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WELCOME AND THANK YOU

Copyright Dr Gary Sharp. Please do not reproduce or plagiarise any material contained in these slides.
Rob
A 70 year old male presents with
Excessive salivation
Intermittent dysphagia
Halitosis
Regurgitation of food
Diagnosis
Pharyngoesophageal (Zenkers)
diverticulum
Pharyngoesophageal (Zenkers) diverticulum
False diverticulum (mucosa and submucosa only)
Most common oesophageal diverticulum
Usually older pts (>70 years)
Aetiology probably due to a loss of tissue elasticity and tone with
age
Pharyngoesophageal (Zenkers) diverticulum
Symptoms
Often asymptomatic until it
enlarges
Pts c/o;
a sticking in the throat
Nagging cough
Excessive salivation
Intermittent dysphagia
As the Zenkers increases in size;
Halitosis
Regurgitation of undigested foul
smelling food
Aspiration pneumonia/abscess high
morbidity & mortality in the elderly
Pharyngoesophageal (Zenkers) diverticulum
Diagnosis and Rx
Diagnosis
Barium swallow - diverticulum
filled with barium
Rx
Remove it!
Open Vs Endoscopic
Nichole
A young women presents with
Drastic weight loss (intentional)
Regurgitation
Dysphagia (progressed over years)
Food seems to be getting stuck!
Shes under severe emotional stress
Diagnosis
Achalasia
Achalasia
Young women and middle aged
men most affected
Hypertonic LOS fails to relax
Pathogenesis Idiopathic
Theories;
Severe emotional stress
Drastic weight loss
Chagas disease (parasitic infection
with Trypanosoma cruzi)
Clinical Features
Classical triad of
1. Dysphagia - developed over
years, initially worse with solids,
worsens with disease
progression
2. Weight loss
3. Regurgitation
Investigations
Manometry
GOLD standard
Confirms high pressure, non-
relaxing LOS
Endoscopy
?oesophagitis or neoplasm
Rx
Medical relaxation of LOS -
sublingual GTN, Ca2+ channel
blockers, Botox
LOS dilatation - bougie dilatation,
endoscopic balloon dilatation
(perforation)
Surgical Rx
Oesophagomyotomy
Outer longitudinal layer of oesophagus
is sliced longitudinal from above the
LOS to the cardia of the stomach
Oesophagectomy
Rus
A 40 year old Caucasian man presents
with
Retrosternal pain
Excessive belching
Reflux
Hes know to have GORD
On his last endoscopy they found
some unusual cells for that area
Diagnosis
Barretts oesophagus
Barretts Oesophagus
Caucasian men >55yrs affected most
GORD stratified squamous cell injury cellular repair initiated
squamous cells replaced by columnar cells
Metaplasia is thought to occur to protect vulnerable tissues from a
hostile environment
Not only are these new columnar cells more prone to injury from
reflux they are also more prone to neoplasia
10% of GORD pts develop Barretts
40 fold increase in oesophageal adenocarcinoma
Pathophysiology
Exact pathophysiological
mechanism unknown
Hiatal hernias
Factors associated with LOS
incompetence are;
age, weight, stress, caffeinated
products, ETOH, smoking, spicy
fatty acidic foods
S+Ss and Diagnosis
Intestinal metaplasia is
asymptomatic
Most present with GORD
symptoms
Retrosternal pain
Reflux
Excessive belching
Dyspepsia (indigestion)
Diagnosis
Endoscopy
Histology
Rx
PPI for all
Annual surveillance endoscopy
If dysplasia found then 6/12
High grade
dysplasia/adenocarcinoma
patients offered oesophagectomy
Fundoplication
~50% post op will have regression
back to squamous epithelium
Disadvantage - may in turn
harbour carcinoma undetected
Pete
A 35 year old male presents with
Solid food dysphagia, especially
with meat or bread
He also suffers from long term
anaemia
Diagnosis
Oesophageal web
Oesophageal webs
Thin membranous structures
that partially or completely
compromise the oesophageal
lumen
Usually only involve the mucosa
and part of the submucosa
Comprised of squamous
epithelium
Can affect any age or sex and
location within the oesophagus
Aetiology
Congenital
Acquired
Most common
Seen in patients with;
Plummer-Vinson syndrome
Pemphigoid
UC
S+Ss and Diagnosis
Children
Poor feeding especially with solids
Adults
Asymptomatic (most acquired)
Solid food dysphagia, especially with
meat or bread
Barium oesophagraphy
Good at picking up small webs
Endoscopy
Webs can be easily missed
Rx
Bougie dilatation
Balloon dilatation
Piecemeal removal via
endoscope
Surgical mucosal resection
Transcervical or transthoracic
approach
Reserved for very thick webs
Chris
A young male presents to ED BIBA
You go to resus
The only history is I went on a
bender last night and have been
vomiting my heart up today
Hes writhing around in pain
holding his chest and neck
Suddenly he vomits blood
Obs - HR 120 SR, RR 30, T38.0
Hes becoming drowsy
Diagnosis
Boerhaaves Syndrome
Boerhaaves syndrome
Postemetic rupture of the oesophagus
Just one of the many causes of oesophageal rupture
In the past there was an 80% mortality rate
Neck, retrosternal or epigastric pain
Vomiting
Dysphagia
Haematemesis
Shock
Low grade fever
Elevated salivary amylase in blood or its presence in pleural fluid
Diagnosis of oesophageal perforation
Oesophogram
Barium used if the perforation is
above the diaphragm
(gastrograffin causes pneumonitis)
Gastrograffin if you think
perforation is in the abdomen
(barium causes peritonitis)
?extravasation
Most perforations are above the
GEJ
+/- CT chest
Rx
Resuscitate
IDC
ETT
IV broad spectrum Abx
NG tube ONLY after the consultant says so
Surgery is not indicated for every perforation and in fact most are
treated conservatively with parenteral feed and re-assessed
Temporary stents can be deployed in the hopes to close the
perforation. Removed after 6-12 weeks
Humphrey
A 60 year old male alcoholic
presents with
Dysphagia
Weight loss
Hes also noticed a change in
voice
Diagnosis
Carcinoma of the Oesophagus
Carcinoma of the Oesophagus
V.high incidence in China
Either SCC (majority worldwide)
or adenocarcinoma
Regardless of type its
Aggressive
Spreads rapidly
(thin walled oesophagus and huge
lymphatic supply)
SCC
Accounts for most oesophageal cancer WORLDWIDE
M:F ratio = 3:1
Rarely seen before 30 years
Found in the upper 2/3rds 70% of the time
Caused by environmental factors such as ETOH and smoking, both of
which increase the risk of foregut Ca fivefold
Food additives including nitrosamines found in pickled, smoked and
fried foods have all been implicated
Adenocarcinoma
Accounts for 70% of cancer in the US
Increasing
M:F ratio 15:1
Rarely seen before 40
Lower oesophagus 25% and cardia 32%
Factors involved in this are;
1. Increasing incidence of GORD
2. Western diet
3. Increased use of acid-suppression meds
Intake of caffeine, fats, acidic and spicy foods all lead to decreased tone in the
LOS and thus an increase in reflux and as such leads to Barretts oesophagus
dysplasia adenocarcinoma
Symptoms of Oesophageal Cancer
Dysphagia and weight loss
GORD
Dyspepsia (indigestion)
Because of the distensibility of
the oesophagus the lumen can
be obstructed by up to 2/3rds
before symptoms arise
Recurrent laryngeal invasion
Mets to liver, bone, lung
Diagnosis
Barium Oesophagraphy
Apple core lesion (non-specific)
Endoscopy
Biopsy histology/cytology
US very important
CT
CAP staging
Positron Emission Tomography (PET)
Can evaluate the primary mass, regional
lymph nodes and distant disease
Laparoscopy
Prior to surgery, ?macroscopic disease
Treatment
Depends on;
1. Histology
2. TNM
3. Co-morbidities
4. Patients wishes
Histology
1. SCC
Treated non-surgically with chemoradiotherapy initially
May achieve complete response to non-surgical management
2. Adenocarcinoma
Surgery
Not as sensitive to chemoradiotherapy
Rx
Chemotherapy
Used to stop/reduce distant
micrometastises
Neoadjuvant chemo improves survival
Cisplatin and 5-Flurouracil
+/- mitomycin C, etoposide or paclitaxel
Radiotherapy
Neoadjuvant
Controls local tumour burden
Given 5 days a week for a period of 6-7
weeks
In combination with chemotherapy
improves survival
Airway and great vessel injury!!!
Surgical Rx
No superior procedure
Transhiatal approach
2 incisions left neck and upper midline abdominal
incision
Cervical oesophagogastric anastomoses
Advantages if leaks easier to access
Disadvantages higher rate of strictures
Ivor Lewis
Right thoracotomy and abdominal upper midline
An intrathoracic oesophagogastric anastomosis is
performed
Benefits low rate of anastomotic leak, but, if it does
then its harder to control than a leak in the neck!
Anastomosis
Leak <48 hours post-op due to
poor arterial supply
Leaks from day 7 onwards - due to
venous compromise
Technique of performing an
anastomosis;
1. Hand sewn
2. Stapled
The new oesophagus, usually
comprised of stomach, placed in
the posterior mediastinum or right
pleural space
Palliation
Can include;
Chemo
Radiotherapy
Stents must get consent for an
oesphagectomy (10% risk of
perforation). Average survival post
stent insertion is 6/12
PEG/JEJ
Mr Mayor
An obese man presents with
Long standing
retrosternal/epigastric stinging
sensation
Bending forwards exacerbates his
symptoms
He tells you previous imaging
suggested his stomachs in his
chest!
Diagnosis
GORD
GORD
Pathophysiology
LOS has the primary role of
preventing GOR
LOS is not a distinct anatomical
structure
Located just cephlad to the
gastroeosophageal sphincter
Associated with;
Obesity/pregnancy increased
abdominal pressure
Coffee, chocolate, fat and ETOH relax
the LOS
Hiatus hernias
Clinical presentation of GORD
Long standing dyspepsia
Retrosternal/epigastric stinging
sensation
Regurgitation
Waterbrash salivation due to
reflex salivary gland stimulation
as acid enters the gullet
Bending forwards exacerbates
reflux
Aspiration may even be woken
abruptly in their sleep
Investigation
pH monitoring
Gold standard
Catheter in oesophagus for 24 hours, electrodes
every 5-10cm apart sense pH fluctuations
Digital clock on the data recorder. Patient notes
time of the event/symptoms correlated with
pH readings
If there is symptoms correlating with a pH<4
then GORD can be expected
Endoscopy
Excludes other disease
Manometry
Flexible tube with pressure sensing devices at
5cm intervals
Measures oesophageal peristalsis and LOS
pressure
CT
?strictures
Rx
Treat cause
Obesity exercise
Coffee etc - cease
Hiatus hernia - fundoplication
GIVE BIRTH!!
PPI
Either single or double dose
6 week trial
Maximal effect occurs after 4/7
Mr Mayor
Hes discharged after 2 days
Hes been booked in to have an
endoscopy and pH monitoring in
the future
He returns with worse
retrosternal pain
His obs are HR 120 SR, RR 35,
SpO2 93% on 15L and feverish
Diagnosis
Paraoesophageal hernia and
ischaemic stomach
Hiatus hernias
1. Sliding (Type 1)
Cardia migrates back and forth
between the posterior mediastinum
and abdominal cavity
2. Rolling (Type 2)
Occur due to a hiatal defect which
allows the fundus or another part of
the stomach (spleen or bowel also) to
roll in and out of the posterior
mediastinum
3. Mixed a mix of both (Type 3)
Pathophysiology
Gastric fundus most common
structure to herniate
Spleen, colon and omentum can
herniate
Repeated herniation's sac
inflammation adhesions
viscera incarcerated acute
strangulation (~1%risk/year)
Hiatus hernia clinical presentation
Intermittent dysphagia to solids
Visceral torsion leads to abdominal or chest pain
Dyspepsia
Regurgitation most likely with large type 3 (mixed) hiatal hernias
GI bleeding from mucosal ischaemia or ulceration from mucosal
irritation (rubbing on itself)
Worrying clinical presentation
Constant thoracic or epigastric
pain, fever or sepsis in a known
paraoesophageal hernia =
ischaemic viscera
Emergency
Rare
Mortality v. high
Emergency repair and
fundoplication
Nissen Fundoplication (360 degree wrap)
Procedure
Fundus mobilised
Vagus nerves preserved
Fundus is then passed behind the
oesophagus from left to right
The wrap is ~2-3cm
Secured with non-absorbable sutures
+/- Synthetic mesh to reinforce the
hiatal defect
Risks - oesophageal erosion,
ulceration, stricture and dysphagia
which has limited its use
Fundoplication risks
General
Post op ileus
Early
Dysphagia - normal for first 6/52
Bloating due to difficulty belching
secondary to the wrap itself
Pneumothorax (5-8%) Occurs due to
violation of the pleural space by carbon
dioxide. Carbon dioxide is absorbed into
tissues rapidly, the lung will expand and
as such there is no need to drain
Late
Failure (5-10%)
Recurrence
Partial wraps
Either partial posterior or partial anterior
wraps
170-270 degree wraps
Intended to reduce post operative bloating
and dysphagia
Dawn
A 50 year old lady presents with
Nausea
Vomiting
Abdo pain
That radiates to the right scapula
and epigastrium
Her poo and wee are normal
WCC normal
T37.0
Diagnosis
Biliary colic
Biliary colic
Occurs when a gallstone blocks or impacts in the
cystic duct OR CBD
Transient (stone falls back into the GB or is
passed)
Correlates with fatty meals and CCK release (in
50%)
RUQ/Epigastric pain - can last up to 2 hours
Inferior angle scapula pain
Restless pt
Sweaty
N+V
If resolution occurs = ?NOT a stone, ?passage of
stone
NOT PYREXIAL
NO RAISED WCC
Distinguishing between biliary colic and
cholecystitis
Absence of Biliary colic
Leucocytosis Because theres no GB
Pyrexia inflammation therefore no
Murphys sign Murphys

