ABDOMEN

Some Important Vessels and related info

Abdominal aorta

Abdominal aortic topography

Origin T12

Termination L4

Posterior relations L1-L4 Vertebral bodies

Anterior relations Lesser omentum

Liver
Left renal vein
Inferior mesenteric vein
Third part of duodenum
Pancreas
Parietal peritoneum
Peritoneal cavity

Right lateral relations Right crus of the diaphragm

Cisterna chyli
Azygos vein
IVC (becomes posterior distally)

Left lateral relations 4th part of duodenum

Duodenal-jejunal flexure
Left sympathetic trunk

Abdominal aortic branches

Branches Level Paired Type

Inferior phrenic T12 (Upper border) Yes Parietal

Coeliac T12 No Visceral

Superior mesenteric L1 No Visceral

Middle suprarenal L1 Yes Visceral

Renal L1-L2 Yes Visceral

Gonadal L2 Yes Visceral

Lumbar L1-L4 Yes Parietal

Inferior mesenteric L3 No Visceral

Median sacral L4 No Parietal

Common iliac L4 Yes Terminal

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● AA Branches (Superior To Inferior): (N-247)
Ventral: (unpaired ant. branches)
- Celiac trunk T12 (branches are: Left Gastric; Hepatic; Splenic → Lt. Hand Side)
- SMA L1
- IMA L3

Dorsal: - Lumber (4pairs; lat. paired parietal) L1-L4

- Median Sacral (unpaired, terminal?) (LAST BRANCH)

Lateral: - Inf. Phrenic (lat. paired parietal) (FIRST BRANCH) T12

[3 lat. paired visceral br.]
- Middle supra-renal
- Renal L1
- Gonadal Arteries

Terminal: - Common Iliacs L4

** If surgical access is difficult for AAA, then Left Renal artery is divided to achieve the access**

Abdominal aorta aneurysm

• Abdominal aortic aneurysms are a common problem in vascular surgery.

• They may occur as either true or false aneurysm. With the former all 3 layers of the arterial wall are involved, in
the latter only a single layer of fibrous tissue forms the aneurysm wall.
• True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people. They are
commonest in elderly men and for this reason the UK is now introducing the aneurysm screening program with
the aim of performing an abdominal aortic ultrasound measurement in all men aged 65 years.

Pathology
Abdominal aortic aneurysms occur primarily as a result of the failure of elastic proteins within the extracellular matrix.
Anuerysms typically represent dilation of all layers of the arterial wall. Most aneurysms are caused by degenerative
disease. After the age of 50 years the normal diameter of the infrarenal aorta is 1.5cm in females and 1.7cm in males.
Diameters of 3cm and greater, are considered aneurysmal. The pathophysiology involved in the development of
aneurysms is complex and the primary event is loss of the intima with loss of elastic fibres from the media. This process
is associated with, and potentiated by, increased proteolytic activity and lymphocytic infiltration.

Major risk factors for the development of aneurysms include smoking and hypertension. Rare but important causes
include syphilis and connective tissues diseases such as Ehlers Danlos type 1 and Marfans syndrome

Causes
• Several different groups of patients suffer from aneurysmal disease.
• The commonest group is those who suffer from standard arterial disease, i.e. Those who are hypertensive,
have diabetes and have been or are smokers.
• Other patients such as those suffering from connective tissue diseases such as Marfan's may also develop
aneurysms. In patients with abdominal aortic aneurysms the extracellular matrix becomes disrupted with a
change in the balance of collagen and elastic fibres.

Management

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 • Most abdominal aortic aneurysms are an incidental finding.
• Symptoms most often relate to rupture or impending rupture.
• 20% rupture anteriorly into the peritoneal cavity. Very poor prognosis.
• 80% rupture posteriorly into the retroperitoneal space
• The risk of rupture is related to aneurysm size, only 2% of aneurysms measuring less than 4cm in diameter will
rupture over a 5 year period. This contrasts with 75% of aneurysms measuring over 7cm in diameter.
• This is well explained by La Places' law which relates size to transmural pressure.
• For this reason most vascular surgeons will subject patients with an aneurysm size of 5cm or greater to CT
scanning of the chest, abdomen and pelvis with the aim of delineating anatomy and planning treatment.
Depending upon co-morbidities, surgery is generally offered once the aneurysm is between 5.5cm and 6cm.

Indications for surgery

• Symptomatic aneurysms (80% annual mortality if untreated)
• Increasing size above 5.5cm if asymptomatic
• Rupture (100% mortality without surgery)

Surgical procedures: Abdominal aortic aneurysm repair

Procedure: GA
Invasive monitoring (A-line, CVP, catheter)
Incision: Midline or transverse
Bowel and distal duodenum mobilised to access aorta.
Aneurysm neck and base dissected out and prepared for cross clamp
Systemic heparinisation
Cross clamp (distal first)
Longitudinal aortotomy
Atherectomy
Deal with back bleeding from lumbar vessels and inferior mesenteric artery
Insert graft either tube or bifurcated depending upon anatomy
Suture using Prolene (3/0 for proximal , distal anastomosis suture varies according to site)
Clamps off: End tidal CO2 will rise owing to effects of reperfusion, at this point major risk of myocardial events.
Haemostasis
Closure of aneurysm sac to minimise risk of aorto-enteric fistula
Closure: Loop 1 PDS or Prolene to abdominal wall
Skin- surgeons preference

Post operatively:

ITU (Almost all)

Greatest risk of complications following emergency repair
Complications: Embolic- gut and foot infarcts
Cardiac - owing to premorbid states, reperfusion injury and effects of cross clamp
Wound problems
Later risks related to graft- infection and aorto-enteric fistula

Special groups
Supra renal AAA
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These patients will require a supra renal clamp and this carries a far higher risk of complications and risk of renal failure.

Ruptured AAA
Preoperatively the management depends upon haemodynamic instability. In patients with symptoms of rupture (typical
pain, haemodynamic compromise and risk factors) then ideally prompt laparotomy. In those with vague symptoms and
haemodynamic stability the ideal test is CT scan to determine whether rupture has occurred or not. Most common
rupture site is retroperitoneal 80%. These patients will tend to develop retroperitoneal haematoma. This can be disrupted
if Bp is allowed to rise too high so aim for Bp 100mmHg.
Operative details are similar to elective repair although surgery should be swift, blind rushing often makes the situation
worse. Plunging vascular clamps blindly into a pool of blood at the aneurysm neck carries the risk of injury the vena cava
that these patients do not withstand. Occasionally a supracoeliac clamp is needed to effect temporary control, although
leaving this applied for more than 20 minutes tends to carry a dismal outcome.

EVAR
Increasingly patients are now being offered endovascular aortic aneurysm repair. This is undertaken by surgeons and
radiologists working jointly. The morphology of the aneurysm is important and not all are suitable. Here is a typical list of
those features favoring a suitable aneurysm:
• Long neck
• Straight iliac vessels
• Healthy groin vessels
Clearly few AAA patients possess the above and compromise has to be made. The use of fenestrated grafts
can allow supra renal AAA to be treated.

