation possible  sepsis  SIRS
SIRS = Sequential - global organ dysfx SIRS severity:
 CVS - hypotension 1 organ failure - 50% mortality
 Liver - jaundice 2 organ failures - 90% mortality
 GIT - paralytic ileus 3 organ failures - 99.9& mortality
 CNS - confusion & LoC
 Resp - ARDS
Resus for Necrotic Bowel Obstruction

Acidotic state is 2-fold

1. Necrotic tissue  ischaemic  Kreb’s cycle not possible  Lactic Acid build-up
2. Vomiting  Alcolosis (ABG)  H+ taken up into cells  K+
K+ released into cells  Na
 Cl

Rx:
 Resus fluids N/Saline provides the Cl ions to the kidneys to produce HCl
Assists correction of Acidosis
R/Lactate only if volumetric depletion has occurred
 Maintenance fluids Ongoing losses & continued support once resus is over
Fluid choice depends on acid-base state

Evaluating Extravascular Fluid State: Evaluating Intravascular Fluid State:

0-5% dry mucosa ATLS classification - depends on vitals
5-10% loss of skin turgor Response to Resus with 2L R/Lactate:
10-15% sunken eyes (& fontanels in babies) 1. compensated without resus
>15% confusion / LoC 2. Responds to resus permanently
3. Responds to resus temporarily
4. Decompensated despite resus
Normal Anatomy: Terms:
- small bowel usually 6-8m (pylorus to ileocaecal valve)  Mechanical vs. functional obstruction
- large bowel usually 1.5m Physical obstruction vs. peristalsis/absorption/secretion/digestion
 Complete vs. incomplete
Bowel wall: Solids & liquids both affected vs. food/gas/liquids can still pass
- serous layer  Closed-loop vs. open-loop
- muscular layer Closed e.g. volvulus / transverse Colon Ca (if ileocaecal valve competent) Any form
- mucosal layer of impeda
Loop closed proximally & distally (cant deflate) - more complications content th nce to no
rough the rmal pass
small or la age o
rge intesti f bowel
ne
Extramural Causes Intramural Causes Intraluminal Causes
 Adhesions  CaColon  Gallstone ileus Investigations :
Most common  Intussusseption Last cause, if even mentioned  Bloods (FBC/CRP/WCC)
Later age Esp in 1st year of life Not common at all
 Abd X-ray
Bands in younger age Most common after viral infections  Foreign body Bowel sebment
Can occur in Crohn’s Short hx of screaming attacks, pallor, drawing up of knees, abd distention, abd  Faecal impaction proximally distended
 Hernias tenderness, anorexia, vomiting, no stool passed  Worm obstruction (tropical areas) Multiple air-fluid levels
 Ca  Volvulus  Strictures Large bowel haustra
Especially in mentally impaired & elderly seen (taenia coli) -
Often Hx of chronic constipation & laxative abuse. around 10cm when
 Diverticular Disease & Merckel’s diverticulum distended
Gas in bowel wall
(pneumatosis)
Clinical: Small bowel obstr Sx: Large bowel obstr Sx: Free fluid in Abd cavity
 Colicky pain & vomiting (early features)  Distended Abd  Incomplete obstr - contrast
 Midgut (small bowel, also Rt & transverse  Constipation (late)  Constipation scan
colon) - painful contractions d/t  Distension (only if distal)  Colicky pain & vomiting less marked (late features)  H2O solution enema if
Obstruction & inflamm = peri-umbilical  Usually short Hx (recurrent event)  Complete obstruction - absolute constipation (failure to pass unsure (not barium)
colic  High pitched tinkling bowel sounds any faecal matter or flatus) = obstruction
 Hindgut (distal lower bowel) painful  Incomplete - frequent passage of soft/liquid stools
contractions d/t obstruction / inflamm = Must exclude strangulation Management :
lower abd colic - abd tenderness (rebound) Causes to remember:
 High small bowel obstr - nausea &
 NGT (decompression)
- guarding - malignancy most common
vomiting - volvulus possible DDx
 Replace fluids lost (drip &
- tachycardia
suck)
 Large bowel obstr - abd distension & - pyrexia & incr Wcc
altered bowel habits (vomiting very late - continuous dull abd pain (not colickly)  Keep pt & bowel alive
 Resus
 Treat the cause
Pathogenesis :
 Distension / stretching  loss of appetite (d/t message sent to brain) distended with fluid & gas bacterial overgrowth is a risk _____________________
 Hyper-peristalsis  spasmotic pain _____________________
 Increased wall tension  decr blood supply  Perfusion pressure < wall pressure  ischaemia risk of perforation _____________________
 Mucosal ischaemia  mucosal ischaemia  barrier disrupted  transmigration of bacteria bacteraemia / sepsis
_____________________
 Severe dehydration  often associated with vomiting as well as poor water absorption  tachycardia / decr urine output / decr renal fx
Signs & Symptoms Sinister Sx Main Sx Spreading…
Wt Loss DDx:
 Weight loss  Intermittent rectal bleeding  Local spread - pain, urinary Sx - Cancer
(remember DDx)  Blood mixed with mucous  Locally advanced rectal Ca - - TB
 Weakness  Altered bowel habits perianal / sciatic type of pain - HIV
 Feeling unwell  Fe deficiency anaemia  Distal spread - acites, - Malnutrition
 Anorexia  Colicky lower abd pain hepatomegaly, jaundice,
 Tenesmus haemoptysis, pleural effusions Colon - Teania coli present
 Abd wall invasion - parietal pain Rectum - no Taenia coli present