Presence of above Cholecystitis


Differential diagnosis of biliary colic
Without jaundice
Renal colic
Intestinal obstruction
Angina
With jaundice;
Benign
Cholangitis
Malignancy
Head of pancreas (usually painless
jaundice), ampulla, SOL
Cholangiocarcinoma
Hepatocellular carcinoma
Ricki
A 40 year old lady with 2 children
presents with
Nausea
Vomiting
Abdo pain
That radiates to the right scapula and
epigastrium
Her poo and wee are normal
Neutrophils 15 (thats raised!)
T38.2
Shes tender in the RUQ
Diagnosis
Acute cholecystitis
Acute calculous cholecystitis
Definition - gallbladder
inflammation, oedema and
subserosal haemorrhage due to
calculi
95% due to cystic duct obstruction
Clinical features;
Dyspepsia, fat intolerance, biliary
colic
RUQ pain, increasing over 1-2 days
Fever
Leucocytosis
Rebound tenderness & guarding in
RUQ
Murphys sign
Gallstones
F>M 2:1
Incidence increases with age
FH = strong predictor
Fair, Fat, Fertile, 40, Female
Biliary sludge (cholesterol, calcium &
mucin) nidus gallstone formation
Types:
Cholesterol 20%
Pigment 5%
Mixed 75%
Biliary sludge increased with fasting and TPN (lack of GB
stimulation secondary to no CKK release)
Complications of acute calculous cholecystitis
Unresolved cystic duct obstruction
stagnant bile infection
Unresolved cystic duct obstruction GB
ischaemia necrosis gangrene
perforation peritonitis
Empyema = pus in the GB.
SEPTIC +++
Elderly
High mortality if it perforates
Rx remove it!
Emphysematous cholecystitis = The end
result of a gangrenous GB infected with gas
forming Clostridium perfringens
SEPTIC+++
Elderly/immunocompromised usually
Rx remove it!
Acute cholecystitis and jaundice
Is unusual as its usually the
cystic duct blocked (not CBD)
If theyre jaundiced ?cholangitis
with CBD stone blockage or
Mirizzi syndrome
Mirizzi syndrome - Inflammation
or a stone in the GB neck leads
to inflammation of the adjoining
biliary system with subsequent
blockage of the common hepatic
duct
Diagnosis of cholecystitis and/or gallstones
USS
Limited by BMI!!!
GB wall thickening
Biliary tree dilatation
Pericholecystic fluid
CT
Less sensitive than US
Useful if unsure (DD) or pt
jaundiced
Mx of Acute cholecystitis
Analgesia
IVF
NBM
G+S, clotting etc
Broad spectrum Abx
Low fat diet
Hot GB Vs cholecystectomy in 6/52 post D/C
Guidelines suggest laparoscopic cholecystectomy within 3/52 after acute pancreatitis due to gallstones
Q. Why have a cholecystectomy?
A.
High risk of recurrent attacks
Life threatening complications (see above)
Asymptomatic gallstones leave alone!
Cholecystectomy
Open = OLD SCHOOL
Kochers incision right subcostal incision
LAP = NEW SCHOOL
Reduced morbidity
Reduced pain = reduced complications
Reduced hospital stay
Quicker return to work
Fully mobilising next day
E+D next day
Home after 24 hours if well
+/- Drain - may dictate longer stay
Always consent for open too!!
Relative CI to lap chole
Pregnancy
Jaundice
Cirrhosis
Previous upper abdominal surgery
High BMI
A Continuum