Procedure:

GA
Radiology or theatre
Bilateral groin incisions
Common femoral artery dissected out
Heparinisation
Arteriotomy and insertion of guide wire
Dilation of arteriotomy
Insertion of EVAR Device
Once in satisfactory position it is released
Arteriotomy closed once check angiogram shows good position and no endoleak

Complications:
Endoleaks depending upon site are either Type I or 2. These may necessitate re-intervention and all EVAR
patients require follow up . Details are not needed for MRCS

Coeliac axis

The coeliac axis has three main branches - Left Hand Side (LHS)
• Lt. gastric
• Hepatic branches. –Rt. Gastric, Gastroduodenal, Rt. Gastroepiploic, Superior Pancreaticoduodenal, Cystic.
• Splenic: branches- Pancreatic, Short Gastric, Left Gastroepiploic

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It occasionally gives off one of the inferior phrenic arteries. The coeliac axis branches off the aorta at T12.

Relations

Anteriorly Lesser omentum

Right Right coeliac ganglion and caudate process of liver

Left Left coeliac ganglion and gastric cardia

Inferiorly Upper border of pancreas and renal vein

● Internal Iliac Artery Branches: I Love Going Places In My Very Own Underwear: (N-369, 373)
I leolumbar
L ateral sacral
G luteal (superior)
[From Posterior Division]

P udendal (internal)
I nferior vesicle (uterine in females)
M iddle rectal
V aginal
O bturator
U mbilical
[From Anterior Division]

Gastroduodenal artery

Supplies
Pylorus, proximal part of the duodenum, and indirectly to the pancreatic head (via the anterior and posterior superior
pancreaticoduodenal arteries)

Path
Most commonly arises from the common hepatic artery of the coeliac trunk
Terminates by bifurcating into the right gastroepiploic artery and the superior pancreaticoduodenal artery

Inferior vena cava

Origin
• L5

Path
• Left and right common iliac veins merge to form the IVC.
• Passes right of midline
• Paired segmental lumbar veins drain into the IVC throughout its length
• The right gonadal vein empties directly into the cava and the left gonadal vein generally empties into the left
renal vein.
• The next major veins are the renal veins and the hepatic veins

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 • Pierces the central tendon of diaphragm at T8
• Right atrium
Relations

Anteriorly Small bowel, first and third part of duodenum, head of pancreas, liver and bile duct, right common iliac
artery, right gonadal artery

Posteriorly Right renal artery, right psoas, right sympathetic chain, coeliac ganglion

Levels

Level Vein

T8 Hepatic vein, inferior phrenic vein, pierces diaphragm

L1 Suprarenal veins, renal vein

L2 Gonadal vein

L1-5 Lumbar veins

L5 Common iliac vein, formation of IVC

● IVC Tributaries: I Like To Rise So High; [Think, IVC wanting to rise high up to heart- NO VALVE.] (N-247,314)
I lilacs (common illiac)
rd th
L umbar (3 & 4 )
T esticular (right) or ovarian
R enal
S uprarenal (right) (It can be injured during the right adrenalectomy)
H epatic vein

● A patient presents with superior vena caval obstruction. How many collateral circulations exist as alternative
pathways of venous return?
Ans: There are 4 collateral venous systems:
Azygos venous system
Internal mammary venous pathway
Long thoracic venous system with connections to the femoral and vertebral veins (2 pathways)
Despite this, venous hypertension still occurs.

Superior mesenteric artery(N-286)

• Branches off aorta at L1
• Supplies small bowel from duodenum (distal to ampulla of vater) through to mid transverse colon
• Takes more oblique angle from aorta and thus more likely to recieve emboli than coeliac axis

Relations of SMA

Superiorly Neck of pancreas

Postero-inferiorly Third part of duodenum

Uncinate process

Posteriorly Left renal vein

Right Superior mesenteric vein

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● SMA BRANCHES: MIIRJa ( ) (N-286)

M iddle colic
I liocolic (Appendicular artery is the branch of iliocolic artery)
I nferior pancreaticoduodenal
R ight colic
J ejunal+ileal

● Occlusn of IMA is seldom asymptomatic bcz it gets supply also by Middle colic artery; usually betn middle & left colic.

● All veins in the body usually run a course parallel to the artery of the same name except Inferior mesenteric

● During development midgut bends around SMA 2form the midgut loop.

Mesenteric vessel disease

Mesenteric ischaemia accounts for 1 in 1000 acute surgical admissions. It is primarily caused by arterial embolism
resulting in infarction of the colon. It is more likely to occur in areas such as the splenic flexure that are located at the
borders of the territory supplied by the superior and inferior mesenteric arteries.

Acute mesenteric • Sudden onset abdominal pain followed by profuse diarrhoea.

embolus (commonest • May be associated with vomiting.
50%)
• Rapid clinical deterioration.
• Serological tests: WCC, lactate, amylase may all be abnormal particularly in
established disease. These can be normal in the early phases.

Acute on chronic • Usually longer prodromal history.

mesenteric ischaemia
• Post prandial abdominal discomfort and weight loss are dominant features. Patients
will usually present with an acute on chronic event, but otherwise will tend not to
present until mesenteric flow is reduced by greater than 80%.
• When acute thrombosis occurs presentation may be as above. In the chronic setting
the symptoms will often be those of ischaemic colitis (mucosa is the most sensitive
area to this insult).

Mesenteric vein • Usually a history over weeks.

thrombosis • Overt abdominal signs and symptoms will not occur until venous thrombosis has
reached a stage to compromise arterial inflow.
• Thrombophilia accounts for 60% of cases.

Low flow mesenteric • This occurs in patients with multiple co morbidities in whom mesenteric perfusion is
infarction significantly compromised by overuse of inotropes or background cardiovascular
compromise.
• The end result is that the bowel is not adequately perfused and infarcts occur from
the mucosa outwards.

Diagnosis
• Serological tests: WCC, lactate, CRP, amylase (can be normal in early disease).

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 • Cornerstone for diagnosis of arterial AND venous mesenteric disease is CT angiography scanning in the
arterial phase with thin slices (<5mm). Venous phase contrast is not helpful.
• SMA duplex USS is useful in the evaluation of proximal SMA disease in patients with chronic mesenteric
ischaemia.
• MRI is of limited use due to gut peristalsis and movement artefact.

Management
• Overt signs of peritonism: Laparotomy
• Mesenteric vein thrombosis: If no peritonism: Medical management with IV heparin
• At operation limited resection of frankly necrotic bowel with view to relook laparotomy at 24-48h. In the interim
urgent bowel revascularisation via endovascular (preferred) or surgery.

Prognosis
Overall poor. Best outlook is from an acute ischaemia from an embolic event where surgery occurs within 12h. Survival
may be 50%. This falls to 30% with treatment delay. The other conditions carry worse survival figures.

Epigastric artery

The inferior epigastric artery arises from the external iliac artery immediately above the inguinal ligament. It then passes
along the medial margin of the deep inguinal ring. From here it continues superiorly to lie behind the rectus abdominis
muscle.