Examination Bowel Obstr X-Ray features: Epidemiology:

 Clinical signs of anaemia
 Clinical signs of hepatomegaly (abd mass) - Lymphatic invasion via portal blood supply to the liver
 Clinical signs of obstruction
 DRE Detect low Cancerous lesions (tumour)
Assess fixity & sphincter involvement (2cm clear margin needed to spare)
 Bloods
 Radiology
 Histo
 Biopsy
Management:
 Chemo pre-opp
 Surgery
 Chemo post-opp
 Gas in bowel wall (pneumatosis intestinalis)  Colon Left side - 60% of Ca
 Distended bowel  Colon Right side - 40% of Ca
 Multiple air-fluid levels  Rectum & sigmoid - most common sites
 Fts of small & large bowel for tumours
FBC HB - anaemia CIs for Colonoscopy: Risk #:
WCC - high  Pt too sick (can’t cope with anaesthesia)  Male gender
MCH / MCV - chronic blood loss picture  Obstruction - lumen ++ narrow  Immunocompromised pts
Plts - if bleeding, check for abN  Incomplete C-scope with partial obstr (up to  > 50yrs of age
LFT Only do albumin - Cancer uses albumin Cecum)  Family Hx (1st degree) & geneics
Only do if jaundiced Hereditary non-polyposis Colon Ca
U&E Baseline - 1/2 of 1 kidney needed to U&E normal FAP (>100 polyps)
Check before any surgery/anaesthetic Tumours of the Large Intestine: 2 close relatives >6x higher risk
INR In any bleeding Pt  Westernised diet
Tumour markers - low sensitivity Squamous Ca Low fibre, high fat
Abd Xray look for features of bowel obstruction (not routinely done) - mets Anal Ca /arise in caecum  Smoking
C-Scope direct visualisation & biopsy possible (most sensitive) - from longstanding metaplasia - E.g. in UC
 Red meat
Barium Enema indirect visualisation (least sensitive) - Adenosquamous pattern - no Chronic inflam
 Inflammatory bowel disease
CT scans complimentary to C-scope & Ba-swallow (mostly used for staging)
UC > Chron’s
Ascitic fluid - cytology will detect malignant cells (indicates local spread) Lymphoma
- 10 arise in rectum/caecum  Lacking exercise
Macroscopic features - polypoidal, ulcerating
Rx - resection + ch/rad  Obesity
- stenosing
- differentiation: good/mod/poor - 20 more common  Previous Ca in same pt
- mucinous mostly (poor prognosis) Rx - ch/rad  Previous radiation
Ca prostate
GIT Stromal Tumours (rare) Ca Cx
- from mm of bowel wall (usually rectum) Ca bladder
Rectal Ca = radio & chemo combo - benign & malignant (can’t distinguish
Colon Ca = radical colectomy clinically)
DRE:
Rectal Ca = sphincter involvement needs cholostomy - mets via blood to liver & lungs (resection )
TNM staging via histo - Dx endoscopically or post-opp biopsy  Often incidental Dx
Fluids, nutrition, Abs, DVT prevention (e.g. chemical & stockings)  Lesion:
No Mechanical bowel preps Carcinoid Tumours (rare) Solitary, spherical, hard, sessile
Regular exams/scans/bloods every 3 yrs then 5yrly - usually metastasised by time of Dx (DRE NB!) Nodules are present.
Epidemiology
Aetiology Crohn’s Disease Ulcerative Colitis

