Abdominal Case Study Compiled

Patients
Age
name: Mr A
: 42 years old
Race: Malay Gentleman
RN : 22111379
Date of admission: 14/03/2016
Presenting Complain
Right sided abdominal pain
associated with fever.
History of Presenting
Complain
1) Persistent right sided abdominal pain

for 1 day.
The pain is at the right hypochondriac region
sudden onset
sharp pain
The pain gradually worsening and radiate to
right iliac fossa
pain even when resting
He did not take any medication
He rated the pain with a score of 7/10.
associated with fever
2. Fever for 1 day

On and off fever
No chill and rigor
Excessive sweating until the whole bed was
sweat.
Paracetamol to relieve the fever
No
vomiting
No diarrhea
No loss of appetite
No loss of weight
No change in bowel movement
No jaundice
Dark urine ?Pale Stool?
Systemic review
No urinary symptoms
no chest pain,no shortness of breath,
no edema,ankle swelling, palpitation
or reduce effort tolerance.
no bleeding and bruising tendencies.
He did not notice any lumps on any
parts of his body.
Past Medical History

He
had pancreatitis on February

when he presented with abdominal
pain at the epigastric area that
radiate to the back, vomit out food
for 2 to 3 times and fever with chill
and rigor for 4 days. He reject the
treatment in hospital.Then, he was
discharged with analgesia and
follow up in the hepatobilliary clinic
in UM.
He
was newly diagnosed with type 2

diabetes one month ago and was
having oral medication (metformin).
He had multiple eyes surgery as he
had blindness since 4 years old.
No asthma, no hypertension, no
dyslipidemia, no ischemic heart
disease.
No past surgical history
No know drug or food allergy
Family History
His mother had diabetes, hypertension and kidney
stone
Social History
He was married with 3 children and divorced 3
years ago. All the children was with his ex wife.
He lives in Taman Melawati alone.
He is a teacher in St John school
He did not smoke
He was a social drinker but quit 15 years ago.
No financial problem.
Drug History
Metformin, no supplemental medication and no
traditional medicine.
EXAMINATION OF ALL SYSTEMS

On
general inspection,Mr A was

Lying supine on the bed with the
head supported by 1 pillow
Alert and conscious
No respiratory distress
Has a branula attached at the
right and left dorsum
Infusing sodium chloride 0.9%
Vital signs
RR: 20 breath per min
BP : 144/86 mmHg
PR : 86 beats/min
T : 37C
SpO2 : 100% in room air
Peripheral examination
Warm
periphery, capillary refill < 2

s , no palmar erythema, no finger
clubbing, no dupuytren's
contracture,no scratch marks and
injection site, no conjuctiva
pallor,no sclera jaundice. Good oral
hygiene and no glossitis, no
angular stomatitis,no
lymphadenopathy,no pitting
edema.
Abdominal examination
Soft
and tender at the right hypochondriac and

right iliac fossa
No dilated vein
No surgical scars
No umbilical hernia
No abdominal distension
No Murphys sign
No hepatomegaly
No splenomegaly
No ballotable kidneys
No shifting dullness
Normal bowel sound
RELEVANT
INVESTIGATION(S
Abdominal AP erect x ray
Chest PA erect
Ultrasound abdomen
Management
Broad spectrum antibiotic- IV
metronidazole
2. Fluid resuscitation and correction of
electrolyte imbalance
.NS 0.9%
3. Stone extraction
4. Midazolam
5. Supplement vitamin
6. Encourage orally
1.
Oesophagus
gastro-esophageal reflux
disease(GERD)
definition
the
term GERD is apllied tp

patients with symtops suggestive
of reflux or complications thereof,
but not necessarily with
oesophageal inflamation
a guideline issued by Amerian
College of Gastroenterology
defines GERD symptoms or
mucosal damage produced by
the abnormal reflux of gastric
content into the oesophagus.
Physiological vs
Pathological
pysiological
typically
occur post-prandial, short,

asymptomatic, and rarely occur during
sleep.
pathological
associated
with symptoms of mucosal

injury, often includes noctural
episodes.
minor patiens can have reflux
oesophangitis secondary to GERD but
risk factor
obese
alcohol & smoking
spicy & fatty food.
aetiology
early stage:
increase TLES
relaxation.
severe: LOS pressure low cousing
loss of sphinter function.
worsen by loss of adequate length of
intra-abdominal oesophagus( leads
to sliding hernia)
clinical features
triad:
retrosternal
heartburn(postprandial),
epigastric pain,
regurgitation( bitter or acidic
taste)
others: odynophagia(hot
beverage, citrus drink or alcohol),
nausea, hypersalivation.
less typical symtomps: anginal
cheat pain, pulomonary or
Diagnosis
assumed
rather than proven,

treatment is emperical.
investigation only required when
patient does't respond to PPI or
have dysphagia.
endoscopy with biopsy
diagnosis:1. 24h ph
recording(gold standard)
:2.manometer- to
measure
pressure at LOS
MANAGEMENT
medical
vs surgical
MEDICAL
counter drug(antacid)
lifestyle changes
proton pump inhibitor(8 week), step
down policy after that.
SURGICAL
indicated in patients choice, failure of
PPI includes volume reflux, hermit
lifestyle, poor compliance
type
of surgery:
total(Nissen's), partial(Toupet)
fundoplication
Besley operation- thoracic
aprroach
the Hill operation
complication
stricture
lower end oesophagus

esophagus shortening
Barret's esohagus
reflux esophangitis
sliding hiatus hernia
carcinoma esophagus
BARRETT'S OESOPHAGUS
Clinical
features:
initialy symptoms associated with
GERD, most of them donthave any
symptoms, but they do hav the most
abnormal pH profile.
DIAGNOSIS
Begin
with simple columnar

epithelium that become
specialized with time, hence
endoscope and biopsy is ideal for
diagnosis.
barrett's epithelium consist of
mucus-secreating goblet
cell( intestinal metaplasia)
barrett's esophagus vs tubular,
sliding hiatus
1.
gastric mucosal folds, has

longitudinal fold in a case of hernia.
2.columnar lining of barrett's is
smooth
3.srticture may occur in barrett's
oesophagus and commomly at the
squamo-columnar junction.
increase risk of adeno carcinoma
regular endoscopic with multiple
biopsy recommende for early
detection of malignancy. as invasive
malignancy may present without any
percipitating symptoms like GERD.
2 year interval endoscopeis provided
no dysplasia detected.
MANAGEMENT
laser,
photodynamic therapy,
argon-beam plasma coagulation
and endoscopic mucosal
resection(EMR) are recomended
treament together with high dose
PPI or anti reflux operation.
COMPLICATION
ulceration
in the columnar lined
segment
stricture formation
dysplasia & susequent carcinoma
esophagus.
carcinoma of the
oesophagus
epidemology
6th
most common cancer in the

world, mid to late adulthood, poor
prognosis
divided into 2 type squamous cell
carcinoma and adenocarcinoma.
squamous cell carcinoma

affect upper
common
risk
2/3 of the esophagus
factors:tobbaco,alcohol,dieterary,bet
elnut cheawing,underlying
disease( achalasia,esophageal
diverticuli, and webs ,plummervinson syndrome and HPV infection)
endoscopy can miss the lession if not
grossly involved, ulcer/fungatting
growth might be seen.
adenocarcinoma
lower
1/3 of oesophagus
rising trend
risk factor: obesity, GERD, Barrett's,
smoking
Adenocarcinoma arising in barrett's
may present as ulcer, a nodule, and
altered mucoasal pattern, or no
visible endoscope abnormalities
history
symptoms coused by local effects:
early-non specific dyspeptic or
feeling something not right,

progressive dysphasia from solid to
liquid, cough regurgitation, vomiting,
odynophagia, loss of appetite, weight
loss, upper gi bleed
symptoms
related to invasion of the

surronding structure
respiratory fistula
hoarness of voice
Horner's syndrome
symptoms
related to distant disease:

metastatic disease to the lung, liver,
bone brain
hypercalcemia-paraneoplastic
syndrome in SCC.
Physical Examination
shows
cachexia, patient with muscle

wasting
palpable neck node especially
supraclavicular region
liver maybe palpable ig metastasis
present
lungs- finding suggestive of pleural
effusion
MANAGEMENT
to
confirm diagnosis- endoscopy

and biopsy
general assesment and staging:
a) potential curative-radical
surgery or chemo-radiotherapy
for squamous cell carcinoma,
especially for ealry
disease( T1/T2,N0)
patient
suitable for potential curative therapies

should proceed to staging investigation, look for
haematogenous spread( ct scan chest/abdomen)
then asses locoregional stage using endoscopic
ultrasound(EUS)
blood test- rduced haemaglobin, abnormal liver
function test
bronchoscopy- to asses the pulmonanry in vasion
laparascopy
b)
palliative therapy-unfit,locally advanced,

refused radical surgery patient.
c)
prognostic factor
depth of tumour penetration through wall
reginal lymph node spread.
TREATMENT
SURGERY
main
treatment for patient with carcinoma

surgery alone is best suited to patient with
disaese confined to the
oesophagus(T1,T2) without node
involment(N0)
neoadjuvant therapy helps operability and
survival rate.
3 methods
a) modified Ivor-Lewis
b) McKeown
C)Transhiatal Esophagectomy
MALLORY-WEISS SYNDROME
Introduction
characterisied
by upper gi bleeding
secondary to logitudinal mucosal
laceration at the gastroesophageal
junction at gastric cardia(90%) or
esophagus(10%), usually produced
by forcefull explosive vomitting( after
alcohol consumption)
risk
factors:
retching,
vomitting,starining,hiccuping,coughing,
hiatus hernia
history:
haematemesis following about of
reatching or vomiting
meleana,snycope, and abdominal pain can
present
Physical
examination
tachycardia,hypotension,orthostatic
changes, overt changes maybe evedent.
Diagnosis
endoscope
FBC
coagulation
profile
blood urea serum electrolyte
rule out boerhaeve syndrome,
esophangitis, gastric ulcer
don't do barium studies-low diagnostic
sensitivy and interfere endoscopic
assesment and therapy
MANAGEMENT
ACUTE-nil
by mouth,NG tube if vommiting,

monitor vital sign, stabelise the
patient.control or eliminate the
percipitating factor
ONCE STABILISED
a) endoscopic management
tears with a clean, fibrinous base or with
flat, pigmented spots are not treated,as
the risk of reebleading are minimal
epinephrine injection
hemoclipping
surgery rarely indicated
PERFORATION
barotrauma(spontaneous
perforation, boerhaave
syndrome):
occur classicaly when vomit
againsta clossed glottis
pressure in crease and brust at
the lower 3rd, cousing
esophageal content leakage in to
the mediastinum and the pleura
cavity
can lead to mediastinitis if left
history:
severe
pain in chest or upper abdomen

following a meal or a bout of vommiting
shortness of breath
maybr miss diagnised with MI, perforated
peptic ulcer disease or pacreatitis
physical examination
rigid upper abdomen
diagnosis:
history+pe
chest x-ray with air in mediastinum or
peritonium
pleural effusion
TREATMENT
the
aim of treament is to limit

mediastinal contamination and
prevent or deal with
infection(mediastinitis)
general guideline for non-operative
management(image guided drainage)
include:
a)pain that is readily controlled with
opiates
b)absencse of crepitus, diffuse
medistinal gas, hydropneumothorax or
pnemoperitoneum.
c) no eveident of on going esophageal
the
decision
between operative
an non operative
management rest
on four factors
factors
conservat
ive
surgical
site
cervical(ne
ck)
thoracic/ab
dominal
event
causing
spontaneo
us
intsrument
al
underlying
patho
benign
malignant
esophageal fasting/em
content
pty
food
content/
residue
STOMACH
Peptic ulcer disease
Definition
Disruption
of the mucosal integrity

of the stomach/ duodenum cause by
local inflammatory , decrease
mucosal resistance or hyper acidity
which leads to well define mucosal
defect (ulcer).
Gastric ulcer due to decrease
resistance of gastric mucosa.
Duodenal ulcer predominantly due
to hyperacidity.
RISK FACTORS
H.Pylori
infection
Penetrates protective surface of mucous

Production of urease, protease, phospholipase,
cytotoxicity
NSAIDs
: inhibits prostaglandins
Reflux : Pancreatic enzymes through pylorus
Age : Reduced surface cell turnover and
generalized mucosal atrophy
Smoking : increase vagal activity and gastric
mucosal atrophy
Alcohol, stress, hyperparathyroidism, blood
group O
63
CLINICAL FEATURES
Cannot differentiate the type based on
symptoms
Pain
: epigastric gnawing, may radiate to

back, intermittent, hunger pain (DU) or
increase with eating (GU)
Vomiting : if stenosis occurred
Alteration of weight : LOW or weight gain
Bleeding : hematemesis or melena or
anemia
Criteria
Peptic ulcer
Duodenal ulcer
Introduction
less common
4 time more common
Age
More the 40 years
20-50 years
Sex
Equal in both sex
More in male
Location
Mostly occur near the

lesser curvature
especially the
incusura angularis
Mostly occur in the 1st

part of duodenum
Abdominal Pain
Pain while eating and

relived by vomiting
Pain before meal and

at middle of the
night . Relived by
taking food.
Episodes of pain
Relatively short in
duration
Relatively longer in
duration
Vomiting
Commonly occur after Uncommon unless

each meal.
there is gastric outlet
Coffee ground
obstruction.
Acidic vomiting
Complication
Upper gastrointestinal bleed