● For CABG - LIMA is used then rectus abdominis muscle is backed up by Inf. Epigastric artery 2maintain supply(N-

238)

● Arteries Encountered In Colorectal Surgery

Hemicolectomy (Rt) : RC; IC; (+ MC, if extended)

Hemicolectomy (Lt) : LC; LLC; S; (+ MC, if extended) (lt. ureter can also be injured,, cz its

under psoas major)

Sigmoid-colectomy : LLC; S
n
Abdominoperineal Resec : S; SR
n
Anterior resec : SR (+ left Ureter)
**RC= Rt.colic; LC= Lt. Colic; IC= Iliocolic; LLC= Lt.lower colic; S= sigmoid; SR= Sup. Rectal**
**Posteriorly Gonadal vessels also can be injured

Some Important Nerve and related infos

● PUDENDAL N. BRANCHES(N-382)
Inf. Rectal N. : EAS; Skin around anus; Anal canal below pectinate line
Perineal N : Med & lat. Post scrotal; Muscular br.urogenital muscle
Dorsal N. Penis : Skin of body & glans of penis

● Vagus supplies parasympathetics to the entire GIT upto last part of transverse colon. Rest parts receive
parasympathetic from pelvic splanchnic nerves.
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● Cremesteric reflex – Genitofemoral Nerve

GENERAL DISCUSSION
Levels & Planes

Transpyloric plane: Level of the body of L1

• Pylorus stomach
• Left kidney hilum (L1- left one!)
• Right hilum of the kidney (1.5cm lower than the left)
• Fundus of the gallbladder
• Neck of pancreas
• Duodenojejunal flexure
• Superior mesenteric artery
• Portal vein
• Left and right colic flexure
• Root of the transverse mesocolon
• 2nd part of the duodenum
• Upper part of conus medullaris
• Spleen

● TRANSPYLORIC PLANE OF ADDISON: remember like an address !!! (N-251)

th
GB; Renal hila; Duodenojejunal junction; 9 rib; Pyloric part; Pancreatic Neck (passes thru’ lower border of L1)

Flat # GB
Renal villa (hila)
Duodenojejunal junction
th
9 (rib) Pyloric street
Pancreatic Neck circus
Dhaka.

Can be identified by asking the supine patient to sit up without using their arms. The plane is located where the lateral
border of the rectus muscle crosses the costal margin.
Anatomical planes

Subcostal plane Lowest margin of 10th costal cartilage

Intercristal plane Level of body L4 (highest point of iliac crest)

Intertubercular plane Level of body L5

Common level landmarks

Inferior mesenteric artery L3

Bifurcation of aorta into common iliac arteries L4

Formation of IVC L5 (union of common iliac veins)

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Diaphragm apertures • Vena cava T8
• Oesophagus T10
• Aortic hiatus T12

Oesophagus

• 25cm long
• Starts at C6 vertebra, pierces diaphragm at T10 and ends at T11
• Squamous epithelium

Constrictions of the oesophagus

Structure Distance from incisors

Cricoid cartilage 15cm – C6

Arch of the Aorta 22.5cm – T4

Left principal bronchus 27cm – T6

Diaphragmatic hiatus 40cm – T10

Relations

Anteriorly • Trachea to T4
• Recurrent laryngeal nerve
• Left bronchus, Left atrium
• Diaphragm

Posteriorly • Thoracic duct to left at T5

• Hemiazygos to the left T8
• Descending aorta
• First 2 intercostal branches of aorta

Left • Thoracic duct

• Left subclavian artery

Right • Azygos vein

Arterial, venous and lymphatic drainage of the oesophagus

Artery Vein Lymphatics Muscularis externa

Upper third Inferior thyroid Inferior thyroid Deep cervical Striated muscle

Mid third Aortic branches Azygos branches Mediastinal Smooth & striated muscle

Lower third Left gastric Posterior mediastinal and coeliac Gastric Smooth muscle

Nerve supply

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 • Upper half is supplied by recurrent laryngeal nerve
• Lower half by oesophageal plexus (vagus)

Histology
• Mucosa :Nonkeratinized stratified squamous epithelium
• Submucosa: glandular tissue
• Muscularis externa (muscularis)
• Adventitia

Oesophageal disease

Disorder Features

Mallory-Weiss Tear ● Usually history of antecedent vomiting. This is then followed by the vomiting of a small
amount of blood.
● There is usually little in the way of systemic disturbance or prior symptoms.

● 90% cases MALLORY-WEISS TEAR spontaneously stopped, others usually

responds to endoscopic adrenaline(1:10000) injection. Usually 3% cases need surgery

(Gastrotomy & underrunning)

Hiatus hernia of gastric cardia Often longstanding history of dyspepsia, patients are often overweight. Uncomplicated
hiatus hernias should not be associated with dysphagia or haematemesis.

Squamous cell carcinoma of History of progressive dysphagia. Often signs of weight loss. Usually little or no history of
the oesophagus previous GORD type symptoms.

Adenocarcinoma of the Progressive dysphagia, may have previous symptoms of GORD or Barretts oesophagus.
oesophagus

Peptic stricture Longer history of dysphagia, often not progressive. Usually symptoms of GORD. Often
lack systemic features seen with malignancy

Dysmotility disorder May have dysphagia that is episodic and non progressive. Retrosternal pain may
accompany the episodes.

Diagnosis
Most of the differential diagnoses listed above can be accurately categorised by upper GI endoscopy (usually most
patients). Where this fails to demonstrate a mechanical stricture the use of pH and manometry studies together with
radiological contrast swallows will facilitate the diagnosis.

Dysphagia

Causes of dysphagia

Extrinsic • Mediastinal masses

• Cervical spondylosis

Oesophageal wall • Achalasia

• Diffuse oesophageal spasm

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 • Hypertensive lower oesophageal sphincter

Intrinsic • Tumours
• Strictures
• Oesophageal web
• Schatzki rings

Neurological • CVA
• Parkinson's disease
• Multiple Sclerosis
• Brainstem pathology
• Myasthenia Gravis

Investigation
All patients require an upper GI endoscopy unless there are compelling reasons for this not to be performed. Motility
disorders may be best appreciated by undertaking fluoroscopic swallowing studies.
A full blood count should be performed.
Ambulatory oesophageal pH and manometry studies will be required to evaluate conditions such as achalasia and
patients with GORD being considered for fundoplication surgery.

Gastroesophageal Reflux Disease

- Weak lower oesophageal sphincter

- pH < 4 for >4% for 24hr monitoring
- C/F
o Angina type pain
o Odynophagia while swallowing hot drinks
o Food reflux(not vomit) specially on bending
o Globus (lump in throat)
- Dx
o pH monitoring (gold standard)
o Endoscopy (Invx of choice)
o Biopsy (80% dxtic)
o Esophageal manometry
o Ba-swallow(not definite)

- Complication
o Stricture
o Barrett’s oesophagus
o Bleeding

- Rx
o Antacid
o H2 blocker
o PPI
o Metochlopromide

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 - Surgery
0
o Floppy Nissen 360 fundoplication(post. Partial & ant. partial)
o Hill repair
o Angel chick prosthesis
o Belsey Mark iv : transthoracic fundoplication
o Roux-en Y (in case of recurrence)

● Endoscopic placement of self-expanding metal stents (SEMS) are now placed most frequently in patients presenting
with malignant dysphagia. Early complications of SEMS are malposition, oesophageal perforation, bleeding and stent
migration. Late complications are most frequently related to eating (food bolus) or tumour overgrowth. Initially
management of a food bolus blocking a stent is for the patient to consume a fizzy drink, which helps to break up the food
bolus, otherwise endoscopy is required to dislodge the food bolus

Barrett's Oesophagus
• Intestinal metaplasia
• Squamous epithelium replaced by columnar epithelium in the lower oesophagus
• 3 types of columnar epithelium:
1. Junctional
2. Atrophic fundal
3. Specialised
• Presence of goblet cells important in identification
• Premalignant change (progress to dysplasia)
• Risk of adenocarcinoma
• Risk factors: middle age, men, smoker, Caucasian, gastro-oesophageal reflux, obesity

Treatment
• Long term proton pump inhibitor.
• Consider pH and manometry studies in younger patients who may prefer to consider an anti reflux procedure.
• Regular endoscopic monitoring (more frequently if moderate dysplasia). With quadrantic biopsies every 2-3 cm.
• If severe dysplasia be very wary of small foci of cancer.