Biliary colic Acute Chronic


cholecystitis cholecystitis
CBD stones
Usually pass conservatively
Hx of painful jaundice (duct dilatation)
Dark urine, pale poo!
Complication is ascending cholangitis
Most surgeons want an MRCP to
ensure no stones in ducts prior to
cholecystectomy
If stone seen, do one of two things;
1. ERCP to remove it, increased
morbidity!
2. Remove the stone intraoperatively
requires II for cholangiogram (stone Px)
MRCP
Magnetic resonance
cholangiopancreatogram (MRCP)
Non-invasive
Diagnostic of benign &
malignant disease
Stone detection
No cytology/histology!!
ERCP
Indications
Diagnostic indications;
Dilated ducts (USS) & deranged LFTS
To Ax benign/malignant duct or pancreatic
disease
Therapeutic indications;
Stone clearance, Stenting, Sphincterotomy
Pre procedure
FBC, U+E, LFT, clotting, G+S
Starved 6 hours prior to ERCP
Informed consent - complications
Contrast medium
Non-ionic (iodine) reduces the chance
of pancreatitis
ERCP procedure
Left lateral px
LA spray to throat
IV sedation (Midazolam causes amnesia also)
IV broad spectrum Abx
Hyoscine butylbromide reduces duodenal
peristalsis
Mouth clamp/protector for endoscope to pass
through
Ampulla identified
Cannulation of bile and/or pancreatic ducts
+/- cholangiogram images saved
Duct images saved
+/- Rx carried out
Observed
Home later that day someone else drives!
ERCP complications
Pancreatitis 3%
Life threatening pancreatitis
0.1%
Contrast reactions
Bacteraemia
Septicaemia
Perforation
Haemorrhage
Tionne
A young African-American lady
presents with
Painful joints
Abdo PAIN
JAUNDICE
RIGORS (FEVER)
Diagnosis
Cholangitis
Cholangitis
Ascending biliary tree infection
Charcots triad
PAIN, JAUNDICE, RIGORS
All 3 may not be present!! (Jaundice is
usually the one missing)
Pts get sick fast
Diagnosis USS/ CT
Rx IV Abx & A-H
Definitive Rx = Decompression of the
biliary tree via endoscopic, percutaneous,
surgical, radiological means
Any restriction on bile flow can
predispose to cholangitis
CBD stones, biliary stricture, post ERCP,
malignancy
Patsy
A 70 year old lady presents with
N+V
No flatus since yesterday
BNO
Diagnosis
SBO
She goes for a AXR
Her AXR shows air-fluid levels and
pneumobilia
Diagnosis
Gallstone ileus
Gallstone ileus
Not an ileus but an obstruction!
Large gallstone chronic GB
inflammation cholecysto-enteric fistula
(duodenum) stone impaction at the
ileocaecal junction (or Meckels
diverticulum)
Pts are usually older
PC SBO +/- RUQ pain, pneumobilia, +/-
opacity (stone) in ileum
CT - usually diagnostic
Rx Drip and suck, laparotomy &
enterotomy
Fistula Rx leave until acute episode is
over then +/- definitive Rx
Cate
A 40 year old lady is in ICU due to severe
trauma
Shes being fed parenterally
She c/o
Nausea
Abdo pain that radiates to the right
scapula
Her poo and wee are normal
A bedside USS shows no gallstones
BUT it does show a thickened gallbladder
wall
Diagnosis
Acalculous cholecystitis
Acute acalculous cholecystitis
Definition - obstruction of the cystic duct in the absence of stones leading to inflammation
Same presentation!
Pathophysiology poorly understood
Risk factors
Older age
Critical illness
Burns
Trauma
Prolonged TPN use
DM
Immunosuppression
Generally more fulminant than calculous cholecystitis & may progress quicker to gangrene
Rx US or CT guided cholecystostomy (drain into GB), cholecystectomy if well enough
Ms Random
A 65 year old Indian female presents with
A palpable non-tender GB
Jaundice
Weight loss
Diagnosis
Gallbladder carcinoma
Gall bladder carcinoma
Rare
Aggressive
Usually present with advanced disease
F>M 3:1
6-7th decade
Indians and Pakistanis +++
90% adenocarcinomas
10% squamous cell carcinoma
Cause chronic inflammation with subsequent cellular proliferation
Risk factors
Gallstones
Especially if large (>3cm).
80% diagnosis with GB Ca have
gallstones!!
Gallbladder polyps
Especially if >10mm
Porcelain gallbladder
Definition extensive calcification
of the GB wall
Causes a brittle GB
Diagnosis and Rx
Diagnosis
USS irregular GB, mass, large polyp (>10mm), thickened wall
CT - mass
Spread
Local and haematogenous = liver
Clinical features
PC similar to chronic cholecystitis
Weight loss etc
Incidental finding
Rx
Cholecystectomy plus hepatic segmentectomy/liver resection
Palliation
Prognosis
POOR, why?
90% found in fundus or body of GB no symptoms until advanced!!
Shane
A 50 year old man presents with
Anorexia
Weight loss
Painless jaundice
Ascites
A history of primary sclerosing
cholangitis
Diagnosis
Cholangiocarcinoma
Cholangiocarcinoma
AKA bile duct Ca
Adenocarcinoma
M=F
50% in hepatic duct, 50% in cystic duct & CBD
Dismal prognosis
Cause chronic inflammation of the biliary tree with cellular proliferation
Predisposing factors;
Bile duct stones (20-30%)
Primary sclerosing cholangitis
UC
Parasitic infection
S+Ss, Diagnosis and Rx
PC
Jaundice (90%), Pain (30%), Ascites, Anorexia, Wt loss, Anaemia
Investigations
USS
ERCP additional risk of cholangitis and pancreatitis in a sick pt!
Percutaneous Transhepatic Cholangiography (PTC)
CT CAP
FNAC via US or ERCP
Mx
Distal cholangiocarcinoma pancreaticoduodenectomy
Proximal cholangiocarcinoma en bloc revision of CBD and hepatic parenchyma to achieve ve
margins
Palliation (80-90%) stents, by pass surgery, percutaneous biliary drainage, radiotherapy
Lindsey
A 40 year old female presents with
Abrupt, severe epigastric, knifelike pain
It radiates to her back
Shes unable to stay still
Obs
T 38.2
BP 85/65
HR 101 SR
GCS 15/15
o/e voluntary guarding in epigastrium, BS
present
Diagnosis
Pancreatitis
Pancreatitis
Either:
Acute
Chronic
Acute = acute presentation WITH resolution
Chronic = may have had previous attacks, no COMPLETE resolution of
S+Ss
Pancreatitis spectrum
Interstitial oedema
Infiltration of inflammatory
Mild cells

As above
Moderate Mild necrosis

Extensive necrosis
Intrapancreatic vascular thrombosis and haemorrhage
Severe Abscess formation, either in or around the pancreas
Chronic pancreatitis
Initial acute
pancreatitis