Perforation
Gastric outlet obstruction
Gastric malignancy
Investigation
FBC,
RP, amylase H.pylori testing
1. Non-invasive Serological test, hydrogen breath

test
2. Invasive rapid and biopsy urease test, culture
Endoscopy-
Esophageal gastro-duodenoscopy
(OGDS) and biopsy. (to exclude malignancy)
Radiology- Chest X-ray and abdominal
radiographs (perforation).
Serum gastrin level and gastric acid analysis
in patient suspected to have Zollinger-Ellison
syndrome.
66
Management
Short-term management
2. Long-term management
1.
Intermittent treatment
Maintenance treatment
Surgical treatment
Short-term management
General
measure
Avoid smoking
Avoid aspirin and NSAIDs (or use less damaging
agents like ibuprofen)
Alcohol to be moderate
Medical
treatment
Antacid Symptomatic relief

. Sodium bicarbonate, MgSo4, AlOH
Histamine H-receptor antagonists

. Inhibit of acid pepsin secretion by blocking H2-receptor
. Cimetidine, ranitidine, famotidine and nizatidine
Proton pump inhibitors

. Irreversible inhibition of acid secretion by the proton
pump.
. Omeprazole, lansoprazole, pantoprazole, rabeprazole
Sucralphate
. Form a protective coating for the ulcers
Misoprosol
. Used to antagonize NSAID induce peptic ulcer
H.pylori
eradication (Triple therapy)
Consists of 2 antibiotic (amoxicilin,

clarithromycin, and/or metronidazole.
plus a proton pump inhibitor.
bismuth
Long term management

Intermittent
treatment
For symptomatic relapse more than

four time a year.
4 week course of one ulcer healing
agent
Maintenance
treatment
Symptomatic relapse > 4 time a year

When risk of complication is low,
operation must be avoid.
With H2-receptor antagonists
Surgical
treatment
Gastric ulcer Partial gastrectomy with

Billroth 1 anastomosis.
Duodenal ulcer
. Truncal vagotomy plus pyloroplasty or
gastroenterostomy.
. Selective vagotomy with pyloroplasty
. Hight selective vagotomy.
COMPLICATIONS
Perforation
Obstruction
Malignancy
Bleeding
PERFORATION
Usually
occurs in acute ulcers on

the anterior wall of duodenum.
CF acute, severe unremitting
epigastric pain, vomiting, tender
and guarding of abdomen
(peritonitis), pale or shocked
Investigations : x-ray free air
under the diaphragm, moderate
hyperamylasaemia
Management
Resuscitation and antibiotics

Operation
Duodenal ulcer : simple closure and application

of an omental patch, then eradication therapy
Gastric ulcer : biopsy, simple closure, omental
patch
Conservative
treatment
Too ill and present late for surgery

Nasogastric suction, eradication therapy, IV
fluids
OBSTRUCTION
CF
Sensation of fullness, constant and

dull epigastric pain, Projectile vomiting,
weight loss
PE Signs of dehydration and weight
loss, visible peristalsis, succession splash
Management Nasogastric aspiration
(large volume non-bilious gastric
contents
Pyloroplasty
Gastrojejunostomy
Anterectomy
BLEEDING
CF
UGIB
Management
Resuscitation
Risk assessment
FORREST CLASSIFICATION
RISK
OF REBLEEDING
Stigmata or Recent Hemorrhage
(SRH)
Major SRH : Forrest 1a, 1b, 2a, 2b
Minor SRH : Forrest
2c, 3
CLASS 1 : ACTIVE BLEEDING
A
SPURTING
OOZING
CLASS 2 : NO ACTIVE BLEED
VISIBLE BLOOD VESSEL
OVERLYING CLOT
HEMATIN COVER BASE

CLASS 3 : CLEAN ULCER GROUND
ROCKALL RISK
ASSESSMENT
COMP
SCORE
ONEN
T
AGE
<60
60-79
>80
HR>100
SYS BP
>100
SYS BP
<100
SHOCK HR<100
SYS BP
>100
COMO
RBIDIT
Y
NONE
DX
MWT
SRH
MINOR
TOTAL
IHD, CCF,
CA
ALL
OTHERS
SCORE
RF, LIVER
3
DISEASE,
DISSEMINATE
D CA
MALIGNANC
Y OF UPPER
GIT
MAJOR
2
11
MANAGEMENT
Endoscopic
intervention
Within 24 hours (major SRH)

Thermal
heater probe, laser

Injection Adrenaline (4-16ml
1:10000)
Prolonged vasoconstriction + platelet
aggregation + local tamponade effects
Mechanical
clips, band ligation,
staples
Combination
80
FOLLOW UP
Discharged
with oral PPI :

Omeprazole 40mg BD for 6
weeks
Re-endoscope in 6 weeks to
assess healing and rule out
malignancy
H.Pylori positive : eradication
Acute Gastritis
Inflammation
of stomach lining
Imbalance between aggressive
and defensive factors
maintaining the integrity of
gastric mucosa
Causes: NSAIDs; alcohol; bile;
ischaemia; infection; acute stress
(shock); autoimmune
82
TYPES OF
GASTRITIS
ETIOLOGY
TREATMENT
1. STRESS
GASTRITIS
Common complication of - Prevention is easier

serious illness, injury or
than treating
- H2-receptor
major surgery or
comorbidity. Most found
antagonist
in ICU
sulfacrate (in ICU
Characterized by
patient)
reduction of blood supply
to the superficial mucosa
2. EROSIVE
GASTRITIS
Caused by agents that

disrupt the gastric
mucosal barrier. (NSAIDs
and alcohol)
- Most bleeding
settles
spontaneously
- Acid suppression
by PPI and H2 RA
3. REFLUX
GASTRITIS
Caused by enterogastric
reflux (common after
gastric surgery or
cholescystectomy)
- Bile-chelating
agent or prokinetic
agent
- Operate in severe
cases
TYPE OF
GASTRITIS
ETIOLOGY
MANAGEMENT
4. TYPE A
GASTRITIS
Autoimmune condition in
Screening
which there are circulating
endoscopically
antibodies to the parietal
cell.
Results in atrophy of parietal
cells, hypochlorhydria and
achlorhydia
5. TYPE B
GASTRITIS
H.Pylori infection : infection

aquired mainly in childhood
and inversely proportionate
to the socio-economic status
Can cause gastric cancer
- H.Pylori
eradication
- Endoscopic
screening
Symptoms and Signs
pain
Abdominal discomfort
(dyspepsia)
Nausea
Vomitting
Haematemesis
Melaena
Complications
Epigastric
Mild
tenderness at
epigastric region
Scarring
and
narrowing of stomach
outlet (pyloric
stenosis)
Stomach ulcer
Stomach CA
Decreased production
of intrinsic factors
(symptoms of
anaemia)
85
Treatment and
Management
Fluids
and electrolytes replacement as

required if presented with vomiting
Discontinue use of drugs such as
NSAIDS
Antacids (Aluminium and magnesium
hydroxide; Rulox)
H2 blockers (Ranitidine, Cimetidine)
PPI (Omeprazole)
Antibiotics (Amoxicillin, Tetracycline,
Metronidazole, Clarithromycin)
86
Gastric cancer
Epidemiology
Second most common cancer
worldwide and causing death.
Increase freuancy after 50myears
old, male > female
Malaysia : 7th commonest cancer
in male
Risk factor
Risk factor
Precancerous lesion
Chronic atrophic gastritis

Partial gastrectomy
Pernicious anemia
Menetrier disease
Chronic gastric ulcer
Gastric polyps
Infection
H Pylori
Diet
Excess intake of salt and nitrosamine

compound
Low intake ascorbic acid
Alcohol
Other
Smoking
Family history
Clinical features
Early
Late
Complication
Vague symptoms
Indigestion
Abdominal pain
-abdominal pain tends
to be vague and mild
early in the disease
Bloating
Flatulance
Decreased appetide
Fatigue
Early satiety
Feeling abdominal
fullness
Marked weight loss
Epigastric mass
Abdominal pain
Hematemesis
Anemia
Metasatasis
Jaundice
Left supraclavicular
mass
Ascites
Pleural effusion
Spurious diarrhea
Physical examination
General
Abdomen
Per rectal
Pallor (anemia)
Cachexia
Juandice
Enlarge lymph node:
Virchows nodes
(troiser sign)
Epigastric mass
Hepatomegaly
Periumbilical
metastasis
Ascites
Blemur shelf
( shelflike tumor of
the anterior rectal
wall indicating
implantation
metastases in
Douglas pouch as in
gastric carcinoma..
Mode of spread
Direct
Lymphatic
Blood borne
Transperitone
al
The tumor
invades
muscularis,
serosa and
ultimately
adjacent organ
like liver,
pancreases and
colon gasro
colic fistula
formation.
Spread via
submucosal and
subserosal
lymphatic
plexus common
mode for
diffuse type of
gastric cancer.
First to liver,
then to lungs
and bone
uncommon in
the absence of
nodal disease
Common mode
of spread once
the tumor has
reached serosa
of stomach may
present with
ascities
Krukenberg
tumor
Investigation
Baseline
FBC : anemia,
BUSE : electrolyte imbalance,
LFT : nutritional status (albumin) and liver
mastestasis
Tumour marker : carcinoembryonic antigen (CEA)
and cancer antigen.
Diagnostic
Esophageal gastro-duodeno scopy (OGDS)

. Visual inspection and biopsy
Staging
CT thorax abdomen
pelvis
Assess the local disease prosess

Local tumour invasion
LN involvement
Distant metastasis
Laparoscopy
To detect small intestine metastasis
Endoscopic US
More precise preoperative assesment of the

tumour staging and depth of penetration.
Management
Radical
total gastrectomy
Removal of entire stomach, nearby

lymph node + distal part of easophagus,
proximal part of duodenum and
surrounding structure with mestastases.
Subtotal
gastrectomy
For the tumaor distal stomach

Removal of : part of the stomach contains cancer,
nearby lymph node, and part of other tissues and
organs near the tumour. Spleen may be remove.
Billroth II remaining stomach will be anestomosed
with remnant of the jejunum.
Esophagogastrectomy
Tumor of the cardia and

gastroesophageal junction
LIVER
Liver Abscess
TYPE
PYOGENIC
AETIOLOGY
Streptococcus milleri
Escherichia coli
Streptococcus faecalis
Proteus vulgaris
MODE OF SPREAD
Haematogenous/ penetrating trauma/ direct

spread from surgery
RISK FACTORS
Elderly, diabetic, Immunosuppressed state
COMMON
PRESENTATION
Symptoms: malaise, intermittent fever, RUQ

pain
Sign: palpable liver and Right subcostal
tenderness
INVESTIGATION
(CONFIRM
DIAGNOSIS)
Ultrasound/ CT scan: moltiloculated cystic

mass in liver
Aspiration for culture and sensitivity
TREATMENT
Antibiotic (penicillin+
aminoglycoside+metronidazole /
cephalosporin+metronidazole)
Extra: Hydatic Liver Cyst

TYPE
TYPE
PYOGENIC
AETIOLOGY
Echinococcus granulosus (tapeworm)

is present in the dog intestine
PATHOGENESIS
Ova is ingested by human and pass in the

portal blood to the liver
COMMON
PRESENTATION
upper abdominal discomfort
PYOGENIC
AETIOLOGY
Streptococcus milleri
INVESTIGATION
Ultrasound: moltiloculated cystic mass in liver
coli
(CONFIRM Escherichia
CT scan: floating
membrane within the cyst
DIAGNOSIS)
on CT scan
Streptococcus
faecalis
Serology(ELISA):
antibodies to hydatid
antigen
TREATMENT
Albendazole puncture of cyst under image

guidance aspiration of the cyst content
instillation of hypertonic saline in the cyst
cavity reaspiration (PAIR)
Surgery: liver resection or local excision of
the cyst
GALL BLADDER
STRUCTURE OF BILIARY SYSTEM

CALOTS
TRIANGLE
= lower edge of
liver above,
cystic duct right
& CBD left
Significance:
contain cystic a.
which supply
gallbladder ->
need to be
ligated in
cholecystectomy
Gall Bladder
Pear shaped
7.5-12 cm long
Capacity of 25-30 ml
Divide into fundus, body and neck
FUNCTIONS OF GALL BLADDER

1. Reservoir for Bile
- Fasting : resistance to flow through sphincter of Oddi
is high
bile excreted by liver diverted to gall
bladder
- Feeding : resistance is reduced
contracts and bile
enters duodenum
gall bladder
2. Concentration of bile
- By active absorption of water, sodium chloride,
and bicarbonate by mucous membrane of gall bladder
3. Secretion of mucus
- Produce approximately 20 mL per day
METABOLISM OF BILIRUBIN
ENTEROHEPATIC CIRCULATION
GALLSTONE (CHOLELITHIASIS)
MAIN CAUSE :
1. Changes in concentration of different constituent of bile
2. Biliary stasis
3. Infection
RISK FACTORS (4 F : female, fat, forty, fertile) :
4. Obesity
5. Increasing age
6. High in fat diet
7. Pregnancy /OCP
8. Chronic Hemolysis (sickle cell anaemia)
9. Primary Biliary Cirrhosis
10.Chronic Biliary Tract infection
PATHOGENESIS
1. Lithogenic bile
Bile salts & phospholipids in bile keep cholesterol in solution
normal ratio bile acid to cholesterol is 20:1, when ratio falls to below 13:1
higher chance of gallstone
Causes of decreased bile salt
Primary biliary cirrhosis