Achalasia; Pseudoachalasia; Diff. esophageal spasm

FEATURES ACHALASIA PSEUDO DOS

ACHALASIA
Age 30-60 yrs >50
Predispose to SCC
n
Pain Retrosternal chest pain Ca @ LOS, Angina type chest pain ē radiat
extrinsic tumor to jaw, Interscapular region –
CAG normal
Clammy & pale
Food prob. Solid + liquid
Dysphagia + recurrent pneumonia Dysphagia+Odynophagia both
Dysphagia exacerbate with stress

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 n
Regurgita Present Absent
Manometry Absent peristalsis Nut-cracker/ Corkscrew
esophagus
Segmental spasm
Pseudodiverticulosis
Endoscopy To exclude stricture / Ca Can’t pass thru’
Ba swallow Bird’s beak
No gastric air bubble
Food residue may present @ esophagus
Double right heart border
n st
Rx Esophageal Bouginage/ballon dilat (1 Nifedipine
line)
nd
Heller’s cardiomyotomy(2 line)
Inj. Botulinum toxin ē endoluminal US
guide

● Corkscrew esophagus - Diffuse oesophageal spasm

Bird’s Beak oesophagus - Achalasia Cardia ... A-B & C-D

● ACHALASIA – Shows the characteristic mega- esophagus on Ba swallow

Manometry reveals high lower oesophageal sphincter pressure ē failure to relax during swallowing

● Oesophageal varices patient, band ligation done, bleeding unstoppable; RX- Balloon temponade (Sengstaken-

Blakemore / Minnesota tube)

Oesophageal cancer

SCC (upper 2/3 assoc. achalasia, PUD, caeliac disease,webs,stricture,vit.A&C def.;),

Adenocarcinoma (lower 1/3 assoc. GORD and Barrett's)
Oat cell carcinoma (very rare,poor Prox)
Commonest benign tumor of oesophagus is leiomyoma
• Incidence is increasing. Barretts oesophagus is a major risk factor for most cases
• In most cases in the Western world most number of cases is Adenocarcinoma - in the UK adenocarcinomas
account for 65% of cases. In other regions of the world Squamous Cancer is more common
• Is linked to smoking, alcohol intake, diets rich in nitrosamines and achalasia.
• Surveillance of Barretts is important as it reports a 30 fold increase in cancer risk.
• If invasive malignancy is diagnosed early then survival may approach 85% at 5 years.

● Oesophageal Ca Dx

• UGI Endoscopy (best 1st line Invx for anyone ē dysphagia)

• Contrast swallow may be of benefit in classifying benign motility disorders but has no place in the
assessment of tumours
• CT scan (to see lung & liver mets.& distant lymphadenopathy). If overt metastatic disease is identified using this
modality then further complex imaging is unnecessary
• If CT does not show metastatic disease, then best method for preoperative local staging is endoscopic US.

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 • Staging laparoscopy is performed to detect occult peritoneal disease.
• If laparoscopy is negative then PET CT is performed.
• Thoracoscopy is not routinely performed. Bronchoscopy can be done in prox & middle 3rd tumor adjacent
tracheobroncheal tree

● Treatment
• In general resections are not offered to those patients with distant metastasis, and usually not to those with N2
disease.
• Local nodal involvement is not in itself a contra indication to resection.
• Surgical resection is the mainstay of treatment.
• Neoadjuvent chemotherapy is given in most cases prior to surgery.

• In more proximal lesion – Total Oesphagectomy (Mckeown Type) with anastomosis to cervical Oesophagus
• In situ disease – Endoscopic Mucosal Resection
• In lower third disease – Ivor – Lewis type procedure.
• In very distal tumors – Transhiatal Procedure. (its an attractive option – as two visceral cavities penetration is
required for Ivor – Lewis type procedure, which increases the morbidity considerably)
• In unresectable disease – Local Ablative Procedures, Palliative Chemotherapy or Stent Insertion.

● Two stage Ivor Lewis (also called Lewis-Tanner) approach-

- Initial laparotomy and construction of a gastric tube,
- Right thoracotomy to excise the tumor and create an esophagogastric anastomosis.
- Preferred for middle & lower third tumor
- Azygos Vein is divided to allow mobilization of oesophagus

● Three stage McKeown approach-

- Ivor Lewis (also called Lewis-Tanner) approach plus neck incision
n
- Third incision in the neck is made to complete anastomosis betw stomach & cervical esophagus.
● Transhiatal resection-
- Laparotomy & incision in the neck.
- Esophagus is mobilized by blunt dissection from above & below.
- Stomach used as conduit & brought up to the neck & cervical anastomosis carried out as in the 3
phase procedure
- For elderly patient ē lower tumor, for whom thoracotomy is not suitable; or ē severe dysplasia ē
Barrett’s

● Operative details of Ivor- Lewis procedure

• Combined laparotomy and right thoracotomy
Indication
• Lower and middle third oesophageal tumours
Preparation
• Staging with a combination of CT chest abdomen and pelvis- if no metastatic disease detected then patients
will undergo a staging laparoscopy to detect peritoneal disease.
• If both these modalities are negative then patients will finally undergo a PET CT scan to detect occult
metastatic disease. Only in those whom no evidence of advanced disease is detected will proceed to resection.
• Patients receive a GA, double lumen endotracheal tube to allow for lung deflation, CVP and arterial monitoring.

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 Procedure
• A Rooftop Incision is made to access the stomach and duodenum.

Laparotomy To mobilize the stomach

• The greater omentum is incised away from its attachment to the right gastroepiploic vessels along the greater
curvature of the stomach.
• Then the short gastric vessels are ligated and detached from the greater curvature from the spleen.
• The lesser omentum is incised, preserving the right gastric artery.
• The retroperitoneal attachments of the duodenum in its second and third portions are incised, allowing the
pylorus to reach the oesophageal hiatus. Some surgeons perform a pyloroplasty at this point to facilitate gastric
emptying.
• The left gastric vessels are then ligated, avoiding any injury to the common hepatic or splenic arteries. Care
must be taken to avoid inadvertently devascularising the liver owing to variations in anatomy.

Right Thoracotomy Oesophageal resection and oesophagogastric anastomosis

• Through 5th intercostal space
• Dissection performed 10cm above the tumour
• This may involve transection of the azygos vein.
• The oesophagus is then removed with the stomach creating a gastric tube.
• An anastomosis is created.
• The chest is closed with underwater seal drainage and tube drains to the abdominal cavity.