+/-
superimposed Cellular
acute destruction
pancreatitis

Loss of
function
Fibrosis
Etiology of pancreatitis
GET SMASHED
70-80% caused by Etoh and
gallstones
Acute usually gallstones
Chronic usually prolonged ETOH
10-15% of pancreatitis cases are
idiopathic
Any pancreatic duct obstruction
can cause pancreatitis
Etoh abuse
What actually causes the pancreatitis?
IDIOPATHIC, but, theories include:
1. ETOH causes hypertryglyceridaemia fatty acid generation
pancreatic injury
2. ETOH free radical production cell destruction
3. ETOH causes direct acinar cell damage
4. ETOH causes the release of proteolytic enzymes cellular damage.
END RESULT IS ALWAYS FIBROSIS!!
OBSTRUCTIVE CAUSES:
Any pancreatic duct obstruction can cause
pancreatitis
INFECTIVE
ascaris lumbricoides (nematode intestinal
worms)
NEOPLASTIC
periampullary tumours
INFLAMMATORY
crohns, DU
TRAUMA
blunt abdo trauma at the point where the
pancreas passes over the vertebrae can lead to
fibrosis and strictures
CONGENITAL
pancreas diversum (due to the larger volume of
flow out of the smaller santorini duct you have a
relative obstruction)
For you creatures of habit...
G - Gall stones
E - Ethanol
T - Trauma
S - Steroids
M - Mumps, COXSACKIE
A - Auto-immune, SLE
S - Scorpion bite!!!!!! Found in Trinidad
H - Hypercalcaemia, Hyperlipidemia
E - ERCP
D - Azathioprine, Furusemide, Metronidazole
S+Ss
N+V
Abrupt, severe epigastric, knifelike pain
Intrascapular radiation
Eased by forward flexion
Cant stay still (Vs perf who lay still)
Pyrexial
DRY (Hypovolaemic)
Due to capillary leak & N+V
Hypotension
Tachycardia
Tachypnea
Rebound tenderness
Voluntary and involuntary guarding
Rare as rocking horse....
Grey turners sign
Cullens sign
Due to retroperitoneal
haemorrhage
Seen DURING severe
pancreatitis
Pancreatitis and the lung
Pleural effusion/s common
usually the left
Atelectasis
If severe +/- Adult Respiratory
Distress Syndrome (ARDS)
Amylase & Lipase
Amylase may or may not be raised!
Amylase normal <130
Should be 3x the upper
Returns to normal within 3-6 days post attack (if resolving)
Lipase (<160), remains elevated for longer than amylase
DD of raised amylase:
1. Acute cholecystitis
2. Perforation
3. Bowel obstruction
4. Bowel infarction
Investigations
CXR
NOT FOR PANCREATITIS DIAGNOSIS
To check the following:
1. Pleural effusions (usually left)?
2. Air under the diaphragm (DD)?
3. Basal atelectasis secondary to poor
inspiration (due to pleuritic pain)?
AXR
USS
Gallstones
Dilated bile ducts
CT abdo
If unsure of cause
?necrosis
Glasgow score
PaO2 <60mmHg <3 mild
Age >55 years >3 severe
WCC >15
Calcium <2
Urea >16
Elevated LDH
Alb <32
BSL >10
Acute attack Rx
Fluids
1. Capillary leak due to proinflammatory factors released=3rd space losses
fluid in lung & retroperitoneal.
2. N+V = fluid loss again and metabolic alkalosis
IDC strict FB
Analgesia
Antiemetics
NG tube
If severe ITU CVP line
Hypoxaemia due to proinflammatory substances causing fluid
sequestration in lungs = shunt/dead space. Pancreatitis also causes
a lung injury similar to ARDS
Prophylactic Abx complicated topic! Check local policy
If stone ERCP within 72 hours
Dietician R/V - ? PEJ. ? TPN
Shazza
A 25 year old smoker presents with
abdo pain
Weight loss
Diarrhoea and mucus PR
Shes off her food too
Shes noted to have a red fat beefy
tongue
Oral ulcers
Diagnosis
Crohns
Introduction
Highest incidence is Scandinavian countries > Scotland > England >
North America
Bimodal age distribution
1st peak is 15-30 years
2nd peak 55-80 years
Idiopathic
Involves all layers of the bowel wall (transmural)
Mouth to anus affected
More common in smokers and is aggravated by it
Crohns clinical presentation
Varies greatly
Characteristic triad of
Abdo pain
Diarrhoea no blood or mucus usually
Weight loss eating provokes pain!
Other symptoms;
Anorexia
Fever
Recurrent oral aphthous ulcers
Terminal ileum and right colon (together) is the most usual presentation
Followed by right colon > colon alone > terminal ileum alone > ileum and jejunum
Anal disease (see later)
Extra-intestinal complications
Eyes
Conjunctivitis, Iritis, Episcleritis
Mouth
Ulcers, Glossitis
Liver
Fatty liver, Abscess/Portal pyaemia
Vascular
Mesenteric or portal vein thrombosis, DVT
Large Joint arthritis
Dermatology
Erythema nodosum, Pyoderma gangrenosum
Sacroilitis/Ankylosing spondylitis
Associated with HLA B27 +ve pts or those with a FH of Ank
spond
Usually IMPROVE post colectomy
Gross appearance
Transmural chronic inflammation
thickened bowel wall
Cobblestone on endoscopy (deep
linear fissures) may ulcerate
through bowel wall abscess or
fistula
Fat wrapping mesenteric fat
literally wraps around the bowel
Strictures (small & large bowel)
Skip lesions normal mucosa
interspersed within inflamed
mucosa
Histological appearance
Pathognomonic histological
feature of Crohns is;
NON-CASEATING
GRANULOMA
Granulomas are found in
only 50% of resected
Crohns specimens!
Transmural inflammation
Submucosal oedema
Lymphoid aggregates
Fibrosis
Diagnosis
Through combination of clinical,
endoscopic and radiological
features
Colonoscopy is the most sensitive
diagnostic modality
Biopsies should be taken but unless
youre lucky enough to biopsy a
granuloma, distinguishing between
the 2 diseases (UC & Crohns) may
still be difficult
Stool MC+S, ova, parasites (rule out
infective causes)
Case 17 cont
After being diagnosed with Crohns shes discharged home on
appropriate Rx
She returns a year later and is now c/o bubbles in my wee
Diagnosis
Enterovesical fistula
Fistulas
Fistulas can occur between bowel and;
Enterocutaneous
Enteroenteric (small), enterocolic (large)
Enterovaginal faecalent vaginal D/C
Enterovesical recurrent UTIs/pneumaturia
Gastrocolic
~35% of Crohns sufferers affected
Most involve small bowel
Rx - Resection of the affected bowel segment,
closure of other viscera, omentum placed
between the bowel and affected organ
Perianal disease in Crohns
Devastating to patients
Painful+++
~20% of Crohns patients will present
with anal disease
Fissures
Fistulas
Abscesses
Pain
From excoriation, maceration,
hemorrhoids and the above
Bleeding
Distal proctitis, hemorrhoids, granulating
fistulas
Fissures usually multiple
Evaluation & Rx
Subjective & objective examination
Endoscopy not in acute flare
Rx;
Fissures
sit baths, stool softeners, analgesics
Abscesses
GA I+D
Fistula
Seton or fistulotomy
Abx cover
+/- bowel resection if really bad
Crohns Induction of Remission
Typical regimen;
Budesonide 9mg od for 6/52
Gradually reduce dose over 2 weeks then stop
No response to budesonide
Prednisolone 40mg od
Reduce by 5mg/week then cease
Vitamin D and calcium should be co-prescribed
Severe disease
Admit
IV hydrocortisone
Or anti-TNF Rx (Infliximab) AND 6-Mercaptopurine (6-MP)/Azathioprine
dual therapy proven to be better
The way I remember acute Crohns Rx

Bloody
(Budesonide)

Painful
(Prednisolone)