OCP/estrogen
Low 7a-hydroxylase
Ileal disease/ileal resection
(decreased enterohepatic
circulation)
2. Nucleation
Cholesterol
crystal formation
3. Stasis
Prolonged fasting
TPN
Pregnancy
Trauma (burn), surgery
Causes of increased cholesterol
Obesity with high cholesterol diet
Types of Stones
A.
B.
C.
D.
Cholesterol stones (15%)

Pigment stones (5%)
Mixed stones (80%)
Calcified stones
CLINICAL PRESENTATION:
Abdominal Pain
S RUQ / epigastric
O Sudden, intermittent
C Sharp
R radiate to scapula
A sometimes associate with nausea vomiting
T can last from 30 min to 5 hrs
E aggravate after eating especially high fat meal
S - severe
DIAGNOSIS :
1. Ultrasound
2. Plain film x-ray
May detect cholesterol stones and pigment stones
MANAGEMENT :
-. Cholecystectomy
Symptomatic gallstone disease
Asymptomatic gallstone when there is reasonable likelihood for
future complications
CHOLEDOCHOLITHIASIS
Stone in common bile duct ->
obstructive jaundice
2 types of stone:
Primary brown pigment stone
due to bile stasis, form
spontaneously in duct
Secondary black pigmented
stone originating from
gallbladder
Same risk factors and epidemiology
as cholelithiasis
Increases with age
Clinical presentation
Intermittent painful obstructive
jaundice dark urine, pale
stool, itchiness
Nausea & vomiting
WHAT HAPPENED IN OBSTRUCTIVE JAUNDICE?
DARK URINE
PALE STOOL
COURVOSIERS LAW
Painless jaundice in the presence of palpable gall bladder is

not due to stone (and therefore likely to be caused by
tumour)
- Stone will cause fibrosis, so gallbladder will be shrunken
Exceptions:
Double impaction of stone (one in CBD, another in cystic
duct)
Stone obstructing ampulla of Vater
Stone with primary oriental cholangiohepatitis
Mucocoele of gallbladder
Causes of palpable gallbladder
Mucocoele
Empyema
Obstructive jaundice due to
pancreatic Ca
Gallbladder Ca
INVESTIGATIONS
LFT increase bilirubin, ALP
Coagulation profile increase PT, APTT (due to vit K

malabsorption)
Renal profile bilirubin is nephrotoxic
Urinalysis may detect urobilinogen
Ultrasound dilated CBD (8mm), acoustic shadow
ERCP/MRCP
MANAGEMENT
Conservative rehydration, monitor vital signs
Definitive ERCP (stenting to drain bile, endoscopic

basketing and stone retrieval)
ACUTE CHOLECYSTITIS
Acute inflammation of gall bladder
Aetiology:
Calculous - 90% caused by gallstone obstruction
Acalculous related to bile stasis (critical illness, prolonged fasting,
TPN, sepsis, major surgery or severe trauma/burns)
Clinical presentation
Severe RUQ pain, after meal
Fever, Nausea, Vomiting
Positive Murphys sign
Investigations
Ultrasound thickened gallbladder, acoustic shadow
Management
Conservative NBM, IV fluid, analgesic, antibiotics
Definitive delayed cholecystectomy after 6 weeks
CHRONIC CHOLECYSTITIS
Chronic inflammation leading to
thick walled and shrunken gall
bladder
Impalpable gall bladder
Can be asymptomatic or recurrent
low grade pain
ASCENDING CHOLANGITIS
Ascending bacterial infection of biliary tract in association
with partial or complete obstruction of bile ducts
Aetiology:
Gallstones (most common)
Others stent, stricture, tumor, choledochal/biliary cyst
Clinical presentation ( Charcots Triad)
Fever
Jaundice
Severe RUQ pain
Complication : Acute Suppurative Cholangitis (Reynold Pentad)
Charcots Triad + Altered Mental Status + Hypotension
This is EMERGENCY!! need to drain the bile duct
urgently, either by surgical or endoscopic sphincterotomy
LABORATORY RESULT :
1. Elevated AST/ALT from obstruction (>1000)
2. Elevated Bilirubin
3. Elevated WBC
IMAGING
4. US and CT show dilatation of ducts
5. ERCP is gold standard
MANAGEMENT
1. Conservative antibiotics, fluid resuscitation, correct electrolyte
imbalance
2. Drain the bile as soon as patient stabilized
- Percutaneous transhepatic biliary drainage (PTBD)
- Endoscopic biliary stent
Pancrease
Pancreas
Retroperitoneal organ
Anteriorly is the ; Stomach
On its right ; joins the Biliary system
Weighs approx 80g
Main duct is lined by columnar epithelium
Ductules are lined by cuboidal epithelium
Neuroendocrine cells ; Islets of Langerhans ; A cells (20%)

(produce glucagon) ; B cells (70%) (produce insulin) ; remainder
are D cells (produce somatostatin)
Within the islet, B cells form an inner core ; capillaries

draining the islet cells drain into the portal vein ; creating a
pancreatic portal system.
Anatomy
Head
( lies within the curve of duodenum )
Neck
( superior mesenteric vessels & aorta)
Body
Tail
( splenic hilum)
Pancreas
Acute Pancreatitis
IEP (interstitial edematous pancreatitis)
NP (necrotizing pancreatitis)
<GET SMASHED>
Chronic Pancreatitis
<TIGARO>
Acute Pancreatitis
Diagnosis ( 2 out of 3 criterias)
1.
Abdominal pain consistent with acute pancreatitis (acute onset of a

persistent, severe, epigastric pain, often radiating to the back)
2.
Serum lipase activity (or amylase) at least 3 times greater than the
upper limit of normal
3.
Characteristic findings of acute pancreatitis on contrast-enhanced

computed tomography (CECT) and less commonly magnetic resonance
imaging (MRI) or transabdominal ultrasonography.
Acute Pancreatitis
x 2 types : 1.
IEP ( Interstitial Edematous Pancreatitis )
2.
NP ( Necrotizing Pancreatitis )
Aetiology : <GET SMASHED>
Possible causes of acute

Gallstones
pancreatitis
Alcoholism (Ethanol)
Trauma (of the abdomen)
Recent Surgery(ies) / Steroids
Mumps(infection), Malnutrition
Autoimmune pancreatitis
Scorpion sting (very rare)
Hyper (Parathyroidism, calcaemia, lipid)
Post-ERCP
Drugs (corticosteroids, azathioprine, valproic acid, thiazides, estrogens)

GET SMASHED!
IEP
Most common type.
Diffuse swelling
Pancreatic tissue enhanced on CECT
May have peripancreatic fluid present.
(APFC :- Acute Peripancreatic Fluid Collection)
Self-limiting and usually resolve
APFC may form pseudocyst after 4 weeks.
NP
Present as
i.
Necrosis of pancreatic parenchyma
ii.
Peripancreatic tissue
iii.
or both
Lack of pancreatic tissue enhancement on CECT.
May have peripancreatic necrosis
(ANC :- Acute Necrotic Collection ; which contain both fluid and necrotic
material)
.
ANC may form WON (Walled-Off Necrosis) after 4 weeks
Acute Pancreatitis
> 4 weeks
Clinical Presentation
Epigastric pain
Throughout the entire abdomen
May radiates to the back
Some relief by sitting or leaning forward
Nausea, vomiting
Mild icterus ; biliary obs in gallstone pancreatitis
Swinging pyrexia ; suggests cholangitis
Grey turners or Cullens sign
Abdominal examination may reveal ; distension (due to ileus), mass can

develop due to inflamm, muscle guarding etc
Cullens sign
Cullens sign is a superficial edema and bruising in

the subcutaneous fatty tissue around the umbilicus.
This sign takes 24-48 hours to appear and can

predict acute pancreatitis.
It may be accompanied by Grey Turners sign

(bruising of the flank), which may be indicative of
pancreatic necrosis with retroperitoneal or
intraabdominal bleeding.
Other causes include,
Ruptured ectopic pregnancy
Aortic ruptured
Blunt intraabdominal trauma
Grey Turners sign
Bruising of the flanks.
Takes 24-48 hours to develop, and can predict a severe

attack of an acute pancreatitis.
May be accompanied by Cullens sign ; both indicative

of pancreatic necrosis with retroperitoneal or
intraabdominal bleeding.
Other causes include,
Pancreatic hemorrhage
Retroperitoneal hemorrhage
Blunt abdominal trauma
Ruptured ectopic pregnancy
Ruptured of AAA.
Investigation
Serum Enzyme Levels
Serum Amylase (3 to 4 times above upper limit) (or serum lipase, if available)
Urine Amylase (because it lasts longer)
Amylase-Creatinine Clearance Ratio
Pancreatic Function Tests
Test Meal ( Lundh test )
Iv injection of a hormone (eg CCK)
(NBT-PABA) test ; indirect measure of pancreatic function
Pancreolauryl test
Faecal elastase ; low level indicates exocrine insufficiency.
Morphology (Imaging)
Ultrasound ; initial investigation.
(bile dust dilated, gallstones, mass of pancreas)
CT
(calcification, necrotic areas, inflammatory collections, cysts, pseudocysts)
MRCP
(less invasive, less expensice c/p ERCP)
ERCP
(side-viewing, ampulla of vater is intubated and contrast is injected into biliary system ; narrowing, double duct sign, obstruction,
strictures, dilatation, brush cytology, placement of stents)
EUS
(can clarify relationship of neuroendocrine tumor to main pancreatic duct ; enucleation)

(distinguish cystic tumors from pseudocysts)
(guide in Transduodenal/ Transgastric FNA or Trucut biopsy)
Severity of Acute Pancreatitis
Mild Acute Pancreatitis
- No organ failure
- No local or systemic complications
Moderately severe Acute Pancreatitis
- Organ failure that resolves within 48hours (Transient Organ Failure)

- Local or systemic complications without persistent organ failure
Severe Pancreatitis
- Persistent organ failure (> 48 hours)

- Single or multiple organ failure
Types of Scoring System
IMRIE or Modified Glassgow
Ransons criteria
Modified Marshall Scoring System
BISAP
APACHE II
Bilthazar
BALI score
Revised Atlanta Criteria
Glassgow prognostic scoring

(note the PANCREAS acronym)
Pa02 decreased
Age increased
Neutrophilia
Calcium decreased
Renal Urea increased
Enzymes (Lactate Dehydrogenase) increased
Albumin low
Sugar Glucose increased
Severe is when > 3 criterias are present within 48 hours.
Ransons Criteria
Criteria:
Admission Risk Factors (*LEGAL*)

Age over 55 years old
Blood Glucose >200
Serum Lactate Dehydrogenase (LDH) >300
Aspartate Aminotransferase (AST, SGOT) (Enzymes) >250
White Blood Cell Count (Leukocytes) >16,0000
Criteria:
At 48 hours Risk Factors (*CHOBBS*)

Hematocrit falls >10%
Blood Urea Nitrogen (BUN) increased >5 mg/dl
Serum Calcium <8.0
Arterial PO2 <60
Base Deficit >4
Estimated fluid Sequestration >6L
Interpretation
Risk
factors <3: 1% mortality

Risk factors 3-4: 15% mortality
Risk factors 5-6: 40% mortality
Risk factors >7: 100% mortality
BISAP
( Bedside Index of Severity in Acute Pancreatitis)
Criteria (*BASAP*)
Altered Mental Status
Blood Urea Nitrogen (BUN) >25
SIRS Criteria positive for 2 or more
Age over 60 years
Pleural Effusion on CT Scan
Interpretation
Score 0: Mortality 0.1%
Management
General measures : -
Analgesia
Hydration
Nutritional support
Antibiotics
Local complications : eg infected collection,
(drainage percutaneously, endoscopically, surgically)
Long term measures : -
Cholecystectomy
Alcohol abstinence
Spleen
Anatomy:
SPLEEN
Functions:
- Immune
system: WBC
- Filter blood,
remove
abnormal
blood cells
- Normally
size of fist
- Pathology
leading to
splenomegal
y
Splenomegaly
Causes
1.
2.
3.
4.
Infection
Cancer
Haematolo
gical
disorder
Others
.Diagnosis
1.
2.
3.
Ultrasound
CT
MRI
.
Complications
1. Ruptured spleen
2. Bleeding
.
Indication for
splenectomy
1. Trauma
2. Oncological
3. Haematological,
4. Portal
hypertension
5. Others
Pre operative preparation
1.
Control coagulation profile
Indications for emergency

splenectomy
2.
Antibiotic prophylaxis
1. Patient unstable
3.
Vaccination
2. Continuous massive bleeding
3. Bleeding associated with hilar injury

.
Post operative complications
1.
Haemorrhage
.Indications for elective splenectomy
2.
Pleural effusion
3.
Fistula of stomach,
pancreases
1. With gastrectomy and

pancreatectomy
4.
Raised platelets count
2. Haematological disorder
3. Variceal surgery
Types of splenectomy
1.
Open splenectomy
2.
Laparoscopic splenectomy
Risk
1.
Blood loss during surgery
2.
Blood clot formation
3.
Infection
4.
Stroke, IHD
5.
Damage to adjacent organs
The Urinary
Tract
Anatomy
Anatomy Course of Ureter

The ureter begins its descent to the bladder by
Common Topics
Urolithiasis (renal, ureteric or bladder calculi)
Urolithiasis
Investigation and Diagnosis
Aetiology
Definition
Management
Common in male than female.
Prevalence is higher in hot and dry climate.
Three main locations kidney, ureter, bladder.
Composition of stones calcium oxalate, calcium phosphate,

ammonium-magnesium phosphate, uric acid or cystine.
Clinical presentations 1) renal/ureteric colic with haematuria