Post operatively
• Patients will typically recover in ITU initially.
• A nasogastric tube will have been inserted intraoperatively and must remain in place during the early phases of
recovery.
• Post operatively these patients are at relatively high risk of developing complications:

* Atelectasis- due to the effects of thoracotomy and lung collapse

* Anastomotic leakage. The risk is relatively high owing to the presence of a relatively devascularised
stomach. Often the only blood supply is from the gastroepiploic artery as all others will have been
divided. If a leak does occur then many will attempt to manage conservatively with prolonged
nasogastric tube drainage and TPN. The reality is that up to 50% of patients developing an
anastomotic leak will not survive to discharge.

* Delayed gastric emptying (may be avoided by performing a pyloroplasty).

Oesophageal candidiasis

- Characterised by white spots in the oropharynx with extension into the oesophagus.
- Associated with broad spectrum antibiotic usage, immunosupression and immunological disorders.
- Patients may present with oropharyngeal symptoms, odynophagia and dysphagia.
- Treatment is directed both at the underlying cause and with oral antifungal agents.

16
Theme: Oesophageal disease Rx

A. Oesophagectomy

B. Endoscopic sub mucosal dissection

C. Photodynamic therapy

D. Insertion of oesophageal stent

E. Chemotherapy

F. Radiotherapy

● A 52 year old man with long standing Barretts oesophagus is diagnosed with high grade dysplasia on recent
endoscopy. The lesions are multifocal and mainly distally sited.
The correct answer is Oesophagectomy
Some may argue for local therapy. However, in young patients who are otherwise fit, multifocal disease such as this
should probably be resected.

● A 72 year old man presents with dysphagia. He is investigated and found to have an adenocarcinoma of the distal
oesophagus. His staging investigations have revealed a solitary metastatic lesion in the right lobe of his liver.
The correct answer is Insertion of oesophageal stent
Although he may be palliated with chemotherapy a stent will produce the quickest clinical response. Metastatic disease
is usually a contra indication to oesophageal resection.

● An 83 year old lady with long standing Barretts oesophagus is diagnosed with a 1cm focus of high grade dysplasia
3cm from the gastrooesophageal junction.
Endoscopic sub mucosal dissection
As she is elderly and the disease localised EMR is an appropriate first line step.

The technique involves raising the mucosa containing the lesion and then using an endoscopic snare to remove it. This
technique is therefore minimally invasive. However, it is only suitable for early superficial lesions. Deeper invasion would
carry a high risk of recurrence

Abdominal wall

The 2 main muscles of the abdominal wall are the rectus abdominis (anterior) and the quadratus
lumborum (posterior).
The remaining abdominal wall consists of 3 muscular layers. Each muscle passes from the lateral aspect of the
quadratus lumborum posteriorly to the lateral margin of the rectus sheath anteriorly. Each layer is muscular
posterolaterally and aponeurotic anteriorly.

Muscles of abdominal wall

External oblique • Lies most superficially

• Originates from 5th to 12th ribs
• Inserts into the anterior half of the outer aspect of the iliac crest, linea alba and pubic
tubercle
• More medially and superiorly to the arcuate line, the aponeurotic layer overlaps the rectus
abdominis muscle

17
 • The lower border forms the inguinal ligament
• The triangular expansion of the medial end of the inguinal ligament is the lacunar ligament.

Internal oblique • Arises from the thoracolumbar fascia, the anterior 2/3 of the iliac crest and the lateral 2/3 of
the inguinal ligament
• The muscle sweeps upwards to insert into the cartilages of the lower 3 ribs
• The lower fibres form an aponeurosis that runs from the tenth costal cartilage to the body of
the pubis
• At its lowermost aspect it joins the fibres of the aponeurosis of transversus abdominis to
form the conjoint tendon.

Transversus • Innermost muscle

abdominis • Arises from the inner aspect of the costal cartilages of the lower 6 ribs , from the anterior
2/3 of the iliac crest and lateral 1/3 of the inguinal ligament
• Its fibres run horizontally around the abdominal wall ending in an aponeurosis. The upper
part runs posterior to the rectus abdominis. Lower down the fibres run anteriorly only.
• The rectus abdominis lies medially running from the pubic crest and symphysis to insert into
the xiphoid process and 5th, 6th and 7th costal cartilages. The muscles lies in a
aponeurosis as described above.
• Nerve supply: anterior primary rami of T7-12

Surgical notes
During abdominal surgery it is usually necessary to divide either the muscles or their aponeuroses. During a midline
laparotomy it is desirable to divide the aponeurosis. This will leave the rectus sheath intact above the arcuate line and
the muscles intact below it. Straying off the midline will often lead to damage to the rectus muscles, particularly below
the arcuate line where they may often be in close proximity to each other.

Rectus abdominis muscle

The rectus sheath is formed by the aponeuroses of the lateral abdominal wall muscles. The rectus sheath has a
composition that varies according to anatomical level.

1. Above the costal margin the anterior sheath is composed of external oblique aponeurosis, the costal cartilages are
posterior to it.
2. From the costal margin to the arcuate line, the anterior rectus sheath is composed of external oblique aponeurosis
and the anterior part of the internal oblique aponeurosis. The posterior part of the internal oblique aponeurosis and
transversus abdominis form the posterior rectus sheath.
3. Below the arcuate line the aponeuroses of all the abdominal muscles lie in anterior aspect of the rectus sheath.
Posteriorly lies the transversalis fascia and peritoneum.

The arcuate line is the point at which the inferior epigastric vessels enter the rectus sheath.

Hesselbach's triangle

Direct hernias pass through Hesselbachs triangle.

Superolaterally Epigastric vessels

18
Medially Lateral edge of rectus muscle

Inferiorly Inguinal ligament

Abdominal signs

• Rovsings sign- appendicitis; palpation of the left iliac fossa causes pain in the right iliac fossa
• Psoas stretch sign - Acute retrocaecal appendicitis is indicated when right thigh is passively extended with
patient lying on their side with their knees extended
• Boas sign –cholecystitis. Hyperesthesia beneath the right scapula
• Murphys sign- cholecystitis - pain/catch of breath, on palpation of right hypochondrium during inspiration
• Cullens sign- pancreatitis (other intra-abdominal haemorrhage); peri-umbilical bruising
• Grey-Turners sign- pancreatitis (or other retroperitoneal haemorrhage); bruising in the flanks.

Abdominal radiology

Plain abdominal x-rays are often used as a first line investigation in patients with acute abdominal pain. A plain
abdominal film may demonstrate free air, evidence of bowel obstruction and possibly other causes of pain (e.g. renal or
gallbladder stones).
Investigation of potential visceral perforation is usually best performed by obtaining an erect chest x-ray, as this is a
more sensitive investigation for suspected visceral perforation.

Features which are usually abnormal

• Large amounts of free air (colonic perforation), smaller volumes seen with more proximal perforations.
• A positive Riglers sign (gas on both sides of the bowel wall).
• Caecal diameter of >8cm
• Fluid levels in the colon
• Ground glass appearance to film (usually due to large amounts of free fluid).
• Sentinel loop in patients with inflammation of other organs (e.g. pancreatitis).