Genetic
- No clear pattern
- Familial recurrence observed
- Chromosime 6: HLA-DR1/DQwS Extra-GIT Sx
Infections
- Measles virus Skin
- Chlamydia
 Pigmentation
- Mycobacteria (M.Paratuberculosis)
Host immunity  Erythema
- ?? inappropriate exposure to luminal/bacterial Ag.  Pyoderma
Eyes
 Iritis
Mediators:
Neutrophils / Eusinophils / Mast cells / Fibroblasts / Lymphocytes / Etc.  Uveitis
 Episcleritis
 Transmural involvement inflammation, mucosal damage  Mucosa & submucosa involvement  distal proximal inflamm.
Signs & Symptoms

Joints
 Granulomatous  non-caseating (no central necrosis)  Non-granulomatous  Ankylosing spondylitis
 Classically starts in ileum  variable involvement of colon,  Mostly rectum proximal spread and may involve entire colon  Migratory polyarthritis
rectum, anus  anywhere may be affected (rare) (pancolitis) Liver
 Hypoalbuminaemia
Features can be variable – depending on site Features can be variable – depending on site  Sclerosing cholangitis – common
 Intermittent attacks of fever/diarrhoea/abd. pain/distension  Relapsing disorder (variable time) (biliary tract)
 Asymptomatic periods  Chronic bloody diarrhoea / rectal bleeding  Pericholangitis
 Blood loss  anaemia  ± mucous  Cirrhosis
 Bowel obstructions - fibrosing strictures  May have remission after single attack  Hepatitis
- fistulae (bowel, bladder, vagina,  Tetanus  Fatty changes
perineum)  Stress can be “onset” or “trigger”
 ↑ risk of Ca (5x)  Serious attacks
++ bleeding Complications
Fluid loss  tachycardia  Extra-GIT manifestations
Electrolyte imbalance  Cancer development (> in UC)
± fever
 Thromboembolisms
Fe2+ - deficiency anaemia
 Toxic megacolon
 Total cessation of bowel habits è toxic megacolon
 Colonic dilatation
 ↑↑↑ risk of Cancer: specifically adenocarcinoma
 Perforation ± sepsis & haemorrhage
Gross patholgoy Crohn’s Disease Ulcerative Colitis
40% only small intestine Can affect:
30% small intestine + colon  Entire Colon (pancolits)  Ca risk
30% colon only  Can involve rectum (extends proximally)
Can affect: Mouth, oesophagus, duodenum too  10% backwash eleitis Investigations:
No skip lesions - Bloods
Bowel wall No fissures FBC
 Thickened No fistulas CRP
 Rigid  Extensive broad-based ulcers LFT
 Fibrotic (hosepipe-like) Mucosa - Stool MC&S
Rule out infections
Serosa  Reddened
 Dusky - Haematinics
 Granularity - Colonoscopy
 Fat entrapped into wall  Friability Monitor disease
Mucosa  Pseudopolyps (isolated islands of regenerating epithelium) Monitor response to Rx
 Variably affected Serosa = normal Screening for Cancer
 Cobble stone appearance  Indolent / healing active disease - attenuated & atrophic in quiescent - Radiology
 Skip lesions phase Barium meals may help
Linear ulcers aka: fissures Severe cases
Fissures  Toxic damage to neurons & nn
 may extend transmurally Management:
 Neuromuscular structures may shut down Crohn’s Disease
 may form fistulas (sinus)  Toxic Megacolon

ALWAYS AS LITTLE AS POSSIBLE SURGERY! SPARE SMALL BOWEL!