A.Hole
(Admit, Hydrocortisone)
Crohns Maintenance Therapy
Only needed in pts with persistent active disease
Treatment can be with either 1, 2 OR 3 (3 is the most expensive)
1. 6-Mercaptopurine (6-MP) OR Azathioprine
2. Methotrexate (teratogenic) once weekly PO or S/C
3. Combination therapy which involves Infliximab and 1 OR 2 above
(only used if 1 and 2 have failed)
Indications for surgery
1. Intractable disease to medical Rx
Most common cause
2. Intestinal obstruction
Causes; - active inflammation, stricture, abscess (mass effect),
adhesions (previous surgery)
SBO > LBO
3. Intra-abdominal abscess
4. Fistulas
5. Fulminant colitis
6. Toxic megacolon
7. Cancer
Not as high risk as UC
8. Growth retardation
Both mental and physical
Poor caloric intake
Chronic active inflammation leads to closure of epiphyseal plates
Surgery does not cure Crohns!
Surgical options
Segmental colon resection
Segmental stricture/obstruction
Ileocaecal resection
Severe ileal disease
Total proctocolectomy with end
ileostomy
Removal of entire colon, rectum &
anus for pancolitis
Total abdominal colectomy with
ileorectal anastomosis or end
ileostomy
Rectal & anal sparing
Case 17 cont
Shes d/c on maintenance therapy
She presents a year later with;
A Ind
B chest clear, RR 30, Spo2 99% on NRBM (15L)
C HS dual, BP 60/40, HR 130 SR
D GCS 14/15
E NAD
F DRY+++
G Abdo guarded, rebound tenderness, no BS, thumbprinting on AXR with bowel loops >10cm
H haemodynamically unstable
Diagnosis
Acute abdomen toxic megacolon
Toxic Megacolon
Life threatening
Bacterial infiltration of the colon wall
colonic dilatation imminent perforation
necrosis
Dilatation mucosa gaps appear
bacteria enter surrounding vasculature
portal system systemic infection
Look for thumbprinting (bowel wall
oedema)
Mx;
IVF
Broad spectrum IV Abx
IV high dose steroids
+/- surgery
Toxic megacolon Rx - Total colectomy with
ileostomy
Bob
A 25 year old male presents with
Abdo pain
>6 bloody stools in the last 24 hours
He also c/o diarrhoea
Mucus PR
A feeling like I havent completely finished pooing when I
have?!!!
His Hb is 75
HR 100 SR
Bloods - CRP 123
Has had a recent cold with stress at work
Brother has something similar
Diagnosis
UC
Epidemiology and cause
More commonly affects those <30
Small second peak in 6th decade
M=F
Whites, Jews and northern Europeans
most affected
Idiopathic
Suggestion of genetic PLUS environmental
factors
Smoking
Protective and therapeutic
Gross appearance
Involves the mucosa and
submucosa only
Rectal involvement is the hallmark
of the disease
Continuous mucosal inflammation
Pseudopolyps = normal or
hypertrophied mucosa within areas
of atrophy
The terminal ileum is ONLY
involved in backwash ileitis
Clinical presentation of UC
First attack usually the worst
Provocation factors in UC
Stress, Infection, Gastroenteritis, Abx, NSAIDS
Rectal bleeding
From marked vascular congestion
Mucus PR (Both IBD)
Abdo pain (not as severe as Crohns)
Diarrhoea
Tenesmus (UC>Crohns)
Almost 100% will have rectal disease
Extraintestinal manifestations of UC
Erythema nodosum 10-15%
Pyoderma gangrenosum
Pretibial erythematous plaque
that progresses into ulcerated
painful wound
Arthritis
Particularly knees, hips, GHJs
Primary sclerosing cholangitis
Those in red usually completely
resolve post colectomy
UC Diagnosis
Colonoscopy
Not in acute setting
Diffuse, symmetrical disease from the dentate line is consistent with
UC biopsies
Upper GI barium follow through
To rule out Crohns/Ca
Stool MC+S, ova & parasites
To rule out infection
Medical therapy
1. Aminosalicylates 3. Immunomodulatory drugs
Sulphasalazine lots of SEs 6-Mercaptopurine (6-MP)
Mesalazine less SEs Azathioprine
2. Corticosteroids Induce remission
Budesonide - less SEs than SE reversible bone marrow
prednisolone suppression, pancreatitis
Highly effective during active UC Cyclosporin
bouts Infliximab
Can be IV/PO or topical (enemas)
Truelove-Witts criteria for acute severe UC
6 bloody stools per 24 hours
Plus one of the following;
Anaemia
Fever
Tachycardia
High CRP/ESR
Case 18 RECAP
A 25 year old male presents with
Abdo pain
>6 bloody stools in the last 24 hours
He also c/o diarrhoea, mucus PR and a feeling like I havent completely
finished pooing when I have?!!!
His Hb is 75
HR 100 SR
Bloods - CRP 123
Diagnosis
UC
Severe UC Rx
Bloods daily
AXR
IVF
IV hydrocortisone 400mg od
If no response by 48-72 hours try ciclosporin (2mg/kg) or infliximab
(5mg/kg)
Broad spectrum Abx
Avoid opiates/loperamide
If still no joy colectomy
Case 18 cont
His abdo pain has become extreme
Hes still passing bloody stools, but
not as regular
T 38.0
RR 28
BP 90/50
HR 110 SR
Bloods - CRP 405
AXR thumbprinting
Diagnosis
Toxic megacolon
Toxic Megacolon
Life threatening
Bacterial infiltration of the colon wall colonic dilatation
leading to imminent perforation necrosis
Dilatation mucosa gaps appear bacteria enter
surrounding blood vessels portal system systemic
infection
Thumbprinting (bowel wall oedema)
Mx;
IVF
AXR
Broad spectrum IV Abx
IV high dose steroids
+/- surgery
Toxic megacolon Rx - Total colectomy with ileostomy
Indications for surgery
1. Intractable disease
Most common
2. Fulminant colitis
Present with high fever, severe abdo pain, tachycardia, WCC
Deterioration or lack of improvement within 48-72hrs of medical management warrants an
urgent procedure
3. Toxic megacolon
4. Massive bleeding
Uncommon
5. Dysplasia
6. Carcinoma
7. Malnutrition and growth retardation may necessitate resection
Surgical options
Segmental resections are not
indicated
Total proctocolectomy with
ileostomy
Restorative proctocolectomy
with ileal pouch-anal
anastomosis (IPAA)
No colon must remain, end of!
Restorative proctocolectomy with ileal pouch-
anal anastomosis (IPAA)
Most common definitive
procedure for UC
The procedure involves;
A near total proctocolectomy
Preservation of the anal sphincter
complex
A single chambered pouch is
fashioned from the distal 30cm of
ileum
Ileum is then sutured or stapled to A
the anus
Case 18 cont...
The specimen is sent
Histology shows carcinoma
BUT
Clear margins and no lymph
nodes
Risk of carcinoma in UC
The most important risk factors are;
1. Length of disease process
25% risk of CRC at 25 years
35% risk at 30 years
45% risk at 35 years
65% risk at 40 years
2. Pancolic disease
3. Continuously active disease
4. Severity of inflammation
CRC in UC tends to be poorly differentiated and highly aggressive
Surveillance colonoscopy in UC pts
1 to 2 yearly colonoscopies 8
years after the onset of
pancolitis
Or 12-15 years after the onset of
left sided disease
At least 30 biopsy specimens
should be taken
If dysplasia is found a
prophylactic colectomy offered
What if you cant be sure its
one or the other?
Indeterminate colitis
Occurs in ~10-15% of those investigated
End of day 1
Will
PC - abdo pain
HPC colicky abdo pain 4-5 minutes apart, nausea
(no vomiting), diarrhoea earlier today
O/E
Tachycardic
Dehydration
Previous surgical scars noted
Audible whooshes on abdominal auscultation
Abdo pain
You cannulate him, take some bloods an ABG and
then review him
O/E now hes
Vomiting
His abdomen is now more tender and distended
Diagnosis?
SBO
Small bowel obstruction
Causes
Extramural
Adhesions
Hernias
SOL nice Vs nasty
Abscesses
Intramural
Nice vs nasty
Intraluminal
Enteroliths
Foreign bodies
Small bowel obstruction causes
1. Adhesions
~60%.
2. Malignant tumours
~20%. Metastatic peritoneal deposits =
extramural compression
3. Hernias
Any hernia
4. Crohns disease
5. Abscess formation
Ileus or compression
6. Miscellaneous
Intussusception
Irradiation
Pathophysiology
1. Diarrhoea early
2. Bowel dilates unable to absorb 3rd space sequestration
dehydration, hypovolaemia.
3. Electrolyte disturbances - hypokalaemia, hypochloraemia.
4. Vomiting Metabolic alkalosis (H+ loss)
5. Raised intra-abdominal pressures elevation of diaphragm and
reduced venous return respiratory compromise & hypovolaemia
6. Intraluminal pressure > capillary perfusion pressure necrosis
perforation
7. Greatest risk is with a closed loop obstruction
Clinical manifestations
Examination
Borborygmus (bor-bo-ryg-mus) = audible whooshes associated with hyper-
peristalsis (early sign)
Tachycardia
Hypotension
Dehydration
Fever suggests strangulation
Distended abdomen
Note any previous surgical scars
Peristaltic waves these are seen in early phase
Min/no BS = late phase
Mild abdo tenderness +/- palpable mass
Hernia examination
Investigations
Bloods
The usual plus
G+S and crossmatch!
ABG met alkalosis, lactate
AXR
Supine AXR = dilated bowel loops (valvulae
coniventi) without colonic dilatation
CT
Good for diagnosing extramural causes of
obstruction e.g. ?Ca
Good in post-op pts - ?collection
Barium studies
Can locate the exact point of obstruction
USS
Good in pregnancy when radiation is an issue
Simple obstruction Vs strangulation