Features which should be expected/ or occur without pathology

• In Chialditis syndrome, a loop of bowel may be interposed between the liver and diaphragm, giving the
mistaken impression that free air is present.
• Following ERCP (and sphincterotomy) air may be identified in the biliary tree.
• Free intra abdominal air following laparoscopy / laparotomy, although usually dissipates after 48-72 hours.

Acute abdominal pain

Acute abdominal pain is a common cause of admission to hospital. The relative proportions of conditions presenting with
abdominal pain is
• Non specific abdominal pain (35%)
• Appendicitis (17%)
• Intestinal obstruction (15%)
• Urological disease (6%)
• Gallstone disease (5%)
19
 • Colonic diverticular disease (4%)
• Abdominal trauma (3%)
• Perforated peptic ulcer (3%)
• Pancreatitis (2%)
Non specific abdominal pain should really be a diagnosis of exclusion and if care is taken in excluding organic disease
the proportion of cases labeled such should decline. It should also be appreciated that a proportion of patients may have
an underlying medical cause for their symptoms such as pneumonia or diabetic ketoacidosis.

Key points in management

• Early administration of adequate analgesia (including opiates).
• Abdominal ultrasound is safe, non invasive and cheap and yields significantly more information than plain
radiology. However, plain radiology is still the main test for suspected perforated viscus, especially out of hours.
• In up to 50% cases with perforated peptic ulcer, the plain x-rays may show no evidence of free air. If clinical
signs suggest otherwise, then a CT scan may be a more accurate investigation, if plain films are normal.
• Plain film radiology usually cannot detect <1mm free air, and is 33% sensitive for detection of 1-13mm pockets
of free air (Stoker et al. Radiology 2009 253: 31-46).
• Think of strangulated intestine when there is fever, raised white cell count, tachycardia and peritonism.
• In suspected large bowel obstruction a key investigation is either a water soluble contrast enema or CT scan.
• Where need for surgery is difficult to define and imaging is inconclusive the use of laparoscopy as a definitive
diagnostic test is both safe and sensible.

Acute abdominal pain-diagnoses

Condition Features Investigations Management

Appendicitis History of migratory pain. Differential white cell count Appendicectomy

Fever. Pregnancy test
Anorexia. C-Reactive protein
Evidence of right iliac fossa Amylase
tenderness. Urine dipstick testing
Mild pyrexia.

Mesenteric Usually recent upper Full blood count- may show Conservative management-
adenitis respiratory tract infection. slightly raised white cell count appendicectomy if diagnostic
High fever. Urine dipstick often normal doubt
Generalised abdominal Abdominal ultrasound scan -
discomfort- true localised pain usually no free fluid
and signs are rare.

Mittelschmerz Only seen in females.
Mid cycle pain.
Usually occurs two weeks
after last menstrual period.
Pain is usually has a supra-
pubic location.
Usually subsides over a 24-
48 hour period.
Full blood count- normal
Urine dipstick- normal
Abdominal and pelvic
ultrasound- may show a trace of
pelvic free fluid
Manage conservatively if doubt or
symptoms fail to settle then
laparoscopy

20
Fitz-Hugh Curtis Disseminated infection with
syndrome Chlamydia.
Usually seen in females.
Consists of evidence of pelvic evidence of sexually transmitted
inflammatory disease
together with peri-hepatic
inflammation and subsequent
adhesion formation.
Abdominal aortic Sudden onset of abdominal
aneurysm pain radiating to the back in
(ruptured) older adults (look for risk
factors).
Collapse.
May be moribund on arrival in
casualty, more stable if
contained haematoma.
Careful clinical assessment
may reveal pulsatile mass.
Perforated peptic Sudden onset of pain (usually Erect CXR may show free air. A
ulcer epigastric).
Often preceding history of
upper abdominal pain.
Soon develop generalised
abdominal pain.
On examination may have
clinical evidence of peritonitis.
Intestinal Colicky abdominal pain and
obstruction vomiting (the nature of which
depends on the level of the
obstruction).
Abdominal distension and
constipation (again depending
upon site of obstruction).
Features of peritonism may
occur where local necrosis of
bowel loops is occurring.
Mesenteric Embolic events present with
infarction sudden pain and forceful
evacuation.
Acute on chronic events
usually have a longer history
and previous weight loss.
On examination the pain is
typically greater than the
physical signs would suggest.
Abdominal ultrasound scan- may Usually medically managed-
show free fluid doxycycline or azithromycin
High vaginal swabs - may show
infections
Patients who are Unstable patients should undergo
haemodynamically stable should immediate surgery (unless it is not
have a CT scan in their best interests).
Those with evidence of contained
leak on CT should undergo
immediate surgery
Increasing aneurysmal size is an
indication for urgent surgical
intervention (that can wait until the
next working day)
Laparotomy (laparoscopic surgery
CT scan may be indicated where for perforated peptic ulcers is both
there is diagnostic doubt safe and feasible in experienced
hands)
A plain abdominal film may help In those with a virgin abdomen
with making the diagnosis. A CT and lower and earlier threshold for
scan may be useful where laparotomy should exist than in
diagnostic uncertainty exists those who may have adhesional
obstruction
Arterial pH and lactate Immediate laparotomy and
Arterial phase CT scanning is the resection of affected segments, in
most sensitive test acute embolic events SMA
embolectomy may be needed.
21
Gynaecological causes of abdominal pain

A number of women will present with abdominal pain and subsequently be diagnosed with a gynaecological disorder. In
addition to routine diagnostic work up of abdominal pain, all female patients should also undergo a bimanual vaginal
examination, urine pregnancy test and consideration given to abdominal and pelvic ultrasound scanning.
When diagnostic doubt persists a laparoscopy provides a reliable method of assessing suspected tubulo-ovarian
pathology.

Differential diagnoses of abdominal pain in females

Diagnosis Features Investigation Treatment

Mittelschmerz Usually mid cycle pain. Full blood count- Conservative

Often sharp onset. usually normal
Little systemic disturbance. Ultrasound- may show
May have recurrent episodes. small quantity of free
Usually settles over 24-48 hours. fluid

Endometriosis 25% asymptomatic, in a further Ultrasound- may show Usually managed medically, complex
25% associated with other pelvic free fluid disease will often require surgery and
organ pathology. Laparoscopy will some patients will even require formal
Remaining 50% may have usually show lesions colonic and rectal resections if these
menstrual irregularity, infertility, areas are involved
pain and deep dyspareurina.
Complex disease may result in
pelvic adhesional formation with
episodes of intermittent small
bowel obstruction.
Intra-abdominal bleeding may
produce localised peritoneal
inflammation.
Recurrent episodes are common.

Ovarian torsion Usually sudden onset of deep Ultrasound may show Laparoscopy
seated colicky abdominal pain. free fluid
Associated with vomiting and Laparoscopy is usually
distress. both diagnostic and
Vaginal examination may reveal therapeutic
adnexial tenderness.

Ectopic Symptoms of pregnancy without Ultrasound showing no Laparoscopy or laparotomy is

gestation evidence of intra uterine gestation.
Present as an emergency with
evidence of rupture or impending
rupture.
Open tubular ruptures may have
sudden onset of abdominal pain
and circulatory collapse, in other
intra uterine pregnancy haemodynamically unstable. A
and beta HCG that is salphingectomy is usually performed.
elevated
May show intra
abdominal free fluid

22
 the symptoms may be more
prolonged and less marked.
Small amount of vaginal discharge
is common.
There is usually adnexial
tenderness.