2) obstruction with infection/renal failure 3) asymptomatic.
3 Constrictions of Ureter
1.
Pelviureteric junction (PUJ)
2.
Pelvic brim
3.
Ureterovesical junction (UVJ)
1.
2.
Pelvic brim
3.
1.
2.
Pelvic brim
3.
1.
2.
Pelvic brim
3.
Which of the followings is

the most common?
Calcium oxalate
B. Calcium phosphate
C. Ammonium-magnesium
phosphate
D. Uric acid
E. Cystine
A.
The most common

A. Calcium
oxalate
Calcium phosphate
phosphate
D. Uric acid
E. Cystine
B.

radiolucent?
Calcium oxalate
phosphate
D. Uric acid
E. Cystine
A.
Radiolucent
Calcium oxalate
phosphate
A.
D. Uric
E.
acid
Cystine

infective calculi?
Calcium oxalate
phosphate
D. Uric acid
E. Cystine
A.
Infective calculus
Calcium oxalate
A.
phosphate
D. Uric
acid
E. Cystine
Renal infection favours
the formation of urinary calculi.
Prolonged immobilisation
Inadequate urinary drainage and urinary stasis
results in skeletal decalcification and an increase in

urinary calcium favouring the formation of calcium phosphate calculi.
stones are liable to form when
urine is static.
Altered urinary solutes and colloids dehydration
concentrates urinary solutes

until they precipitate. Reduction of urinary colloids, which adsorb
solutes, or mucoproteins, which chelate calcium, might tend to crystal
and stone formation.
Decreased urinary citrate presence
Hyperparathyroidism
Dietetic - deficiency
of citrate as citric acid, keeps relatively

insoluble calcium phosphate and citrate in solution.
hypercalcaemia, hypercalciuria and hyperphosphaturia.
of vitamin A causes desquamation of epithelium

forming a nidus on which a stone is deposited.
Imaging
Non-contrast-enhanced helical computed tomography

(CT urography)
Plain kidney-ureter-bladder radiography (KUB X-ray)
Kidney-ureter-bladder ultrasonography (KUB ultrasound)
Intravenous urography/pyelography (IVU/IVP)
Non-contrast-enhanced helical computed tomography (
Gold
standard.
Can
detect both radio-opaque and

radiolucent calculi.
Detect
secondary signs of urinary

tract obstruction i.e. hydronephosis
and/or hydroureter.
Plain kidney-ureter-bladder radiography (
Can
only detect radio-opaque

calculi.
Cannot
detect urinary tract

obstruction.
choice for pregnant women (no

radiation).
Can
detect both radio-opaque and

radiolucent calculi.
Also
can detect urinary obstruction.
Uses
contrast.
Invasive.
Can
detect urinary tract obstruction.
Rarely
done now.
Acute Therapy of Acute Renal Colic
Indications for Urological Consultation
Management of Obstructive Uropathy (AKI/Urosepsis)
Surgical Management of Urinary Tract Stone
Managed conservatively with analgesia (NSAIDs or narcotics)

and hydration until the stone passes out spontaneously.
Likelihood that stones will pass depends on size and location.
Smaller (less than 5mm) and more distal stones are likely to
pass.
Average time to pass stone is anywhere from 8-22 days

depending on size of stone.
Alpha blocker medication (such as Cardura or Xatral) can

be used as Medical Expulsion Therapy (MET) for distal
ureteric stone less than 7-8 mm.
MET reduce the duration of pain and increase the

chances of stone to pass out spontaneously.
Indications for Urological Consultation
Urgent referral for obstructive uropathy (AKI or

urosepsis).
Outpatient referral indicated for stones > 5 mm, or

failure to pass stone within 2 to 4 weeks.
Management of Obstructive Uropathy (AKI/Urosepsis)
Obstructive uropathy, with AKI or urosepsis, need an urgent

referral to urology as it can lead to irreversible renal damage
and is life threatening to patient.
Urgent intervention to relieve the obstruction is required

either by:
Retrograde insertion of double J stent or
Percutaneous nephrostomy and antegrade insertion of double J

stent.
The definitive management of the obstructing stone is usually

delayed until patient has fully recovered from acute episode of
AKI or urosepsis.
Surgical Management of Urinary Tract Stone
Types of surgical management to clear the urinary tract

stones depends on the site and size of stone:
1.
Extracorporeal Shock Wave Lithotripsy (ESWL)
2.
Ureterorenoscopy (URS) and Lithotripsy
3.
Percutaneous Nephrolithotomy (PCNL)
4.
Cystolitholapaxy / open vesicolithotomy
Extracorporeal Shock Wave

Lithotripsy (ESWL)
Treatment of choice in 80% of patients.
Employs high energy shock waves which are transmitted

through water and focused on stone via fluoroscopy or
ultrasound.
Particularly good for renal and upper ureteric stone.
Not ideal method for large (> 2 cm) or very hard

(cystine) stones, or in patients with odd anatomy.
Ureterorenoscopy (URS) and

Lithotripsy
Stone is reached by using semi-rigid or flexible

ureterorenoscope depending on location.
The scope is passed up through urethra, bladder, ureteric

orifice and ureter.
Small stones are extracted by dormia basket.
Larger stone is fragmented by either mechanical or laser

lithotripters.
Small fragmented stone can either be retrieved by

dormia basket or allowed to pass out spontaneously
when patient pass urine.
Chronic pyelonephritis
Aetiology
Definition
Management
An important cause of renal damage and end-stage renal

failure.
More common in women than men.
Pathology interstitial inflammation and scarring of

renal parenchyma.
Clinical features dull lumbar pain, increased urinary

frequency, dysuria, hypertension, lethargy, malaise,
anorexia, nausea, headache.
Ascending infection in the urinary tract is the most

common route, and it is most likely to occur when there
is vesicoureteric reflux.
Urinary stasis and the presence of calculi are common

contributory factors.
Urine full examination and microscopic examination

(UFEME)
Proteinuria is less marked than glomerulonephritis.
Casts are not present but white cells are plentiful.
Escherichia coli, Streptococcus faecalis, Proteus spp. or

Pseudomonas spp. are found in the urine.
Treatment aims at eradicating predisposing factors such

as obstruction or stones and treating the infection, often
with repeated courses of antibiotic (confer only
temporary benefit and progressive renal damage is
common).
Surgery is indicated only when the disease is confined to

one kidney.
Patients with end-stage renal failure require renal

replacement therapy.
Cystitis
Aetiology
Definition
Management
1-3% of all GP consultations.
5% of women each year with symptoms. Up to 50% of

women will suffer from a symptomatic UTI during their
lifetime.
UTI in men is much rarer.
A proportion of patients may be symptomatic in the

absence of infection - called 'urethral syndrome'.
Symptoms Dysuria, frequency, nocturia, urgency of

micturition.
Other symptoms include suprapubic pain, cloudy or foul

smelling urine and haematuria.
The most common cause is bacterial infection:
Eschericia coli is the pathogen in 70% of uncomplicated case

of lower urinary tract infections.
Other organisms include Proteus mirabilis, Klebsiella

pneumoniae, Staphylococcus saprophyticus, Staphylococcus
aureus and Pseudomonas spp.
Urethral Syndrome not associated with any infection.
Rarely kidney or bladder stones, prostatism, diabetes.
Urine dipstick
Can be done in the surgery and will be positive for nitrates

and leucocytes (leukocyte esterase test). This helps to
differentiate those with UTI from the 50% with urethral
syndrome.
Urine microscopy and culture reveals significant

bacteruria (usually >105 /ml).
Asymptomatic bacteruria
Is present in 12-20% of women aged 65-70 years and does

not impair renal function or shorten life.
In 4-7% of pregnant women and associated with premature

delivery and low birth weight and therefore, always
requires treatment.
Differential Diagnosis
Urethral syndrome.
Bladder lesion e.g. calculi, tumour.
Candidal infection.
Chlamydia or other sexually transmitted disease.
Urethritis.
Drug induced cystitis (e.g. with cyclophosphamide,

allopurinol, danazol, tiaprofenic acid and possibly other
NSAIDs)
Complication and Prognosis
Ascending infection can occur, leading to development of

pyelonephritis, renal failure and sepsis.
In children, the combination of vesicoureteric reflux and

urinary tract infection can lead to permanent renal scarring,
which may ultimately lead to the development of hypertension
or renal failure. 12-20% of children already have radiological
evidence of scarring on their first investigation for UTI.
Urinary tract infection during pregnancy is associated with

prematurity, low birth weight of the baby and a high incidence
of pyelonephritis in women.
Recurrent infection occurs in up to 20% of young women with

acute cystitis.
50% will resolve in 3 days without treatment.
No evidence to support drink plenty
It is reasonable to start treatment without culture if the

dipstick is positive for nitrates or leucocytes.
MSU if dipstick negative but suspicion.
Culture is always indicated in:
Men
Pregnant women
Children
Those with failure of empirical treatment
Those with complicated infection
Femoral Hernia
Anatomy
Borders of femoral canal:
Anterior = inguinal ligament
Posterior =
o
Pectineal ligament
Superior rami of the pubic bone
Pectineus muscle
Medial = lacunar ligament, pubic bone
Lateral = femoral vein
Content of femoral canal:
Loose areolar/connective tissue
Nodes of Cloquet = the superior-most node is located

under the inguinal ligament. It is part of deep inguinal
LN.
Femoral ring is the base of the femoral canal.
Pathology
Course of hernia:
femoral ring femoral canal saphenous opening (4cm inferior &

lateral to pubic tubercle) travel upwards in subcutaneous tissue may
reach inguinal ligament
Covering (from outside to inside):

o
Skin
Superficial fascia
Cribriform (Hesselbach's) fascia
Anterior layer of femoral sheath
Fatty content of femoral canal
Femoral septum
peritoneum
History
Age: middle-aged or elderly woman
Sex: female
Side: Right 2x more common than Left
Local symptoms:
Swelling apparently on standing & straining
Pain if adhere to greater omentum
General symptoms:
Obstruction abdominal colic, vomiting, distension, constipation
Strangulation sudden pain at local side immediately spread all over

abdomen + vomiting
Partial strangulation of bowel wall (Richters hernia) due to the narrow

neck
Can be unilateral or bilateral
Diagnosis of femoral hernia
Site:
below & lateral to pubic tubercle
Lies in the upper leg rather than in lower abdomen
Rapidly becomes irreducible & loss of cough impulse due

to tightness (narrowed) of the neck. Femoral canal
cannot distend easily with bone & ligament on 3 sides
while 1 side with major vessel.
A characteristics but not invariable feature:

- The sac of femoral hernia is thick walled with layers of fat and
connective tissue, which when cut across look like an onion.
- This means that the sac remains palpable even when empty (seems to
be irreducible).
Differential diagnosis
Direct inguinal hernia
LN
Saphena varix
Femoral artery aneurysm
Psoas abscess
Ruptured adductor longus with hematoma
Investigations
In routine cases, no specific investigations are required.
If uncertain, do US or CT.
CT is done for bowel obstruction TRO malignancy.
In emergency setting, AXR to show small bowel

obstruction (associated feature of femoral hernia)
All patient with unexplained small bowel obstruction

should undergo careful examination for a femoral hernia.
Treatment: Surgery
1. Low approach (Lockwood)
Simplest but ONLY suitable when no risk of bowel resection

Below inguinal ligament via groin crease incision
Does not prevent inguinal hernia
Done under LA
2. Inguinal approach (Lotheissen)

Initial incision into inguinal canal
The spermatic cord/round ligament is mobilized and the transversalis fascia opened from
deep inguinal ring to pubic tubercle. A femoral hernia lies immediately below this incision
and can be reduced by a combination of pulling from above & pushing from below.
Advantage: sac can be removed flush with parietal peritoneum & can prevent inguinal
hernia
3. High approach (McEvedy)

More complex. Incision made over femoral canal and continued above to inguinal canal.
Ideal in emergency setting where risk of bowel strangulation is high (strangulated &
irreducible)
Done under regional/general anaesthesia
4. Laparoscopic approach
TEP and TAPP approach
Insert a standard mesh
Ideal for reducible femoral hernia presenting electively
INGUINAL
HERNIA
Clinical features
1. Asymptomatic hernias
Swelling or fullness at the hernia site

Aching sensation (radiates into the area of the hernia)
No true pain or tenderness upon examination
Enlarges with increasing intra-abdominal pressure and/or standing
2. Incarcerated hernias
Painful enlargement of a previous hernia or defect
Cannot be manipulated (either spontaneously or manually) through the fascial
defect
Nausea, vomiting, and symptoms of bowel obstruction (possible)
3. Strangulated hernias
Have symptoms of an incarcerated hernia
Systemic toxicity secondary to ischemic bowel is possible
Strangulation is probable if pain and tenderness of an incarcerated hernia persist
after reduction
Suspect an alternative diagnosis in patients who have a substantial amount of
pain without evidence of incarceration or strangulation
Physical examination
Ask patient to stand up
Proper exposure
Examine one side first then go to the other side.
Inspect the lump from front
Site
Shape
Palpation
1. From front
can get above it?
2. From side
Position
Temperature
Tenderness
Shape
Size
Tension
Composition (solid, fluid, gaseous)
Reducibility
Expansile cough impulse

If the swelling become tense and expands
with coughing, it has cough impulse.
Movement in one direction of the swelling is
not a cough impulse.
Is the swelling reducible?