Poor success with drugs
Fistulas!
Poor success with surgery
 communications with vagina/etc.
Medical Management:
- 5-ASA (helps in some cases)
-
Micro Pathology

Transmural disease – entire depth of bowel wall Can affect  mucosa & superficial submucosa
Mucosal inflammation Diffuse inflammation in lamina propria
Ulcerative Colitis
 Focal neutrophil infiltration into epithelium Neutrophil infiltration  crypt abscesses (mostly seen in attacks)
Good success with drugs
 Crypt abscess No granulomas
Great success with surgery
Chronic mucosal damage Epithelial dysplasia
 Architectural changes  Low grade Medical Management:
 Metaplasia  High grade - 5-ASA (gold standard)
Non-caseating granulomas (60% of CD) Severe disease - a-TNF
Ulceration (usually deep) Ulceration
 fistulae ↓ Can cure with surgery:
 complication of inflammation Healing - Remove affected area
Trans-mural inflammation ↓ - Make pouch to replace rectum
 All layers Submucosal fibrosis - Preserve sphincters
Paneth cell metaplasia
 Serosal lymphoid aggregates - Ileostomy sometimes
↓ mucin production necessary
Other mural changes
 Hypertrophy of muscularis mucosa
Fibrosis  causes strictures
Causes:
 Fibre content in diet
IBS Sx can present identically to Sx of cancer
 Food allergies
and/or inflammatory bowel disorders.
 Disorders of bowel motility
 Abnormalities of visceral perception Functiona
l disorder
 Psychological disorders aetiology, of bowel,
which cau of unknow
pain, chan ses n
 Social & behavioural problems ges in bow chronic abdominal
defaecatio el habit an
n, and abd d
ominal dis
Abdominal pain or discomfort which is: tension.
Diagnosis: Don’t need to scope if…
 History  Continuous / recurrent at least 3 months (and only if all of the following applies)
 Clinical examination  Relieved by defaecation and/or
 Associated with change in frequency of - No family Hx of bowel Ca
Diagnostic process must exclude: defaecation and/or - No weight loss
 Anaemia  Associated with change in consistence of stool - No blood

Epidemiology:
- Sx usually begin in early adulthood.
- considered a variant, not a disease
- almost 10% of the world-wide population
 Bleeding  Feeling of incomplete emptying - Good general health
- Onset <35yrs
 Weight loss Sx above = diagnostic when presenting with 2 or > of
 Fever the following and these are not ass with the pain:
If any of these are not applicable to your
 Recent development of abdominal pain - altered frequency
- bloated feeling of abd distension patient, there is no reason why a scope should
 Changed bowel habits not be done!!
- altered consistence of stool
 Peritonism - problems with defaecation
** Ca - passage of mucus
**Diverticulosis - gastrocolic reflex (Sx after meals)
** Spastic bowel

Management:
Identify triggers!
 Diet Meal-routine Manage from there…
Small, regular meals
Slow eating
Increase chewing time of meals but avoid chewing continuously (e.g. gum)
Increased fluid intake
Avoid caffeine
Avoid fatty foods (incl full fat dairy, fried foods, fatty meats, chocolate)
Include fibre in every meal

 Natural Flora Probiotics (incl. Lactobacillus, Bifidobacterium, etc)

 Brain-Gut Axis Reduce stress, anxiety and depression

 Antispasmodics Smooth mm relaxation for relief of cramping - Buscopan / Colofac / etc.

Hot bath / hot water bottle No real proof that any of it works - No cure, no true sense of relief.
- Educate patient that it is not cancer, and not dangerous
 Herbs Mint - BMJ 2008 - Educate patient that they are not “crazy” or imagining the symptoms
Calcium - slowing gut motility - Tell them that there is no pharmacological cure - can sort of manage symptoms a little bit.
Turmeric - anti-inflammatory properties, slowing gut motility, etc.
Causes:
 Diet & Exercise
 Lack of fluid intake (no real evidence)
 Drugs
 Neurology
Hard stoo
Strokes l
Infrequen
MS t stool
Plegias
 Metabolic
Myxoedema
Hyperparathyroidism
Diabetes
 Young females
Any kind of abuse
Childhood bereavement
Failure of gender-specific fulfilment

Treat according to stepwise approach:

 Eat sensibly
 Bran
 Medical bran / bulking agents
 Osmotic laxatives
Salts (MgSO4) & (NaPO4)
Sugars (Mannitol)
 Stimulants
Senna (sencot)
Bisicoda (dulcolax)
 Everything else
E.g. liquid paraffin