Pelvic Bilateral lower abdominal pain Full blood count- Usually medical management
inflammatory associated with vaginal discharge. Leucocytosis
disease Dysuria may also be present. Pregnancy test
Peri-hepatic inflammation negative (Although
secondary to Chlamydia (Fitz Hugh infection and
Curtis Syndrome) may produce pregnancy may co-
right upper quadrant discomfort. exist)
o
Fever >38 Amylase - usually
normal or slightly
raised
High vaginal and
urethral swabs

Right iliac fossa pain

Differential diagnosis

Appendicitis • Pain radiating to right iliac fossa

• Anorexia
• Typically short history
• Diarrhoea and profuse vomiting rare

Crohn's disease • Often long history

• Signs of malnutrition
• Change in bowel habit, especially diarrhoea

Mesenteric adenitis • Mainly affects children

• Causes include Adenoviruses, Epstein Barr Virus, beta-
haemolyticStreptococcus, Staphylococcus spp., Escherichia
coli, Streptococcusviridans and Yersinia spp.
• Patients have a higher temperature than those with appendicitis
• If laparotomy is performed, enlarged mesenteric lymph nodes will be present

Diverticulitis • Both left and right sided disease may present with right iliac fossa pain
• Clinical history may be similar, although some change in bowel habit is usual
• When suspected a CT scan may help in refining the diagnosis

Meckel's diverticulitis • A Meckel's diverticulum is a congenital abnormality that is present in about 2%

of the population
• Typically 2 feet proximal to the ileocaecal valve
• May be lined by ectopic gastric mucosal tissue and produce bleeding

Perforated peptic ulcer • This usually produces upper quadrant pain but pain may be lower

23
 • Perforations typically have a sharp sudden onset of pain in the history

Incarcerated right inguinal • Usually only right iliac fossa pain if right sided or bowel obstruction.
or femoral hernia

Bowel perforation • Seldom localised to right iliac fossa, although complete large bowel obstruction
secondary to caecal or with caecal distension may cause pain prior to perforation.
colon carcinoma

Gynaecological causes • Pelvic inflammatory disease/salpingitis/pelvic abscess/Ectopic

pregnancy/Ovarian torsion/Threatened or complete abortion/Mittelschmerz

Urological causes • Ureteric colic/UTI/Testicular torsion

Other causes • TB/Typhoid/Herpes Zoster/AAA/Situs inversus

Abdominal compartment syndrome

Background
Intra-abdominal pressure is the steady state pressure concealed within the abdominal cavity.
• In critically ill adults the normal intra abdominal pressure = 5-7mmHg
• Intra abdominal hypertension has pressures of 12-25mmHg
• Changes >15mmHg are associated with microvascular hypoperfusion
• Abdominal compartment syndrome is defined as sustained intra abdominal pressure >20mmHg coupled
with new organ dysfunction / failure
• It may occur either primarily without previous surgical intervention e.g. Following intestinal ischaemia or
secondarily following a surgical procedure
• Diagnosis is typically made by transvesical pressure measurements coupled with an index of clinical suspicion.

Management
Once the diagnosis is made non operative measures should be instituted including:
• Gastric decompression
• Improve abdominal wall compliance e.g. muscle relaxants/ sedation
• Drain abdominal fluid collections.
• Consider fluid restriction/ diuretics if clinically indicated.

In those whom non operative treatment is failing; the correct treatment is laparotomy and laparostomy. Options for
laparostomy are many although the Bogota bag or VAC techniques are the most widely practised. Re-look laparotomy
and attempts at delayed closure will follow in due course
Abdominal wound dehiscence
• This is a significant problem facing all surgeons who undertake abdominal surgery on a regular basis.
Traditionally it is said to occur when all layers of an abdominal mass closure fail and the viscera protrude
externally (associated with 30% mortality).
• It can be subdivided into superficial, in which the skin wound alone fails andcomplete, implying failure of all
layers.

Factors which increase the risk are:

* Malnutrition

24
* Vitamin deficiencies
* Jaundice
* Steroid use
* Major wound contamination (e.g. faecal peritonitis)
* Poor surgical technique (Mass closure technique is the preferred method-Jenkins Rule)

When sudden full dehiscence occurs the management is as follows:

* Analgesia
* Intravenous fluids
* Intravenous broad spectrum antibiotics
* Coverage of the wound with saline impregnated gauze (on the ward)
* Arrangements made for a return to theatre

Surgical strategy
• Correct the underlying cause (eg TPN or NG feed if malnourished)
• Determine the most appropriate strategy for managing the wound

Options

Resuturing of the This may be an option if the wound edges are healthy and there is enough tissue for sufficient
wound coverage. Deep tension sutures are traditionally used for this purpose.

Application of a This is a clear dressing with removable front. Particularly suitable when some granulation tissue is
wound manager present over the viscera or where there is a high output bowel fistula present in the dehisced
wound.

Application of a This is a clear plastic bag that is cut and sutured to the wound edges and is only a temporary
'Bogota bag' measure to be adopted when the wound cannot be closed and will necessitate a return to theatre
for definitive management.

Application of a These can be safely used BUT ONLY if the correct layer is interposed between the suction device
VAC dressing and the bowel. Failure to adhere to this absolute rule will almost invariably result in the
system development of multiple bowel fistulae and create an extremely difficult management problem.

Derivatives of Dorsal Mesogastrium

Spleen
Pancreas
G. omentum (gastrosplenic, gastrophrenic, gastrocolic)
Splenorenal ligament (pancreas tail is here…)

n
Stomach Bed Form (N-256)
- Diaphragm
- Lt. suprarenal gland
- Lt. Kidney
- Left colic flexure
- Splenic artery
- Transverse mesocolon
- Ant. Surface pancreas (body & tail)
- Spleen(±)

25
Peristalsis
• Circular smooth muscle contracts behind the food bolus and longitudinal smooth muscle propels the food
through the oesophagus
• Primary peristalsis spontaneously moves the food from the oesophagus into the stomach (9 seconds)
• Secondary peristalsis occurs when food, which doesn't enter the stomach, stimulates stretch receptors to cause
peristalsis
• In the small intestine each peristalsis waves slows to a few seconds and causes mixture of chyme
• In the colon three main types of peristaltic activity are recognised (see below)

Colonic peristalsis

Segmentation contractions Localised contractions in which the bolus is subjected to local forces to maximise
mucosal absorption

Antiperistaltic contractions Localised reverse peristaltic waves to slow entry into colon and maximise
towards ileum absorption

Mass movements Waves migratory peristaltic waves along the entire colon to empty the organ prior
to the ingestion of food bolus

Omentum
• The omentum is divided into two parts which invest the stomach. Giving rise to the greater and lesser
omentum. The greater omentum is attached to the inferolateral border of the stomach and houses the gastro-
epiploic arteries.
• It is of variable size but is less well developed in children. This is important as the omentum confers protection
against visceral perforation (e.g. Appendicitis).
• Inferiorly between the omentum and transverse colon is one potential entry point into the lesser sac.
• Several malignant processes may involve the omentum of which ovarian cancer is the most notable.