Strangulation obstruction usually


involves a closed loop which in turn
compromises blood flow necrosis
infarction perforation
Classic signs of strangulation include;
Fever
Constant non-cramping abdo pain
Investigations
ABG raised lactate
CT
DD
Mesenteric infarct
Conservative Rx
Fluid resuscitation
IDC strict FB and UO
Abx
+/- Broad spectrum depends on surgeon
Decompression
NG decompresses and reduces aspiration risk
Pneumonitis KILLS!
Reassess
Surgical Mx
If its complete obstruction then the Rx is surgical!
Choices;
Strictureplasty
Bowel resection
Bypass the obstruction Defunctioning stoma
Abscess drainage
Goldie
Day 1 surgical rotation
Nurse
Dr, bed 4s unwell can you come and see her,
thanks, bye!
You
SH*T
Day 3 post hysterectomy (open)
Drug chart shows large consumption of PRN
opiates
BNO
Feels sick
Passing some flatus (she thinks)
Diagnosis?
Ileus
Ileus
Intestinal distention and the slowing or absence
of passage of luminal contents without a
demonstrable mechanical obstruction
PC
Same as obstruction BUT may still be able to pass
flatus, diarrhoea and may not c/o N+V
Causes;
Post laparotomy+++
Drug induced opiates
Investigations
As obstruction
Bloods, ABG
AXR
Barium studies
Rx
Supportive
Drip and suck
Find cause and treat that!
Kevin
PC abdo pain
Poor historian
O/E
RIF pain on palpation
Feels unwell
Looks unwell
No vomiting
Testicular examination nil
Bloods Hb 80
Diagnosis?
Meckels diverticulum
Meckels Diverticulum
Most common congenital small bowel abnormality
Due to failure of closure of the vitelline duct
Cells lining the vitelline duct are pluripotent therefore its not
uncommon to find gastric mucosa (50%) or pancreatic mucosa (5%)
within them
M=F
Occurs in ~2% of population
2 feet from ileocacal junction
~2cm in size
Meckels PC
Usually incidental finding
Most common presentation
however is GI bleeding (25-50%)
Can manifest as acute
haemorrhagic shock, anaemia
(acute/chronic). Acidic secretion
adjacent ileum ulceration &
bleeding
Obstruction can also occur due to;
Volvulus around fibrous band
attached to ant abdo wall
Intussusception
Incarceration of the diverticulum in
an inguinal hernia Littres hernia
Meckels cont...
DD Investigation
Appendicitis clinically AXR, USS, CT rarely helpful
indistinguishable Diagnostic laparoscopy
Complications Rx
Ischaemia Antiemetics
Necrosis Analgesia
Perforation Diverticulectomy
Peritonitis Ileal resection
Dynamo
Known Crohns
Several small bowel resections in
the past
Another recent small bowel
resection and ileostomy
formation
Now c/o large stoma output,
lethargy and weight loss
Diagnosis?
Short bowel syndrome
Short bowel syndrome (SBS)
A bowel length that is inadequate to support nutrition
75% due to resection
Up to 70% of the small bowel can be resected and tolerated as long as the terminal ileum and
ileocaecal valve are preserved.
Bowel compensation adaptive hyperplasia
Causes;
Trauma to superior mesenteric a. leading to ischaemia, necrosis
Mesenteric occlusion bowel ischaemia, necrosis
Midgut volvulus
Crohns multiple resections
In neonates NEC (necrotising enterocolitis)
Hallmark S+Ss of SBS;
Diarrhoea, steatorrhoea
Malnutrition
Fluid and electrolyte disturbances
Rx
Prevention, NUTRITION, ?TPN
Kevin
PC abdo pain
Poor historian
O/E
RIF pain on palpation
Feels unwell
Looks unwell
No vomiting
Testicular examination nil
Diagnosis?
Appendicitis
Appendicitis
Peak incidence 10-30yrs
The most common surgical emergency
Obstruction faecolith etc
Obstruction bacterial overgrowth increased intraluminal pressure
& distention
Increased luminal pressure = periumbilical visceral pain (midgut pain!)
Intraluminal pressure > capillary perfusion pressure
Inflammation of surrounding peritoneum causes somatic pain in RIF
Inflammation necrosis gangrene perforation
Perf can be walled off or free
Free perforation peritonitis septic shock
Diagnosis
Hx
Periumbilical pain (visceral)
Anorexia
N&V
RIF pain (parietal peritoneum irritated)
Fever
Leucocytosis if v.high ? gangrene/perforation
+/- reduced/absent BS
+/- diarrhoea
Urine dip microscopic haematuria is common as the appendix sits by the
ureter and can cause irritation. Gross haematuria is NOT common.
Physical examination
Lye still
Voluntary guarding
Percussion/rebound tenderness
Dunphys sign if painful
McBurneys point tenderness
1/3rd from ASIS
Rovsings
Appendicitis exam cont...
Obturator sign pain on internal rotation of the hip indicates
a pelvic appendicitis
Iliopsoas sign pain on extension of the hip indicates a
retrocaecal appendicitis
Ruptured appendix - peritonitic
Diagnosis
USS
CT
If atypical picture
Not used in children due to Ca risk
Diagnostic laparoscopy
Child bearing aged females due to the wider DD
In males if there's any doubt whip it out!
Rx
NBM
IVF
Analgesia
Antiemetics
EXPLANATION to parents+++
Lap
Open
Clint
PC abdo pain
Some weight loss recently
No night sweats
No other red flags
Severe LIF pain for some time now
T
Rigors
Leucocytosis
Diagnosis?
Diverticulitis
Diverticulitis
Is the result of a perforation of
a colonic diverticulum
Diverticulitis is a misnomer
It is actually an EXTRALUMINAL,
PERICOLIC infection due to the
escape of faeces through the
perforated diverticulum
Perforation usually sealed off
Pathogenesis
Diverticula are herniations of mucosa
through the bowel wall at points of
vascular entry by arterioles
Sigmoid colon most affected

Mesenteric border
Diverticulitis
PC
LIF pain
+/- radiation to left suprapubic, groin or back
Change in bowel habits is common
T
Rigors
Voluntary guarding
+/- Tender mass (?abscess)
Abdominal distention ileus or if a secondary small bowel obstruction
DRE painful - ?pelvic abscess
Complications see later
Diagnosis
Usually by Hx and examination
alone
If unsure;
AXR rule out obstruction
USS allows percutaneous
drainage if needed
CT if ?Ca
Do not introduce a
sigmoidoscope
Do not perform a barium enema
Rx
Uncomplicated
Abx as out-pt
These pts show a marked improvement within 48 hours of Abx Rx
Recurrent attacks
Consider surgical intervention
?Sigmoidectomy
High fibre diet
Colonoscopy after 3/52 symptom free
Complicated diverticulitis
Abscess
Usually pelvic
Pain, fever, leucocytosis, DRE
painful
Rx drainage
IV Abx
Definitive Rx may require sigmoid
resection and primary
anastomosis ~6/52 post recovery
Complicated diverticulitis
Fistula
Enterocutaneous (sigmoid to skin)
Vaginal
Bladder
Diagnosed via CT, cystoscopy
RX
IV Abx
Colonoscopy to exclude Crohns &
Ca
Resection once stable
Bladder openings - seal
independently with IDC to assist
healing
Complicated diverticulitis
Haemorrhage Generalised peritonitis
<15% of those with diverticulosis Rare
will experience bleeding, 75% stop Rx - Hartmanns procedure
spontaneously
Diagnosis
Colonoscopy
Rx adrenaline, electrocautery,
clipped
Diverticular disease
Diverticulum an abnormal sac
or pouch protruding from the
wall of a hollow organ
Diverticulosis = multiple
diverticula
The increase in diverticular
disease is directly related to the
reduction of fibre intake
Rare in those <30yrs
Edna
PC abdo pain
O/E
Severe pain
Tympanic abdomen
Distended
Hx of chronic constipation
BNO
No flatus
AXR shows a bean shaped mass
Diagnosis?
Volvulus
Volulus
the condition in which the bowel becomes twisted on its
mesentery
Partial or complete obstruction & vascular compromise
Sigmoid most affected
PC
70-80 yrs
Chronic constipation
Obstructed picture
Tympanic
Distended
+/- Ischaemia = severe pain, shock, tachycardic, rebound tenderness
Volulus
Investigations
Bloods
ABG
AXR Bean shaped bowel with
apex in LUQ
No air in the rectum usually
Volulus
Rx
Decompression - flatus tube
Rigid vs flexible sigmoidoscopy
Decompression results in a sudden
gush of air and fluid!
Confirm decompression via AXR
V.HIGH recurrence rate may
therefore need a sigmoidectomy
If no joy with decompression
Hartmanns procedure
Barny
PC abdo pain
O/E
Generalised tender abdomen
off legs
Abdo distention
BNO
No flatus
Diagnosis?
LBO
Causes of mechanical obstruction
Colorectal Ca most common cause
Intraluminal causes
Faecal impaction
Foreign bodies
Intramural
Carcinoma
Extramural
Hernias
SOL
Abscesses
Volvulus
S+Ss of mechanical obstruction
Obstipation
Cramping abdo pain
Distention intraluminal pressure > capillary perfusion pressure =
necrosis
Vascular compromise e.g. Volvulus initially venous return is
compromised, then arterial = ischaemia, gangrene, necrosis =
perforation
Important
Q. Which is worse small or large bowel obstruction?
A. Large
Q. Why
A. Colonic tumour coupled with a competent ileocaecal valve
pressure builds up within the caecum
Capillary perfusion pressure exceeded = perforation
Diagnosis & Mx of mechanical obstruction

Bloods
ABG
G+S
IVF
Analgesia
Check for hernias
DRE rectal mass/ impacted
AXR
Water soluble contrast enema
CT for inflammatory processes e.g.
Abscess. Malignancy
Colonoscopy
Stomas
Colostomy
Temporary vs permanent
Loop vs end
Loop used to rest the distal
bowel, requires a supportive
plastic stoma rod. The plastic
stoma rod is removed on day 5
post op.
End after bowel resection e.g.
Hartmanns procedure
Flush with skin
LIF
Ileostomy
Temporary vs permanent
Loop vs end
Loop used to rest the distal bowel
End following resections
Physiological considerations and practical
implications;
The ileum normally delivers ~2L of faecal
fluid to the caecum every 24 hours. Once
an ileostomy is fashioned the ileum
somehow recognises this and its absorptive
capacity increases (over several months)
thus producing only ~1L/24 hours!
Must increase fluid intake to match output
Spout due to Ileal chyme
RIF
Logistic considerations
Appropriate stoma site marked pre-op
Marked with pt standing up
Permanent marker applied
An area of no skin creases is chosen to ensure maximal skin-stoma bag seal
Stoma must be visible to the pt (pendulous abdomen)
Easily accessible for the pt
Usually placed lateral to and slightly lower to the umbilicus at the natural apex of the
abdomen
Pt counselled
Educated
Given leaflet
Explained stoma nurse will return and re-train post op
Helen
PC abdo pain
O/E;
PAIN+++
Bloody diarrhoea
Fever
Tachycardia
Rebound tenderness
Guarding
Bloods show;
Raised WCC
Raised amylase
ABG
Acidosis
PMH AF
Diagnosis
Acute Mesenteric Ischaemic
Ischaemic bowel
Inadequate blood flow bowel ischaemia
Uncommon
High mortality (>50%)
Most significant factor in survival is time to diagnosis and Rx!
Usually watershed areas affected splenic flexure and rectosigmoid
junction
Characterised according to aetiology
Acute arterio-occlusive mesenteric
ischaemia
Severe, acute, non-remitting abdo pain
strikingly out of proportion to the
physical findings
N+V
Transient diarrhoea or bloody stools
Later findings include peritonism and
shock
Disruption of blood flow by an embolus
or progressive thrombosis in a major
artery
Risk factors - AF, recent MI, valvular heart
disease, recent cardiac or vascular
catheterisation
75% of emboli are cardiac in origin
SMA preferentially affected
Characterised according to aetiology
Non-occlusive mesenteric
ischaemia
Due to arteriolar vasospasm of the
mesenteric vessel/s in response to
a severe stress such as
dehydration or shock
Digoxin causes splanchnic
constriction
Aortic surgery (clamping of aorta)
Characterised according to aetiology
Mesenteric venous thrombosis
Hypercoaguable states (factor V leiden, Protein C + S deficiency)
Best prognosis of the 3!