Examine abdomen.
Assess cardiovascular & respiratory for
fitness for operation.
Inguinal hernia
2 types:
1. Indirect
2. Direct
Indirect inguinal hernia

Most common
It follows the tract through the inguinal
canal.
Caused by defect in the abdominal wall
that is present at birth. It results from a
persistent processus vaginalis.
Direct inguinal hernia

usually occurs as a consequence of a defect or
weakness in the transversalis fascia area of the
Hesselbach triangle.
More common in male adults as aging and stress or
strain weaken the abdominal muscles around the
inguinal canal. Previous surgery in the lower
abdomen can also weaken the abdominal muscles.
Females rarely form this type of inguinal hernia. In
females, the broad ligament of the uterus acts as an
additional barrier behind the muscle layer of the
lower abdominal wall. The broad ligament of the
uterus is a sheet of tissue that supports the uterus
and other reproductive organs.
Risk factor
Any condition that increases the pressure in
the intra-abdominal cavity may contribute to
the formation of a hernia:
Marked obesity
Heavy lifting
Coughing
Straining with defecation or urination
Ascites
Peritoneal dialysis
Ventriculoperitoneal shunt
Chronic obstructive pulmonary disease (COPD)
Family history of hernias
Investigation
Laboratory studies include the following:
Stain or culture of nodal tissue

Complete blood count (CBC)
Electrolytes, blood urea nitrogen (BUN), and creatinine
Urinalysis
Lactate
Imaging studies are not required in the normal workup of a

hernia. However, they may be useful in certain scenarios:
Ultrasonography can be used in differentiating masses in the groin
or abdominal wall or in differentiating testicular sources of swelling
If an incarcerated or strangulated hernia is suspected, upright
chest films or flat and upright abdominal films may be obtained
Computed tomography (CT) or ultrasonography may be necessary
if a good examination cannot be obtained, because of the patients
body habitus, or in order to diagnose a spigelian or obturator hernia
Management
Non-operative therapeutic measures include:
Trusses
Binders or corsets
Hernia reduction
Topical therapy
Compression dressings
Surgical options depend on type and location of

hernia. Basic types of inguinal hernia repair include:
Herniotomy children and young adults with good
musculature
Herniorrhapy all cases of indirect hernia except in children
Hernioplasty especially for direct hernia and recurrent
hernia
Complication of inguinal
hernia repair
Hernia recurrence
Infarcted testis or ovary with subsequent
atrophy (see the images below)
Wound infection
Bladder injury
Iatrogenic orchiectomy or vasectomy
Intestinal injury
Small & Large Intestine
Small &
Large
Bowels
Inflammatory Bowel
Disease
Tumors of Small & Large
Intestine
Diverticulum
Intestinal Obstruction
Inflammatory bowel disease
intestines.
It includes a group of chronic disorders

that cause inflammation or ulceration
in large and small intestines.
TYPES
Crohns
disease
Extends into the deeper
layers of the intestinal wall,
and may affect the mouth,
esophagus, stomach, and
small intestine.
Transmural inflammation
and skip lesions.
In 50% cases -ileocolic,30%
ileal and 20% -colic region.
Regional enteritis
Ulcerative colitis
causes ulceration and

inflammation of the
inner lining of the
colon and rectum.
It is usually in the form
of characteristic ulcers
or open sores.
Other forms of IBD
Collagenous colitis
Lymphocytic colitis
Ischemic colitis
Behcets syndrome
Infective colitis
Intermediate colitis
Epidemiology
Incidence / 1 lac.
Ulcerative colitis
Crohns
2.2-14.3
3.1-14.6
Age of onset
15-30, 60-80
Ethnicity
Jewish
Male: Female
1:1
1.1-1.8 : 1
Smoking
May prevent
Causative
Oral contraceptives
No risk
1.4 odds ratio
Appedicectomy
Protective
Not
Monozygotic
6%
58%
Dizygotic
0%
4%
Etiopathogenesis
Exact cause is unknown.

Genetic factors
Immunological factors
Microbial factors
Psychosocial factors
Genetic factors
Ulcerative colitis is more common in
DR2-related genes
Crohns disease is more common in
DR5 DQ1 alleles
3-20 times higher incidence in first
degree relatives
Immunologic factors
Defective regulation of
immunesuppresion
Activated CD+4 cells activate other
inflammatory cells like macrophages
& B-cells or recruit more
inflammatory cells by stimulation of
homing receptor on leucocytes &
vascular epithelium.
Pathogenesis of IBD
Tolerance
Acute Injury
Normal
Gut
Tolerancecontrolled
inflammatio
n
Environmental
trigger
Complete Healing
(Infection, NSAID,
other)
Genetically
Acute Inflammation
American Gastroenterological Association Institute, Bethesda, MD.

Sartor RB. Nat Clin Pract Gastroenterol Hepatol. 2006;3:390-407.
Susceptible
Immunoregulation,
failure of repair or
bacterial clearance
Host
Chronic Inflammation
Pathology
Macrocopic features
Ulcerative colitis
Usually involves rectum & extends
proximally to involve all or part of colon.
Spread is in continuity.
May be limited colitis( proctitis &
proctosigmoiditis)
in total colitis there is back wash ileitis
(lumpy-bumpy appearance)
Mild disease- erythema & sand paper

appearance(fine granularity)
Moderate-marked erythema,coarse
granularity,contact bleeding & no ulceration
Severe- spontaneous bleeding, edematous
& ulcerated(collar button ulcer).
Long standing-epithelial regeneration so
pseudopolyps , mucosal atrophy &
disorientation leads to a precancerous
condition.
Eventually can lead to shortening and
narrowing of colon.
Fulminant disease-Toxic colitis/megacolon
Ulcerative colitis
Ulcer
pseudopoly
ps
Microscopic features
Crypts atrophy & irregularity
Superficial erosion
Diffuse mixed inflammation
Basal lymphoplasmacytosis
Diffuse
inflammatio
n
Crypt
distortio
n
Macroscopic features
Crohns disease
Can affect any part of GIT
Transmural
Segmental with skip lesions
Cobblestone appearance
Creeping fat- adhesions & fistula
Microscopic features
Aphthous ulcerations
Focal crypt abscesses
Granuloma-pathognomic
Submucosal or subserosal lymphoid
aggregates
Transmural with fissure formation
Aphthous
ulcer
Granulom
a
Clinical features
Ulcerative colitis
Diarrhea
Rectal bleeding
Tenesmus
Passage of mucus
Crampy abdominal pain
Diarrhea & bleeding blood-intermittent

&mild. do not seek medical attention.
Patient with proctatis-pass fresh or blood
stained mucus with formed or semi formed
stool. They also have tenesmus , urgency
with feeling of incomplete evacuation.
With proctosigmoiditis-constipation
Severe disease-liquid stools with blood ,
pus & fecal matter.
Physical signs
Proctitis Tender anal canal & blood
on rectal examination
Extensive disease-tenderness on
palpation of colon
Toxic colitis-severe pain &bleeding
If perforation-signs of peritonitis
Clinical Severity of UC
Mild
Severe
Fulminant
<4
>6
>10
Blood in stool
Intermittent
Frequent
Continuous
Temperature
Normal
>37.5
>37.5
Pulse
Normal
>90 bpm
>90 bpm
Hemoglobin
Normal
<75% normal
rate
Transfusion
required
<30 mm/hour
>30 mm/hour
>30 mm/hour
Abdominal
tenderness
Abdominal
distension and
tenderness
Bowel movement
ESR
Moderate
Intermediate
Clinical signs
1. Truelove SC, et al. Br Med J. 1955;2:1041-1045.
2. Sandborn WJ. Curr Treat Options Gastroenterol.1999;2:113-118.
Diagnosis
Laboratory tests
Endoscopy
Radiography
Biopsy
Laboratory tests
CBC
C-reactive protein is increased
ESR is increased
Platelet count-increased
Hemoglobin-decreased
Fecal Calponectin levels correlate
with histological inflammation,predict
relapses &detect pouchitis
Barium
enema
Barium enema
Fine mucosal granularity

Superficial ulcers seen
Collar button ulcers
Pipe stem appearanceloss of haustrations
Narrow & short colonribbon contour colon
Sigmoidoscopy
Always abnormal
Loss of vascular patterns
Granularity
Friability
ulceration
Extra intestinal
manifestations
Clinical features
Ileal Crohns Disease
Abdominal pain
Diarrhea
Weight loss
Low grade fever
Jejunoileitis disease
Malabsorption
Steatorrhea
Colitis and perianal disease

Bloody diarrohea
Passage of mucus
Lethargy
Malaise
Anorexia
Weight loss
Diagnosis
Laboratory tests
Endoscopy
Radiography
Biopsy
CT enterography
Laboratory tests
CRP-elevated
ESR-elevated
Anemia
Leukocytosis
hypoalbuminemia
Barium enema
String
sign
Colonoscopy
Treatment
Treatment
Diet change
Lifestyle changes
Surgery
Drugs
Lifestyle changes
Taking rest
Doing exercise
No smoking
Stress reduction
Drugs
5-ASA agents
Glucocorticoids
Antibiotics
Immunosuppresants
Biological therapy
5-ASA Agents
Sulfasalazine (5aminosalicylic acid and
sulfapyridine as carrier
substance)
Mesalazine (5-ASA), e.g.
Asacol, Pentasa
Balsalazide (prodrug of 5ASA)
Olsalazine (5-ASA dimer
cleaves
in colon)
Topical Action of 5-ASA: Extent of

Disease Impacts Formulation Choice
Distribution of 5-ASA
Preparations
Oral
Varies by agent: may be released in the

distal/terminal ileum, or colon1
Liquid Enemas
May reach the splenic flexure2-4

Do not frequently concentrate in the
rectum3
Suppositories
Reach the upper rectum2,5

(15-20 cm beyond the anal verge)
1. Sandborn WJ, et al. Aliment Pharmacol Ther. 2003;17:29-42; 2. Regueiro M, et al. Inflamm Bowel Dis. 2006;12:972978; 3. Van
Bodegraven AA,
et al. Aliment Pharmacol Ther. 1996; 10:327-332; 4. Chapman NJ, et al. Mayo Clin Proc. 1992;62:245-248; 5. Williams CN, et al. Dig
Dis Sci. 1987;32:71S-75S.
Use
In mild to moderate UC & crohns colitis
Maintaining remission
May reduce risk of colorectal cancer
Adverse effects
Nausea, headache, epigastric pain, diarrhoea,
hypersensitivity, pancreatitis
Caution in renal impairment, pregnancy, breast feeding
Glucocorticoids
Anti inflammatory agents for
moderate to severe relapses.
Inhibition of inflammatory pathways
Budesonide- 9mg/dl used for 2-3
months & then tapered.
Prednisone-40-60mg/day
No role in maintainence therapy
Antibiotics
No role in active/quienscent UC
Metronidazole is effective in active
inflammatory,fistulous & perianal CD.
Dose-15-20mg/kg/day in 3 divided
doses.
Ciprofloxacin
Rifaximin
Immunosuppresants
Thiopurines
Azathioprine
6-mercaptopurin
Methotrexate
Cyclosporine
Cyclosporine
Preventing clonal expansion of T cell
subsets
Use
Steroid sparing
Active and chronic disease
Side effects
Tremor, paraesthesiae, malaise, headache,
gingival hyperplasia, hirsutism Major: renal
impairment, infections, neurotoxicity
Biological therapy
Infliximab
Anti TNF monoclonal antibody
Infliximab binds to TNF trimers with high affinity, preventing
cytokine from binding to its receptors
It also binds to membrane-bound TNF- a and neutralizes its activity
& also reduces serum TNF levels.
Use
Fistulizing CD
Severe active CD
Refractory/intolerant of steroids or immunosuppression
Side effects
Infusion reactions, Sepsis, Reactivation of Tb, Increased risk of Tb
Other medications
Anti- diarrheals - Loperamide
(Imodium)
Laxatives - senna, bisacodyl
Pain relievers. acetaminophen
(Tylenol).
Iron supplements
Nutrition
Surgery
Ulcerative colitis
Indications:
Fulminating disease
Chronic disease with anemia, frequent
stools, urgency & tenesmus
Steriod dependant disease
Risk of neoplastic change
Extraintestinal manifestations
Severe hemorrhage or stenosis
Reconstruct
ive
Proctocolectomy
with
Ileoanal pouch
Others
Proctocolectomy & ileostomy
Rectal &anal dissection
Colectomy with ileorectal
anastomosis
Ileostomy with intraabdominal
pouch
Crohns disease
Ileocaecal resection
Segmental resection
Colectomy & ileorectal anastamosis
Temporary loop ileostomy
Proctocolectomy
Stricturoplasty
Strictureplasty
Intestinal Diverticula
Diverticula (hollow out-pouchings) : common
structural abnormality that can occur from the
oesophagus to the rectosigmoid junction (but
not usually in the rectum).
They can beclassified as:
-Congenital. All three coats of the bowel are
present in the wall of the diverticulum, e.g.
Meckels diverticulum.
-Acquired. There is no muscularis layer
present in thediverticulum, e.g. sigmoid
diverticula.
Jejunal Diverticulum
Arise from the mesenteric side of the bowel as a result of mucosal herniation at the point of
entry of the blood vessels.
Vary in size and are often multiple.
Asymptomatic and an incidental finding at surgery or on
radiological imaging.
Present in: malabsorption, as a result of bacterial stasis, or present as anacute abdominal
emergency (inflamed or perforate).
Bleeding from a jejunal diverticulum is a rare complication.
Management
Elective resection of an affected small bowel segment that is causing malabsorption can be
effective.
If perforated jejunal diverticulitis is found at emergency laparotomy, a small bowel resection
should be performed and a decision made between anastomosis and stoma formation.
Extensive jejunal diverticulosis can be very difficult to treat. In severe cases, much of the
proximal small intestine may be involved,effectively precluding resection. In addition, limited
resection,while feasible, may fail to deal adequately with recurrent attacks of inflammation or
bleeding.
Meckels Diverticulum
Features of Meckels Diverticulum
Remnant of vitellointestinal duct
Contains allthree coats of the bowel wall and has its own
blood supply.
Occurs in 2 per cent of patients, 2 inches (5 cm long), 2
feet (60 cm) from the ileocaecal valve, 20 per cent
heterotopic epithelium
Should be looked for when a normal appendix is found at
surgery for suspected appendicitis
If a Meckels is found incidentally at surgery, it can be left
provided it has a wide mouth and is not thickened
Can be source of gastrointestinal bleeding if it contains
ectopic gastric mucosa
Clinical Presentation
Haemorrhage. If gastric mucosa is present, peptic ulcerationcan occur and present
as painless maroon rectal bleeding or melaena. If the stomach, duodenum and colon
are cleared by endoscopy, radioisotope scanning with technetium-99m may
demonstrate a Meckels. (A Meckels is notoriously difficult to see with contrast
radiology.)
Diverticulitis. Meckels diverticulitis presents like appendicitis, although if
perforation occurs the presentation may resemble a perforated duodenal ulcer.
Intussusception. A Meckels can be the lead point for ileoileal or ileocolic
intussusception.
Chronic ulceration. Pain is felt around the umbilicus, as the site of the diverticulum
is midgut in origin.
Intestinal obstruction. A band between the apexof the diverticulum and the
umbilicus (also part of the vitellointestinal duct) may cause obstruction directly or by
avolvulus around it.
Perforation. The vast majority of Meckels are asymptomatic. When found in the
course of abdominal surgery, a Meckels can safely be left alone provided it has a wide
mouth and is not thickened. When there is doubt, it can be resected. The finding of a
Meckels diverticulum in an inguinal or femoral hernia has been described as Littres
hernia.
Meckels Diverticulectomy
Meckels diverticulectomy
Should not be amputated at its base and invaginated
(as for an appendix),
there is the risk of stricture and of leaving
heterotopic epithelium behind.
safer simply to excise the diverticulum: resecting it
and suturing the defect at its base, or with a linear
stapler-cutter.
If the base of the diverticulum is indurated, it is on
balance more logical to perform a limited small
bowel resection of the involved segment followed by
an anastomosis.
Diverticular Disease of Large