Regardless of the type if left untreated mucosal stress ulceration will


progress to full thickness ischaemia
PC of acute mesenteric ischaemia
Pain out of proportion to clinical findings
Pain centrally (visceral) then generalised (due to peritonitis)
Bloody diarrhoea
N+V
Fever
Raised WCC
Raised amylase
Tachycardia
Acidosis
Peritonitis
Investigations
Bloods, G+H
ABG
ECG
Erect CXR/FAST
AXR
Ischaemic bowel may show pneumatosis
intestinalis (air in the bowel wall)
CT - mesenteric angiography (contrast -
?GFR)
MRI angiography if CT angiography and
contrast CI
Laparotomy inspect the whole bowel
which may give you a pattern of the
vessel occluded
Rx of acute mesenteric ischaemia
IVF try to reverse hypovolaemia
Broad spectrum IV Abx for all
If emboli embolectomy/on-table angiography and arteriotomy
Resect necrotic bowel
Heparinise
No primary bowel anastomosis - stoma
24 hour second look laparotomy
Chronic bowel ischaemia
PC
Abdominal bruit
Weight loss
Signs of peripheral vascular disease
Post-prandial pain intestinal angina
Intermittent crampy abdominal pain
Investigations
Same as acute mesenteric ischaemia
Rx
Exercise, smoking cessation
Statin
?endovascular stent placement
?aorta SMA bypass
Inspect bowel wall post intervention to
ensure pink
Heparinise
Tony
A 65 year old male
Presents with weight loss
Anaemia
Lethargy
Change in bowel habits
Diagnosis
CRC
CRC

Common in those >50 years old


Environmental factors account for ~70% of all sporadic CRC (e.g.
diet)
Diet is the most important environmental factor known
Increased risk red meat, saturated animal fat (inconclusive
evidence)
Decreased risk fibre, fruit and vegetables (reduced transit time)
Non-dietary adenomas, UC/Crohns, acromegaly, pelvic
radiotherapy, obesity (diet related), smoking (RR 1.5-3.0)
CRC pathogenesis
CRC can arise from either one of the two following pathways;
1. Chromosomal instability two hit theory
2. Microsatellite instability
Staging and features of CRC
Clinical clues
Left sided tumours
Fresh rectal bleeding, obstruction which occurs early
Right sided tumours
Occult bleeding, altered bowel habits, anaemia, obstruction is a late feature,
colicky abdo pain, rectal bleeding (50%)
Rectal tumours
Early bleeding, mucus, tenesmus, palpable mass, Fe def anaemia
Investigations
Colonoscopy
More sensitive and specific than barium enema
Allows biopsies and polypectomy
CT
Can detect polyps 6mm
Post CRC DIAGNOSIS;
CT CAP
Pelvic MRI (anorectal Ca)
CEA (carcinoembryonic antigen) helpful in monitoring effects of Rx (chemo).
Can be normal in CRC!
Management
What does the patient want done?
Generic Mx;
MDT discussion
Cancer nurse specialists to contact pts
Stoma nurse specialist
Social workers
Psychologists
Bowel resections
Pre-op
Informed consent
Anaesthetics
Mallampati (grade 1-4), Thyromental distance
(thyroid cartilage to tip of chin, <7cm = difficult),
Teeth, CXR, ECG, Previous GA, PMH, DH & allergies,
SH smoke, Exercise tolerance
Pre-op bloods
G+H
+/- X-match
Book the patient in theatre
Other
IDC usually done in OT
Access GREEN only people!!!
Imaging
Mark the stoma site
Abdominoperineal (AP) resection
Indications
Pathology situated in the distal 1/3rd of
the rectum (within 2cm of anal verge)
Procedure
Lap versus open
Open - 2 incisions
Abdominal laparotomy
Perineal incision
Whats removed
Anus, rectum, part of sigmoid colon
End result
End-colostomy
Hints theyve had this procedure
NO ANUS!!!!
Anterior resection
Indications
Pathology situated in the middle
and/or upper rectum
Procedure
Laparoscopic
Laparotomy
Whats removed
Part of rectum and sigmoid
End result
+/- colostomy
Hints theyve had this procedure
Colostomy with AN ANUS
Hartmanns procedure
Indications
Emergency procedure for gross
contamination
Palliative
Procedure
Laparotomy
Whats removed
Part of distal colon (depends)
End result
Colostomy
Permanent versus reversal (6/12)
Hints theyve had this procedure
Have they perforated recently!!!
They have an anus!!!!
Left hemicolectomy
Indications
Pathology situated in the descending colon or
splenic flexure
Procedure
Laparoscopic
Open
Whats removed
Part of if not all of the descending bowel
Extended part of transverse colon also taken
beyond the middle colic artery
End result
Primary anastomosis
Colostomy
Defunctioning ileostomy
Hints theyve had this procedure
NAD
Right hemicolectomy
Indications
Pathology situated in the caecum,
ascending, hepatic flexure, transverse colon
Procedure
Laparoscopic
Open
Whats removed
Caecum, ascending, hepatic flexure
Beyond middle colic artery = extended
End result
Ileostomy
Primary anastomosis
Hints theyve had this procedure
Ileostomy
Total colectomy
Indications
Refractory pancolitis
Elective UC curative
Procedure
Laparoscopic
Open
Whats removed
Entire colon
End result
+/- End ileostomy
+/- Primary anastomosis
Proctocolectomy
Indications
Refractory pancolitis
UC
Procedure
Laparoscopic
Open
Whats removed
Rectum and entire colon
End result
+/- End ileostomy
+/- Primary anastomosis
Ileoanal pouch
Adjuvant therapy
Chemo
5-flurouracil and oxaliplatin
Dukes C and some high risk Dukes B cancers
Radiotherapy
Reduces recurrence risk in rectal disease if resection margins were not clear
Palliation
Palliative surgery to relieve obstruction/bleeding
Endoscopic technology stenting obstructions with metal stents
Palliative chemo
Pelvic radiotherapy for pain/bleeding/tenesmus
Prevention and screening
FOB tests - >50.
Reduces CRC mortality through early detection
Colonoscopy
Gold standard
Expensive
Risks - perforation
Flexi-sigmoidoscopy
Only reaches the splenic flexure!
Can be done in out-patients
No sedation
Lizzie
An older aged lady presents with
Tenesmus
Vague rectal sensations and
A history of constipation
A mass is noted during and after
defecation
Diagnosis
Rectal prolapse
Rectal prolapse
F>M 6:1
Peaks in women >60
Full thickness eversion of the rectal wall
through the anus
The exact cause is unclear
Intussusception theory of rectal prolapse
Pudendal nerve injury theory
Chronic constipation
Psychological disorders
Rectal prolapse S+Ss
Tenesmus
Vague rectal sensations
Pressure sensations
A long history of constipation
Mass (complete prolapse), noted
during and after defecation
A full thickness rectal prolapse will
demonstrate rectal protrusion
with concentric rings
Management
Conservative versus surgical
Surgical mx (complete prolapse)
Perineal approaches, less taxing on patients, recurrence
Abdominal approaches larger procedure therefore younger/fitter patients
Kylie
Painless dripping of bright red
blood PR
Sometimes a lump appears
when I poo!
I have an itchy bum too!
Diagnosis
Internal haemorrhoids
Internal haemorrhoids
Anal cushions are subepithelial vascular cushions
Consist of connective tissue, smooth muscle and
arteriovenous communications
Terminal branches of superior rectal artery and the
rectal veins
Theyre normal!
3 primary locations, right anterior, right posterior, left
lateral (3, 7, 11, lithotomy px)
Supported by elastic connective tissue and smooth
muscle
Become engorged during increased abdo pressure to
maintain a water tight seal
Uncomplicated internal haemorrhoids are neither
painful nor palpable
Cause painless bright red bleeding, can be drips or
spurts of blood
Can prolapse with defecation leading to mucus
discharge, faecal leaking and pruritus
Internal haemorrhoid grading and treatment
Are classified according to the extent of prolapse, which influences treatment options