Intestine
Found in the left colon in around 75 per cent of
over 70 year olds in the Western world.
Usually found in the sigmoid, but diverticula are
found in the caecum and can affect the whole
colon (but not the rectum).
In South-East Asia, right-sided diverticular
disease is more common.
Most often asymptomatic (diverticulosis) and
found incidentally.
Can present clinically with sepsis or
haemorrhage.
Aetiology
Consequence of a refined Western diet deficient in dietary
fibre.
The combination of altered collagen structure with ageing,
disordered motility and increased intraluminal pressure
most notably in the narrow sigmoid colon results in
herniation of mucosa,
protruding through the circular muscle at the points where
blood vessels penetrate the bowel wall.
The rectum has a complete muscular coat and a wider
lumen and is thus very rarely affected.
Diverticular disease is rare in Africa and Asia where the
diet is high in natural fibre.
Complications
Pain and inflammation (diverticulitis).
Perforation: most often contained leading to pericolic
abscess formation, but occasionally free leading to
generalised peritonitis.
Intestinal obstruction: progressive fibrosis can cause
stenosis of the sigmoid and large bowel obstruction or
loops of small intestine can adhere to an inflamed
sigmoid resulting in small bowel obstruction.
Haemorrhage: diverticulitis may present with profuse
colonic haemorrhage.
Fistula formation: (colovesical, colovaginal,
enterocolic, colocutaneous) occurs in 5 per cent of cases,
colovesical
Clinical Features
In mild cases, symptoms such as distension, flatulence and a sensation
of heaviness in the lower abdomen
-increased luminal pressure affecting wall tension and increased
visceral hypersensitivity.
Persistent lower abdominalpain, usually in the left iliac fossa
accompanied by loose stoolsor indeed constipation.
Fever, malaise and leukocytosis can differentiate diverticulitis from
painful diverticulosis.
The lower abdomen is tender, especially on the left, but occasionally
also in the right iliac fossa, if the sigmoid loop lies across the midline.
The sigmoid colon may be tender and thickened on palpation and rectal
examination may reveal a tender mass if an abscess has formed.
Generalised peritonitis as a result of free perforation presents in the
typical manner with systemic upset and generalised tenderness,
guarding and rebound.
Haemorrhage from colonic diverticula is typically painlessand profuse.

When from the sigmoid, it will be bright red with clots, whereas right-sided
bleeding will be darker.
Torrential bleeding is fortunately rare and in fact more commonly due to
angiodysplasia but diverticular bleeding may persist or recur requiring
transfusion and indeed resection.
The presentation of a fistula resulting from diverticular disease depends on
the site.
The most common colovesical fistula results in recurrent urinary tract
infections and pneumaturia (flatus in the urine) or even
faeces in the urine.
Colovaginal fistulae are more common in patients who have had a
hysterectomy. Colocutaneous fistulation is rare in the absence of prior
intervention (e.g. radiological
drainage).
Rarely, diverticular disease may perforate into the retroperitoneum leading to
a psoas abscess, and then presentingin the groin with fistulation.
Classification of
Contamination
The degree of sepsis has a major impact on
outcome in acute diverticulitis. Those with
inflammatory masses have a lowermortality than
those with perforation (3 versus 33 per cent).
Hinchey classification of complicated diverticulitis.
Grade
I Mesenteric or pericolic abscess
II Pelvic abscess
III Purulent peritonitis
IV Faecal peritonitis
Diagnosis
Plain chest and abdominal radiographs can demonstrate a
pneumoperitoneum.
CT has excellent sensitivity and specificity for identifying bowel wall
thickening, abscess formation and extraluminal disease and has
revolutionised
If access to CT is limited, a watersoluble contrast enema can
demonstrate intraluminal inflammation and contrast extravasation
Barium enemas (and colonoscopy/flexible sigmoidoscopy)are usually
avoided in the acute setting for fear of causing perforation or peritonitis.
However, they are used after anattack has settled to exclude a coexisting
carcinoma and assess the extent of diverticular disease.
Colovesical fistulae should be evaluated with cystoscopy and biopsy in
addition.
Contrast examinations or CT may demonstrate thefistula clearly. The
differential diagnosis for colovesical fistula includes cancer, radiation
injury, Crohns disease, tuberculosis and actinomycosis.
Management
Management
Recommended to take a high-fibre diet and bulk-forming laxatives.
Acute diverticulitis is treated by intravenousantibiotics (to cover
Gram-negative bacilli and anaerobes) alongside appropriate
resuscitation and analgesia.
Nil by mouth to rest the bowel and catheterisation to reduce the risk
of colovesical fistulation are often advocated.
A CT scan can confirm the diagnosis and assess for complications.
After the acute attack has subsided and if CT has not already
confirmed the diagnosis,
the bowel should be investigated by endoscopy, barium enema
or CT virtual colonoscopy.
An abscess can be drained percutaneously, 5 cm is frequently
regarded as a cut off between an abscess likely to settle with
antibiotics and one likely to require intervention.
Principles of surgical management of

diverticular disease
Hartmanns procedure is the safest option in

emergency surgery (sigmoid resection with
formation of left iliac fossa colostomy and
closure of the rectalstump)
Primary anastomosis can be considered in
selected patients
Elective resection may be offered for recurrent
attacks
Definitive treatment of colovesical fistula will
require resection
NEOPLASM OF THE SMALL

BOWEL
Neoplasm
Rare:
1. Rapid transit time
2. Local immune system of the small bowel
mucosa (IgA)
3. Alkaline pH
4. Relatively low concentration of bacteria; low
concentration of carcinogenic products of
bacterial metabolism.
5. Presence of mucosal enzymes (hydrolases)
that destroy certain carcinogens
6. Efficient epithelial cellular apoptotic
mechanisms that serve to eliminate clones
harboring genetic mutation
Neoplasm
50 60 y/o
Risk factors:
1.
2.
3.
4.
5.
Red meat
Ingestion of smoked or cured foods
Crohns dse
Celiac sprue
Hereditary nonpolyposis colorectal
cancer (HNPCC)
6. Familial adenomatous polyposis (FAD)
100% to develop duodenal CA
7. Peutz-Jeghers syndrome
Neoplasm
Symptoms:
Most are asymptomatic

Symptoms:
1. Vague abdominal pain (epigastric discomfort,

N/V, abd. pain, diarrhea).
2. Bleeding (hematochezia or hematemesis)
3. Obstruction (intussuception, circumferencial
growth, kinking of the bowel, intramural
growth).
Most common mode of presentation is

---> crampy abd. pain, distention,
nausea / vomiting
Hemorrhage usually indolent 2nd
common mode of presentation
Neoplasm
Diagnosis:
For most are asymptomatic it is
rarely diagnosed preoperatively
Serological examination
Serum 5-hydroxyindole acetic acid

(HIAA) for carcinoid.
CEA associated w/ small intestinal
adenocarcinoma but only if w/ liver
metastasis.
Neoplasm
Diagnosis:
Radiological examination:
1. Enteroclysis (test of choice 90%
sensitivity)
2. UGIS w/ intestinal follow through
3. CT scan
4. Angiography / RBC scan --> bleeding
lesions
Endoscopy:
. EGD (esophagus, gastric, and duodenum)
. Colonoscopy
I.
Benign tumors:
A. Adenomas: (most common benign

neoplasm):
1. True adenomas:
Associated w/ bleeding and obstruction
Usually seen in the ileum
Majority are asymptomatic
2. Villous adenoma:
Most common in the duodenum
soap bubble appearance on contrast radiography
No report of secretory diarrhea
3. Brunners gland adenoma

In the duodenum
No malignant potential
Mimic PUD
B. Leiomyoma:
Most common
symptomatic benign lesion
Associated w/ bleeding
Diagnosed by
angiography and
commonly located in the
jejunum
2 growth pattern:
1. Intramurally ----> obstruction
2. Both intramural and
extramural (Dumbbell
shaped)
Benign
tumors:
Benign tumors:
C. Lipoma:
Most common in
the ileum
Causes
obstruction (lead
point of an
intussusception)
Bleeding due to
ulcer formation
No malignant
degeneration
Benign tumors:
D. Peutz-Jeghers
Syndrome:
Autosomal dominant,
Inherited syndrome of:
1. Mucocutaneous
melatonic pigmentation
(face, buccal mucosa, palm,
sole, peri-anal area)
2. Gastrointestinal polyp
(enteric jejunum and ileum
are most frequent part of
GIT followed by colon,
rectum and stomach).
Benign tumors:
D. Peutz-Jeghers
Syndrome:
Inherited syndrome
of:
1. Mucocutaneous
melatonic
pigmentation (face,
buccal mucosa, palm,
sole, peri-anal area)
2. Gastrointestinal
polyp (enteric jejunum
and ileum are most
frequent part of GIT
followed by colon,
rectum and stomach).
Diagnosis
Gastrointestinal
polyps and pigmented
spots
X-irradiation of
abdomen or
endoscopy detects
polyps
Polyps have distinct
shape and histological
composition
DNA test available for
asymptomatic
individuals
Benign tumors:
D. Peutz-Jeghers Syndrome:
Sign & Symptoms:

1. colicky abd. pain (due to intermittent
intussuception)
2. Hemorrhage
3. Benign growths (polyps) in small

intestine (stomach/bowel)
4.Dark-brown or dark-blue spots on lips,
gums, inside mouth, around mouth,
eyes, nostrils (mucocutaneous
macules)
Treatment:
. Polyps removed surgically

. Electrocautery snare
. Exams for cancer and treatment
II. Malignant neoplasm:

Histologic types:
Tumor type
Cell of origin Frequency Predominant

Site
adenocarcinoma
Epithelial cell
35 50%
Duodenum
carcinoid
Enterochromaffin
cell
20 40%
Ileum
lymphoma
lymphocyte
10 15%
Ileum
GIST
? Interstitial cell
of Cajal
10 15%
(gastrointestinal
stromal tumors)
Malignant neoplasm:
1. Adenocarcinom
a:
Most common CA
of small bowel
Most common in
duodenum and
proximal jejunum
Half involve the
ampulla of Vater.
Malignant neoplasm:
2. Carcinoid:
From Enterochromaffin cells or
Kultchitsky cells
Arise from foregut, midgut &
hindgut
Appendix (46%) > Ileum (28%) >
Rectum (17%)
Malignant neoplasm:
2. Carcinoid:
Aggressive behavior than the
appendiceal carcinoid.
appendix 3% metastasize; Ileum 35%

metastasize
Appendix solitary; Ileum 30% multiple
25-50% w/ carcinoid tumor with liver

metastasis develops carcinoid
syndrome.
Secretes serotonin, bradykinin and

substance P
1.
2.
3.
4.
Diarrhea
Flushing
Hypotension
tachycardia
Malignant neoplasm:
3. Lymphomas:
Most common
intestinal
neoplasm in
children under
10y/o.
In adult = 10-15%
of small bowel
malignant tumors
Most common
presentation
1. intestinal
obstruction
2. Perforation (10%)
Malignant neoplasm:
3. Lymphomas:
Criteria of primary lymphomas of the
small bowel:
1. Absence of peripheral lymphadenopathy
2. Normal chest x-ray w/o evidence of
mediastinal LN enlargement.
3. Normal WBC count and differential
4. At operation, the bowel lesion must
predominate and the only nodes are
associated w/ the bowel lesion
5. Absence of disease in the liver and
spleen
Treatment:
I.
For Benign lesions:
All symptomatic benign tumors should

be surgically resected or removed
endoscopically (EGD / colonoscopy).
Duodenal tumors:
1 cm. ----> endoscopic polypectomy

2cm. ----> surgically resected (Whipples
located near the ampulla of Vater).
Duodenal adenomas w/ FAP shd
undergo Whipples for it is usually multiple
and sessile and has 100% degenerate to
CA.
Treatment:
II. Malignant lesions:
1. Adenocarcinoma:
Wide local resection w/ its mesentery to

achieve regional lymphadenectomy
Chemotherapy has no proven efficacy in
the adjuvant or palliative treatment of
small-intestinal adenoCA.
2. Small intestinal lymphoma:
For localized: segmental resection w/

adjacent mesentery
If w/ diffused involvement:
-->chemotherapy rather than surgery, is
primary therapy
Treatment:
3.Carcinoid:
Segmental intestinal resection &
regional lymphadenectomy.
< 1cm rarely has LN metastases
> 3cm 75 to 90% LN metastases
30% are multiple, hence entire small

bowel shd be examined prior to
surgery.
Treatment:
3.Carcinoid:
If w/ metastatic lesions--->
debulking, associated w/ long-term
survival & amelioration of symptoms
of carcinoid syndrome
Chemotherapy: ---> 30 -50%
response
1. Doxorubicin
2. 5-fluorouracil
3. Streptozocin
Octreotide: - most effective for

management of symptoms of
carcinoid syndrome
Treatment:
4. Metastatic cancers:
Melanoma associated
w/ propensity for
metastasis to the small
bowel.
Palliative resection /
bypass procedure
Systemic therapy
depends on the
responds of the primary
site.
Tumours of Large Intestine
Anatomic Location of CRC
Cecum 14 %
Ascending colon 10 %
Transverse colon12 %
Descending colon 7 %
Sigmoid colon 25 %
Rectosigmoid junct.9 %
Rectum 23 %
Symptoms associated with CRC
Colon cancers result from a series of pathologic changes

that transform normal epithelium into invasive
carcinoma. Specific genetic events, shown by vertical
arrows, accompany this multistep process.
WHO Classification of CRC

Adenocarcinoma in situ / severe dysplasia
Adenocarcinoma
Mucinous (colloid) adenocarcinoma (>50%
mucinous)
Signet ring cell carcinoma (>50% signet ring
cells)
Squamous cell (epidermoid) carcinoma
Adenosquamous carcinoma
Small-cell (oat cell) carcinoma
Medullary carcinoma
Undifferentiated Carcinoma
Risk factors for CRC
Age
Adenomas, Polyps
Sedentary lifestyle, Diet, Obesity
Family History of CRC
Inflammatory Bowel Disease (IBD)
Hereditary Syndromes (familial adenomatous
polyposis (FAP))
Dietary factors implicated in

colorectal carcinogenesis
consumption of red
meat
Increased risk
animal and saturated

fat
refined carbohydrates
alcohol
Dietary factors implicated in

colorectal carcinogenesis
dietary fiber
vegetables
Decreased risk
fruits
antioxidant vitamins
calcium
folate (B Vitamin)
Specimen containing an invasive colorectal

carcinoma and two adenomatous polyps.
Multiple adenomatous polyps of the cecum are

seen here in a case of familial polyposis .
Familial polyposis in which mucosal surface of the colon is a

carpet of small adenomatous polyps. Even though they are
small , there is a 100% risk over time for development of
adenocarcinoma, for which total colectomy is recommended
Adenocarcinoma of the cecum demonstrates an

exophytic growth pattern.
Staging of CRC
TNM system
Primary tumor (T)
Regional lymph nodes (N)
Distant metastasis (M)
*Note: Tis includes cancer cells confined within the glandular basement
membrane (intraepithelial) or lamina propria (intramucosal) with no extension

through the muscularis mucosae into the submucosa.
**Note: Direct invasion in T4 includes invasion of other segments of the

colorectum by way of the serosa; for example, invasion of the sigmoid colon by
a carcinoma of the cecum.
Dukes staging system

A Mucosa
80%
B Into or through M. propria
C1Into M. propria, + LN !
C2Through M. propria, + LN!
D distant metastatic spread
50%
40%
12%
<5%
Sites of metastasis
Via blood
Via lymphatics
Liver
Abdominal
wall
Lung
Lymph nodes
Brain
Bone
Per
continuitatem
Nerves
Vessels
Diagnosis
Colonoscopy is the preferred diagnostic test for
colorectal cancer
Barium enema and fl exible sigmoidoscopy.
Biopsy of suspicious lesions is required to establish
a diagnosis.
Tumor markers such as carcinoembryonic antigen
(cea) or carbohydrate antigen (ca).
Radiologic studies are used to evaluate the extent of
local disease and to screen for metastatic disease.
Therapy
Surgical resection the only curative treatment.
The aim of surgery is to prevent the development of colorectal cancer.
The surgical options are:
-colectomy with ileorectal anastomosis (IRA);
-restorative proctocolectomy (RPC) with an ileal pouch-anal
anastomosis, the anastomosis may be defunctioned with aloop
ileostomy;
-total proctectomy and end ileostomy (normally reserved forpatients
with a low rectal cancer).
Likelihood of cure is greater when disease is detected at an early stage

Early detection and screening is of pivotal
importance
INTESTINAL
OBSTRUCTION
INTRODUCTION
Accounts for 5% of all acute surgical admissions
Patients are often extremely ill requiring prompt
assessment, resuscitation and intensive monitoring
Obstruction
A mechanical blockage arising from a structural abnormality
that presents a physical barrier to the progression of gut
contents.
Ileus
is a paralytic or functional variety of obstruction
Obstruction is:
-Partial or complete
-Simple or strangulated
CLASSIFICATION
DYNAMIC
OBSTRUCTION
(MECHANICAL)
CAUSES OF I.O (DYNAMIC)
Proximal bowel dilated & develops altered motility
Pathophysiology:
Obstruction by Adhesions
Peritoneal irritation local fibrin production produces

adhesions between apposed surfaces
As early as 4 weeks post laparotomy. The majority of patients
present between 1-5 years
Colorectal Surgery 25%
Gynaecological
20%
Appendectomy
14%
Prevention: good surgical technique, washing of the peritoneal
TREATMENT OF ADHESIVE
OBSTRUCTION
Initially treat conservatively provided
there is no signs of strangulation; should
rarely continue conservative treatment
for longer than 72 hours
At operation, divide only the causative
adhesion and limit dissection
Laparoscopic adhesiolysis in cases of
chronic subacute obstruction
HERNIA
ACCOUNTS FOR 20% OF SBO
COMMONEST 1. FEMORAL HERNIA

2. ID INGUINAL
3. UMBILICAL
4. OTHERS: INCISIONAL
THE SITE OF OBSTRUCTION IS THE NECK OF HERNIA
THE COMPROMISED VISCUS IS WITH IN THE SAC.
ISCHAEMIA OCCURS INITIALLY BY VENOUS

OCCLUSION, FOLLOWED BY OEDEMA AND ARTERIALC
OMPROMISE.
ATTEMPT TO DISTINGUISH THE DIFFERENCE BETWEEN:
INCARCERATION
SLIDING
OBSTRUCTION
STRANGULATION IS NOTED BY:
PERSISTENT PAIN
DISCOLOURATION
TENDERNESS
CONSTITUTIONAL SYMPTOMS
Volvulus
A twisting or axial rotation of
a portion of bowel about its
mesentery. When complete it
forms a closed loop
obstruction ischemia
Can be primary or secondary:
1: congenital malformation of the gut
(e.g: volvulus neonatorum, cecal or
sigmoid volvulus)
2: more common, due to rotation of a
piece of bowel around an acquired
adhesion or stoma
Commonest spontaneous
type in adult is sigmoid, can
be relieved by
decompression per anum
Surgery is required to prevent
or relieve ischaemia
Features: palpable
tympanic lump
(sausage shape) in
the midline or left
side of abdomen.
Constipation,
abdominal distension
(early & progressive)
Acute
intussusception
Occurs when one portion
of the gut becomes
invaginated within an
immediately adjacent
segment.
Common in 1st year of life
Common after viral
illness enlargement of
Peyers patches
Ileocolic is the commonest
variety in child.
Colocolic intussusception
commonest in adult
An intussusception is
composed of three
parts :
the entering or inner
tube;
the returning or
middle tube;
the sheath or outer
tube (intussuscipiens).
Classically, a previously
healthy infant presents
with colicky pain and
vomiting (milk then bile).
Between episodes the
child initially appears
well.
Later, they may pass a
redcurrant jelly stool.
Red currant
jelly stools
LARGE BOWEL OBSTRUCTION

DISTINGUISHING ILEUS FROM MECHANICAL OBSTRUCTION IS
CHALLENGING
ACCORDING TO LAPLACES LAW: MAXIMUM PRESSURE IS AT
THE MAXIMUM DIAMETER AREA
CAECUM IS AT THE GREATEST RISK OF PERFORATION
PERFORATION RESULTS IN THE RELEASE OF FORMED FEACES
WITH HEAVY BACTERIAL CONTAMINATION
AETIOLOGY:
1.
CARCINOMA:
THE COMMONEST CAUSE, 18% OF COLONIC CA. PRESENT WITH

OBSTRUCTION
2. BENIGN STRICTURE:
DUE TO DIVERTICULAR DISEASE, ISCHEMIA, INFLAMMATORY
BOWEL DISEASE.
3. VOLVULUS:
-SIGMOID VOLVULUS/ CAECAL VOLVULUS
CLINICAL FEATURES
High small bowel obstruction
vomiting occurs early and is
profuse with rapid dehydration.
Distension is minimal with little
evidence of fluid levels on
abdominal radiography
Low small bowel obstruction

pain is predominant with central
distension.
Vomiting is delayed.
Multiple central fluid levels are
seen on radiography
Large bowel obstruction

distension is early and pronounced.
Pain is mild and vomiting and
dehydration are late.
The proximal colon and caecum are
distended on abdominal
radiography
CARDINAL
FEATURES:
Colicky pain
Vomiting
Abd
distention
Constipation
OTHER
FEATURES:
Dehydration
Hypokalaemia
Pyrexia
Abd
tenderness
PHYSICAL EXAMINATION
INSPECTION
Abdominal distention, scars, visible
peristalsis.
PALPATION
Mass, tenderness, guarding
PERCUSSION
Tymphanic, dullness
AUSCULTATION
Bowel sound are high pitch and
increase in frequency
INVESTIGATIONS:
Lab:
FBC (leukocytosis, anaemia, hematocrit, platelets)
Clotting profile
Arterial blood gasses
U& Crt, Na, K, Amylase, LFT and glucose, LDH
Group and save (x-match if needed)
Optional (ESR, CRP, Hepatitis profile)
RadiOlogical:
Plain ABDOMINAL xrays
USS ( free fluid, masses, mucosal folds, pattern of
paristalsis, Doppler of mesenteric vasulature, solid organs)
Other advanced studies (CT, MRI, Contrast studieS)
Fluid levels with gas

above; stepladder
pattern. Ileal
obstruction by adhesions;
patient erect.
Supine radiograph from a

patient with complete small
bowel obstruction shows
distended small bowel
loops in the central
abdomen with prominent
valvulae conniventes (small
Figure 3. Lateral
decubitus view of the
abdomen, showing
air-fluid levels
consistent with
intestinal obstruction
(arrows).
The Difference between small

and large bowel obstruction
Small Bowel
Central ( diameter 3
cm max)
Vulvulae coniventae
Ileum: may appear
tubeless
Large bowel
Peripheral ( diameter
6 cm max)
Presence of
haustration
Role of CT
Used with iv contrast, oral and rectal contrast

(triple contrast).
Able to demonstrate abnormality in the bowel
wall, mesentery, mesenteric vessels and
peritoneum.
It can define:
the level of obstruction
The degree of obstruction
The cause: volvulus, hernia, luminal and
mural causes
The degree of ischaemia
Free fluid and gas
Ensure: patient vitally stable with no renal
failure and no previous alergy to iodine
Figure: Axial computed tomography scan

showing dilated, contrast-filled loops of
bowel on the patients left (yellow arrows),
with decompressed distal small bowel on the
patients right (red arrows). The cause of
obstruction, an incarcerated umbilical hernia,
can also be seen (green arrow), with
proximally dilated bowel entering the hernia
and decompressed bowel exiting the hernia.
Source: Jackson, PG. & Raiji M., Evaluation and Management of Intestinal Obstruction, January
Role of barium gastrografin

studies
Barium should not be used in
a patient with peritonitis
As: follow through, enema