Grade S+Ss Management


First Bleeding; no prolapse Dietary modifications for all
degree (increased fibre, bran, water)
Second Prolapse with spontaneous reduction Rubber band ligation
degree
Bleeding, seepage Coagulation
Third Prolapse requiring digital reduction Surgical haemorrhoidectomy
degree
Bleeding, seepage Rubber band ligation
Fourth Prolapsed, cannot be reduced Surgical haemorrhoidectomy
degree
Strangulated Urgent haemorrhoidectomy
Cause of internal haemorrhoids
Activities that increase venous
pressure;
Straining
Constipation
Prolonged sitting
Pregnancy
Obesity
With time redundancy and
enlargement of the venous
cushions may develop and result
in bleeding or protrusion
Haemorrhoidectomy
For chronic bleeding 3rd degree hemorrhoids or 4th degree
GA Lithotomy position
Proctoscope inserted
The internal hemorrhoids are then visualised and either dissected
Haemostasis
Anal pack may or may not be left in situ that will pass within 2 days
The skin defect can be left open (Milligan Morgan technique) or closed (Hil-Ferguson)
D/C home with analgesia and laxatives
Return to work within 1-2 weeks
Complications;
Early - urinary retention 20%, faecal impaction, bleeding (can also occur 7-10 days later),
subcutaneous abscess
Late anal fissure/stenosis, incontinence, fistula
Stapled Haemorroidplexy
GA Lithotomy
Anal dilator inserted
Hemorrhoid falls into the dilator
Purse strings applied to the base of the hemorrhoid
A circular stapler is then applied to the purse string
and the hemorrhoid removed
Haemostasis
D/C home with analgesia and laxatives
Return to work within 1-2 weeks
Complications
Bleeding, faecal impaction, rectal perforation, anal stenosis,
temporary faecal incontinence has also be recorded but
settles within 3/12
Sly
Acute onset of an exquisitely
painful, tense, bluish perianal
nodule
Pain seems to be reducing
especially when Im in the bath
Diagnosis
Thrombosed external
hemorrhoids
External haemorrhoids
Inferior haemorrhoidal veins
(located below the dentate line)
They are covered with
squamous epithelium - painful
Can swell discomfort and
difficult hygiene
Only cause pain if thrombosed
Thrombosed external haemorrhoids
Should really be called external haematoma
Thrombosis of the perianal venous plexus
perianal haematoma
May be precipitated by heavy lifting, straining
Acute exquisite pain, tense, bluish perianal
nodule
Pain ceases over 2-3 days as oedema subsides
Rx warm baths, topical analgesia
Surgery if the pt is seen within the first 24-
48 hours then the haematoma can be
evacuated via an elliptical incision and dry
gauze applied post op
Pat
A 45 year old male presents with pain
on defecation
He feels that the pain is most
pronounced in his posterior anus
Associated with minimal bleeding
Diagnosis
Anal fissure
Anal fissure
M+F
Usually 30-50 yrs
Mild bleeding (less than hemorrhoids)
Visible fissure
DRE painful!
Hx of constipation
A linear ulcer of the distal half of the anal canal
Usually located in the posterior midline
ONLY involve the anus, not the rectum
Painful+++ because it involves the highly sensitive squamous epithelium
Fissures that are not in the anterior or posterior midline should raise the suspicion of
Crohns, hidradenitis suppurativa or an STI
Pathogenesis
Many associated factors;
Large hard stools
Inappropriate diet
Previous anal surgery
Childbirth
Laxative abuse
Higher than normal resting anal canal pressure anal sphincter
hypertonia mucosal ischaemia
Medical Rx
1. Conservative
Sit baths ~15min twice daily
Bran or bulking agents
Proper diet
2. Topical treatments to correct anal sphincter hypertonia
Nitroglycerin causes headaches & tachyphylaxis
Diltiazem (2%) fewer side effects
Both above offer success is healing the fissure in ~70%
3. Botulinum toxin
Injected into the internal sphincter
Reduces constriction = greater blood flow and a period of time to allow the ulcer to heal
60-80% success rate
Most common SE is temporary incontinence to flatus in ~10%
Surgical Rx
Chronic fissures refractory to medical Mx
Most commonly performed technique is partial lateral internal
sphincterotomy
Local or GA
A small incision is made in the internal sphincter to relieve the spasm
Day case
Home with analgesia and stool softeners
Risks infection, haemorrhage, incontinence ~2% (must check for
incontinence prior to the procedure)
Mr Magic J
A 50 year old male with HIV
presents with vague throbbing
anal pain
A fluctuant tender swelling
Pyrexial
Diagnosis
Abscess
Abscess
M>F 3.1
Peak incidence 30-50 yrs
More prevalent in immunocompromised individuals DM, HIV
Infection anal canal gland/s
Glands normally secrete mucus which aids defecation faeces enters
the glands infected abscess
Causes;
Most common is a non-specific infection of cryptoglandular origin (crypts of
Morgagni)
Crohns
Abscess
Infection originates in the
intersphincteric plane, most likely
in one of the anal glands
The intersphincteric plane is the
plane between the internal and
external, remember the external
wraps around the internal
This may result in a simple
intersphincteric abscess or it may
extend vertically upward or
downward, horizontally or
circumferentially with varied
clinical presentations
Clinical presentation of various types of
abscesses
1. Intersphincteric abscess
Is limited to the primary site of origin
May be asymptomatic
May result in throbbing pain
2. Perianal abscess
Results from the vertical downward
spread of the intersphincteric
infection to the anal margin
Tender, fluctuant swelling
3. Intermuscular abscess
4. Supralevator abscess
5. Horizontal spread
6. Circumferential spread
Treatment
I+D
If simple use LA otherwise GA
Ensure theres no fistula
Digitalised to break down loculations
Washed out - copious saline or hydrogen
peroxide
Left open - heal by secondary intention
Packed and changed regularly by nurse
PO/IV Abx
Follow up
Beware the neglected abscesses nec
fas/Fourniers
Failure to respond post I+D may indicate
residual pus, fistula or immunocompetence,
these pts require a CT/MRI
I+D risks
Bleeding
Infection
Sphincter mechanism damage
Potential for faecal incontinence
Fistula in ano formation
Recurrence
Urinary retention
Even with I+D ~60% will develop a fistula in later life and ~ 30% will
HAVE a fistula o/e
Hughie
An upset man presents with
Constant anal drainage
Previously treated surgically for
a perianal abscess
On DRE a palpable nodule in the
anal canal is noted
My brother has some sort of
gut problem
Diagnosis
Fistula
Fistula presentation and evaluation
Presentation;
The first presentation may indeed be an abscess
Constant anal drainage
Examination
Palpable induration running from external opening to internal anal opening
DRE +/- palpable nodule in the anal canal (the primary opening)
A probe can be passed, gently, from external to internal
Fistulas
Primary fistula the result of an abscess
Secondary Crohns, malignancy, hidradenitis suppurativa, TB
The internal opening most commonly located at the dentate line
where anal glands enter the anal canal
Continued drainage following Rx of an anal abscess ?fistula
Parks classification of fistulas in ano
A. Intersphincteric (most
common)
B. Trans-sphincteric
C. Suprasphincteric
D. Extra-sphincteric (least
common)
Goodalls rule
States that;
A posterior external fistula will
enter the anal canal in the posterior
midline
An anterior fistula will enter the
anal canal at the nearest crypt
(usually within the dentate line)
A fistula >3cm from the anal
verge may have a complicated
upward extension and may not
obey Goodalls rule
Management
Should include the following steps;
1. Under GA palpate locate the external and internal opening
2. Drainage of the primary intersphincteric track, and any other
located tracks
3. Close follow up of the wound by patient and the wound care
specialist
Setons
Q. What are they?
A. Non-absourable monofilament sutures or silk
placed in the fistula track
Q. How many types are there?
A. Two. A cutting seton and a draining seton
Q. How do they work?
A. A draining seton is placed through the track, tied
loosely and left in situ track remains patent
allows drainage and healing of track. Seton removed
2-3/12 later track may heal spontaneously or can
then be assessed properly
A cutting seton is tied tightly and subsequently
tightened every 2 weeks for ~8 weeks. Track heals by
fibrosis until it finally either cuts through the skin,
hopefully obliterating the track
Risks pain, bleeding, incontinence (~12%),
recurrence (~6%), delayed healing
Fistulotomy
Conventional fistulotomy the
track is located and then laid
open by cautery secondary
intention. Relatively
contraindicated if the fistula is
high (involves a large amount
of the external sphincter)
Risks pain, bleeding,
incontinence (4-12%),
recurrence (1-12%)
Fistulectomy
Fistulectomy the entire fistulous tract is identified and removed.
The wound can then be laid open, closed primarily with sutures or
closed with a flap
Risks pain, bleeding, incontinence, recurrence
Kev
A young male presents with
A painful
Erythematous
Fluctuant mass
Its just at the top of my crack!
Diagnosis
Pilonidal sinus
Pilonidal sinus
A pilonidal sinus is a small tract
present in or near the natal cleft
Typically young hairy men
Painful fluctuant mass
Hair seems to play a central role
in the process of infection and
perpetuation of granulation
tissue in sinuses
The exact pathogenesis remains
elusive
Treatment
Acute treatment
Most can be managed with LA I+D
If not then GA
The sinus tracts are then
obliterated
Irrigated +++
Wound is either closed, partially
closed or left open to heal by
secondary intention
Risks pain, haemorrhage, scar,
infection, need for meticulous
cleaning if left open, recurrence