Limited use in the acute setting
Gastrografin is used in acute
abdomen but is diluted
Useful in recurrent and chronic
obstruction
May able to define the level
and mural causes.
Can be used to distinguish
adynamic and mechanical
obstruction
TREATMENT OF INTESTINAL
OBSTRUCTION
Supportive
1. Resuscitation
2. Ryle tube free flow with 4 hourly aspiration
-Decompression of proximal to the obstruction,
reduce subsequent aspiration during induction
of anesthesia and post extubation.
3. IV drip normal saline / Hartmann (Sodium &
water loss during IO)
4. Broad spectrum antibiotic (not mandatory
but need in all patient undergoing surgery.
Surgical
Ind: obstructed / strangulated

external hernia, Internal
intestinal strangulation and
acute obstruction
1.Midline incision usually look on
CAECUM
2.Operative decompression
3.Look at viability of intestine
4.Large bowel obstruction:
colostomy
INDICATIONS FOR
SURGERY
Absolute
Generalised peritonitis
Localised peritonitis
Visceral perforation
Irreducible hernia
Relative
Palpable mass lesion
'Virgin' abdomen
Failure to improve
Trial of conservatism
Incomplete obstruction
Previous surgery
Advanced malignancy
Diagnostic doubt - possible ileus
Source: http: Surgical Tutor.co.uk
MANAGEMENT FOR
LARGE BOWEL
All patients require
OBSTRUCTION
Adequate resuscitation
Prophylactic antibiotics
Consenting and marking for potential stoma
formation
At operation
Full laparotomy should be performed
Liver should be palpated for metastases
Colon should be inspected for synchronous
tumours
Appropriate operations include:
Right sided lesions right hemicolectomy
Transverse colonic lesion Source:
extended
right
http:
Surgical Tutor.co.uk
Three-staged procedure
Defunctioning colostomy
Resection and anastomosis
Closure of colostomy
Two-staged procedure
Hartmanns procedure
Closure of colostomy
One-stage procedure
Resection, on-table lavage and primary anastomosis
Three stage procedure will involve 3 operations!
Associated with prolonged total hospital stay
Transverse loop colostomy can be difficult to manage
With two-staged procedure only 60% of stomas are ever reversed
With one-stage procedure stoma is avoided
Anastomotic leak rate of less than 4% have been reported
Irrespective of option total perioperative mortality is about 10%
Source: http: Surgical Tutor.co.uk
Complications
associated with
intestinal obstruction
include excessive bleeding
repair
infection
formation of abscesses (pockets of
pus)
leakage of stool from an
anastomosis
adhesion formation
paralytic ileus (temporary
Source: http://www.surgeryencyclopedia.com/Fi-La/Intestinalparalysis of the intestines)
Obstruction-Repair.html
PARALYTIC ILEUS
A state in which there is a failure of

transmission of peristaltic waves 2 to
neuromuscular failure ( in Auerbachs and
Meissners plexuses)
Stasis leads to accumulation of fluid and gas
within bowel a/w distension, vomiting,
absence of bowel sound and absolute
constipation
Varieties factors: postoperative, infection,
reflex ileus and metabolic
Radiological: gas filled loops of intestines with
multiple fluid levels
Management:
Essence of treatment prevention with use of
nasogastric suction and restriction of oral
intake until bowel sound and passage of flatus
return
Maintain electrolyte balance
Specific treatment:
Removed primary cause
Decompressed GI distension
If prolong paralytic ileus , consider laparotomy
exclude hidden cause and facilitate bowel
decompression
PSEUDO-OBSTRUCTION
Obstruction usually colon- occur in
the absence of mechanical cause
or acute intra-abdominal disease.
Associated with a variety of
syndromes in which there is
underlying neuropathy and/or a
range of other factors
IDIOPATHIC
SEPTICAEMIA
Metabolic
Retroperitoneal
irritation
Severe trauma at
lumbar area
Drugs
Shock
Secondary GI
involvement
Small intestinal pseudoobstruction
Colonic pseudoobstruction (Ogilvies

syndrome, )
This condition may be

primary (i.e. idiopathic or
associated with
familial visceral myopathy)
or secondary.
The clinical picture
consists of recurrent
subacute obstruction.
The diagnosis is made by
the exclusion of a
mechanical cause.
Treatment consists of
initial correction of any
underlying disorder.
Metoclopramide and
erythromycin may be of use.
This may occur in an acute

or a chronic form.
presents as acute large
bowel
obstruction.
Abdominal radiographs
show evidence of colonic
obstruction, with marked
caecal distension being a
common
feature.
AXR shows colonic
obstruction with marked
caecal distension
Confirmation of absence
mechanical cause by
colonoscopy or single
Acute Mesenteric
Occlusion
Acute ischemic of mesenteric vessel. Commonly SMA
Causes: AF, mural thrombosis, atheromatous plaque

from aortic aneurysm and valave vegetation from
endocarditis
Features:
-Sudden onset of severe abd. pain in pt
with AF and atherosclerosis
-Persistent vomiting and defecation then passage of
altered blood
-Hypovolumic shock
Investigations: - Neutrophil leukocytosis
- Abd Xray: Absence of gas in thickened small intestines
Treatment:
- Anti-coagulant
- Embolectomy
- Revascularization
- Colectomy
Acute Abdominal
Pain
Anus & Anal Canal
Anatomy of Anal canal

4 cm long
commences at the level where
the rectum passes through the
pelvic diaphragm and ends at
the anal verge.
o Anatomic anal canal extends
from anal verge to dentate line
o Surgical anal canal is anal verge
to anorectal ring, the circular
upper border of puborectalis
that is palpable by rectal exam.
Mucous membrane of upper half

of anal canal
derived from hindgut endoderm & has
following features:
1. lined by columnar epithelium.
2. thrown into vertical folds (anal
columns), joined together at their lower
ends by small semilunar folds (anal
valves)
3. Nerve supply is same as that for rectal
mucosa & is derived from autonomic
hypogastric plexuses) & it is sensitive only
to stretch.
4. Arterial supply: Superior rectal artery, a
branch of inferior mesenteric artery.
5. Venous drainage: Superior rectal vein,
a tributary of inferior mesenteric vein, &
portal vein.
6. Lymphatic drainage is mainly upward
along superior rectal artery to pararectal
nodes
Mucous membrane of lower half

of anal canal
derived from ectoderm of proctodeum & has

following features:
1. It is lined by stratified squamous epithelium,
which gradually merges at anus with perianal
epidermis.
2. There are no anal columns.
3. Nerve supply is from somatic inferior rectal
nerve; sensitive to pain, temperature, touch &
pressure.
4. Arterial supply: inferior rectal artery, a
branch of internal pudendal artery.
5. Venous drainage: inferior rectal vein, a
tributary of internal pudendal vein, which
drains into internal iliac vein.
6. Lymph drainage: downward to medial group
of superficial inguinal nodes.
Dentate line: is upper half of anal canal joins
lower half.
Anal sphincters
1. Internal:
. Involuntary
. Circular muscle layer
2. External
. Voluntary
. Striated muscle layer
. Inferior rectal nerve & sacral nerve
. Three parts: Subcutaneous,
superficial, deep
Haemorrhoids Definition
Varicose dilations of the venous plexus at
the anorectal junction that result from
prolonged pelvic vascular congestion.
(Robbins Basic Pathology 9th Edition)
Haemorrhoids
Aetiology
Constipation
Pregnancy
Prolonged toilet sitting
Lack of fibre rich diet
Constipation
Straining during constipation raises intra-abdominal
pressure obstructs venous return causing venous
plexus to be engorged
The bulging mucosa is dragged distally by hard stools.
Persistent straining causes pelvic floor to sag
downwards, extruding the anal mucosa
Causing a small degree of prolapse
(Hard stools also could cause obstruction of venous return)
Pregnancy
(which will resolve spontaneously soon after birth)
Main mechanisms:
Venous engorgement
Mucosal prolapse
The fetus obstructs pelvic venous return
Progesterone mediates venous dilatation
Fibre-deficient diet
results in a prolonged gut transit time, which is

associated with the passage of smaller, harder stools
that require more straining to expel.
The presence of a hard faecal mass in the rectum could
obstruct venous return,
resulting in engorgement of the anal veins with the act of
straining at stool or sitting for prolonged periods on the
lavatory with a relaxed perineum,
causing a disturbance of vascular flow.
Type of Haemorrhoids
Internal haemorrhoids
Proximal to dentate line
Covered by columnar or transitional epithelium
Not sensitive to touch, pain, temperature
External haemorrhoids
Distal to dentate line
Covered by skin
Somatically innervated
Sensitive to touch, pain, stretch and temperature
Mixed haemorrhoids
Presence of both internal and external haemorrhoids
Common Position of
Haemorrhoids
Classically, they occur in the 3,
7 and 11 oclock positions with
the patient in the lithotomy
position
(according to the main branches
of the superior haemorrhoidal
veins)
lithotomy
position
Golighers classification (Internal

haemorrhoids)
Normal
appearance
externally with
haemorrhoids
which may bleed
but do not
prolapse
Haemorrhoids
prolapse
through the
anus on
straining but
reduce
spontaneously
Haemorrhoids
prolapse
through the
anus on
straining or
exertion and
require manual
replacement
into the anal
The prolapse
stays out at all
times and is
irreducible
Symptoms & Signs of

Haemorrhoids
Bleeding
Fresh blood, separate from the motion, on the wiping
paper
Mucous leakage due to imperfect closure of anal
cushions
Perianal irritation and itching (pruritus ani)
Cause by mucous leakage
Mild incontinence of flatus due to imperfect closure of
anal cushions
Haemorrhoidal prolapse
Histroy Taking
Rectal bleeding: bright red
Pain in the anal area (when they are complicated by 2
infection or strangulation)
Prolapse from anal canal and its reducibility (for grading of
haemorrhoids)
Any presence of pruritus
History of risk factors
Physical Examination
Patient should be in lithotomy position
Inspection:
Look for anal tags, prolapsed, swelling, lumps or bleeding
If there is hx of prolapse, ask patient to strain and look for any
protruded mass (is protrusion is less than an inch- partial prolapsed,
more than 2 inches- complete prolapsed)
External haemorrhoids- covered by skin
Internal haemorrhoids- covered with mucous membrane
Palpation:
Perianal region should be palpated for any lumps
Digital rectal examination should be done
Investigations
Diagnostic
Proctoscopy- to look for internal haemorrhoids, note the
position ( usually located at 3, 7, 11 oclock positioned
according to the main branches of the superior
haemorrhoidal veins)
Sigmoidoscopy/ Colonoscopy: transmit images of the
rectum and the colon to rule out carcinoma
Others
Full blood count: to assess hemoglobin status and white
cells count for identification for any infections
Management
Conservative:
Take high fibre diet
Pt should be advised not to spend a long time on the
straining
Most effective tropical treatment is warm (40C) Sitz baths
(type of bath in which only the hips and buttocks are soake
d in water, started at 35C & gradually increased to 40 to
43C, bath lasts 3 to 10 minutes. The primary effect is
analgesic)
Medical
Daflon- to increase venous tone
Stool softeners (Docustae Sodium)
Management (Cont.)
1. Injection of sclerosants
For 1st degree haemorrhoids eventhough it is profusely bleeding, 2 nd
degree where prolapse is slightly noticeable
Contraindication: acute prolapse thrombosis, severe bleeding &
ulceration, fissure & fistula
Irritant solution is injected submucossaly around the pediclesof 3 major
haemorrhoids, in upper canal
Provokes a fibrotic reaction
2. Rubberband ligation
Can be used in 1st, 2nd, 3rd degree haemorrhoids
Rubber band is placed on redundant mucosa
Minimum of 2cm above dentate line
Causes strangulation of blood supply
Sloughs in 5-7 days
Leaves small ulcer that heals & fixes tissue to underlying sphincter
Contraindicated in pt on Coumadin or heparin
Management (Cont.)
Surgical procedures
Cadidates for surgery
Pt who do not respond to office based procedures
Pt with large external haemorrhoidal disease
Pt with garde 3 or 4 or mixed haemorrhoidal disease
Open hemorrhoidectomy (Milligan-Morgan)
Bridges must be left between the excision
Cloval leaf shaped defect in anal canal & perianal skin. Wound are left
open
Healing with scar contracture draws tissue back into anal canal &
reattached it to muscle coat
Closed hemorrhoidectomy
Newer techniques: laser hemorrhoidectomy
Milligan-Morgan
technique
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Patients

1) Persistent right sided abdominal pain

2. Fever for 1 day

Past Medical History

had pancreatitis on February

was newly diagnosed with type 2

EXAMINATION OF ALL SYSTEMS

general inspection,Mr A was

periphery, capillary refill < 2

and tender at the right hypochondriac and

Abdominal AP erect x ray

term GERD is apllied tp

occur post-prandial, short,

with symptoms of mucosal

rather than proven,

lower end oesophagus

with simple columnar

gastric mucosal folds, has

in the columnar lined

most common cancer in the

squamous cell carcinoma

2/3 of the esophagus

feeling something not right,

related to invasion of the

related to distant disease:

cachexia, patient with muscle

confirm diagnosis- endoscopy

suitable for potential curative therapies

palliative therapy-unfit,locally advanced,

treatment for patient with carcinoma

by mouth,NG tube if vommiting,

pain in chest or upper abdomen

aim of treament is to limit

Peptic ulcer disease

of the mucosal integrity

Penetrates protective surface of mucous

: epigastric gnawing, may radiate to

4 time more common

More the 40 years

Equal in both sex

Mostly occur near the

Mostly occur in the 1st

Pain while eating and

Pain before meal and

Commonly occur after Uncommon unless

Upper gastrointestinal bleed

RP, amylase H.pylori testing

1. Non-invasive Serological test, hydrogen breath

Antacid Symptomatic relief

Histamine H-receptor antagonists

Proton pump inhibitors

eradication (Triple therapy)

Consists of 2 antibiotic (amoxicilin,

Long term management

For symptomatic relapse more than

Symptomatic relapse > 4 time a year

Gastric ulcer Partial gastrectomy with

occurs in acute ulcers on

Resuscitation and antibiotics

Duodenal ulcer : simple closure and application

Too ill and present late for surgery

Sensation of fullness, constant and