Ulcers Cause (N-282)

Post. Gastric : Splenic artery← celiac trunk
Lesser curvature : Left. Gastric artery ← celiac trunk
Greater curvature : Gastro-epiploic vessels← GDA← CHA← celiac trunk
Post. Duodenal : Gastro-duodenal artery ← CHA

Various Types of Cells

Chief / zymogenic cell : Pepsinogen (Fundus)
H
Parietal / oxyntic cell : HCl; IF; Na; Ca; Mg (p ) (Body)
–
Mucous neck cell : Mucous, HCO3 (Pylorus)
G cell : Gastrin, (Pylorus)
Pancreatic acinar cell : Chymotrypsinogen; Collipase; Amylase; Phospholypase
Enterochromaffin cell : Serotonin; Bradykinin, Histamin

Gastrointestinal secretions

Up to 7 litres of gastrointestinal secretions enter the lumen of the GI tract in a 24 hour period. The absorptive function of
the small bowel is such that by the time a formed stool is created, it will contain, on average 200ml water.
The common secretions together with their approximate volumes are demonstrated below:

26
 + + -
Origin of secretion Volume in ml / 24 hour period Na mmol/L K mmol/L Cl mmol/L HCO3

Salivary glands 1500 10 26 10 30

Stomach 1500 60 10 130

Duodenum 100-2000 140 80 80

Pancreas 800 140 5 70 115

Bile 50-800 145 100 100 35

Jejunum/ileum 3000 140 104 104 30

Colon 100 60 30 40

The regulation of these secretions is dependent upon location. In the salivary glands a complex interaction of flow rate
governed by the autonomic nervous system. The exact composition of sodium and potassium is regulated by
aldosterone. In the stomach hormones such as gastrin play a role and feedback is both endocrine and neurologically
mediated (vagus). In the duodenum CCK is released in response to duodenal distension and this causes contraction of
the gallbladder and release of bile. Pancreatic secretions are affected by somatostatin. The secretions in the small bowel
are affected by the osmolality of the luminal contents. This is in part due to the tightness of cellular junctions and in this
regard the jejunum is more permeable than the ileum. The practical implication of this is that if an individual has an
extensive intestinal resection and a high output, proximally sited stoma then administration of hypotonic rather than
isotonic solutions will result in worsening of electrolyte disturbances as electrolyte rich secretions will enter the jejunum.
In some individuals a colectomy or similar procedure results in formation of an end or loop ileostomy. Ileostomies
typically lose between 500 and 1000ml over a 24 hour period and patients with high output ileostomies can rapidly
become dehydrated. Ileostomy effluent typically contains 126mmol/L of sodium and 22mmol/L of potassium. Knowledge
of this fluid composition should guide fluid prescribing in replacing losses

Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic ulcers are common, surgeons
frequently prescribe anti secretory drugs and because there are still patients around who will have undergone acid
lowering procedures (Vagotomy) in the past.

Gastric acid
• Is produced by the parietal cells in the stomach
+ +
• pH of gastric acid is around 2 with acidity being maintained by the H /K ATP ase pump. As part of the process
bicarbonate ions will be secreted into the surrounding vessels.

27
 • Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus. This sets up a
negative potential across the membrane and as a result sodium and potassium ions diffuse across into the
canaliculus.
• Carbonic anhydrase forms carbonic acid which dissociates and the hydrogen ions formed by dissociation leave
+ +
the cell via the H /K antiporter pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted into the lumen of the oxyntic gland.

Phases of gastric acid secretion – 3phases

1. Cephalic phase (smell / taste of food)
• 30% acid produced
• Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells

2. Gastric phase (distension of stomach )

• 60% acid produced
• Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)

• 10% acid produced
• High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion via enterogastrones
(CCK, secretin) and neural reflexes.

Regulation of gastric acid production

Factors increasing production include:
• Vagal nerve stimulation
• Gastrin release
• Histamine release (indirectly following gastrin release) from enterchromaffin like cells

Factors decreasing production include:

• Somatostatin (inhibits histamine release)
• Cholecystokinin
• Secretin

Below is a brief summary of the major hormones involved in food digestion:

Source Stimulus Actions

Gastrin G cells in antrum of Distension of stomach, Increase HCL, pepsinogen and IF

the stomach extrinsic nerves secretion, increases gastric motility,
Inhibited by: low antral pH, trophic effect on gastric mucosa
somatostatin

CCK I cells in upper small Partially digested proteins Increases secretion of enzyme-rich fluid
intestine & Tg from pancreas, contraction of GB &
relaxation of sphincter of Oddi, decreases
gastric emptying, trophic effect on
pancreatic acinar cells, induces satiety

28
Secretin S cells in upper Acidic chyme, fatty acids Increases secretion of bicarbonate-rich
small intestine fluid from pancreas and hepatic duct cells,
decreases gastric acid secretion, trophic
effect on pancreatic acinar cells

VIP Small intestine, Neural Stimulates secretion by pancreas and

pancreas intestines, inhibits acid and pepsinogen
secretion

Somatostatin D cells of pancreas Fat, bile salts and glucose Decreases acid and pepsin secretion,
In the gut in the intestinal lumen Decreases gastrin secretion,
All secretion (enterochromaffin Inhibits trophic effects of gastrin,
Inhibitor cells) Delays gastric emptying,
except Found in brain tissue Decreases pancreatic exocrine secretion
Gastric mucous (and may be used therapeutically to treat
secretion pancreatic fistulae),
Decreases Insulin & Glucagon secretion,
Inhibits Growth hormone (released by
hypothalamus causing negative feedback
response on GH ),
Stimulates gastric mucous production

● Intestinal motility is increased by : CCK, Gastrin, Insulin, Motilin

● Only Gastrin secretion is stimulated by protein, but rests secretions are by fat or fatty acid.

Gastric emptying
• The stomach serves both a mechanical and immunological function. Solid and liquid are retained in the
stomach during which time repeated peristaltic activity against a closed pyloric sphincter will cause
fragmentation of food bolus material. Contact with gastric acid will help to neutralise any pathogens present.
• The amount of time material spends in the stomach is related to its composition and volume. For example a
glass of water will empty more quickly than a large meal. The presence of amino acids and fat will all serve to
delay gastric emptying.
Controlling factors
Neuronal stimulation of the stomach is mediated via the vagus and the parasympathetic nervous system will tend to
favor an increase in gastric motility. It is for this reason that individuals who have undergone truncal vagotomy will tend
to routinely require either a pyloroplasty or gastro-enterostomy as they would otherwise have delayed gastric
emptying. The following hormonal factors are all involved:

Delay emptying Increase emptying

Gastric inhibitory peptide Gastrin

Cholecystokinin

Enteroglucagon

Diseases affecting gastric emptying

All diseases that affect gastric emptying may result in bacterial overgrowth, retained food and eventually the formation of
bezoars that may occlude the pylorus and make gastric emptying even worse. Fermentation of food may cause
dyspepsia, reflux and foul smelling belches of gas.

29
Iatrogenic
Gastric surgery can have profound effects on gastric emptying. As stated above any procedure that disrupts the vagus
can cause delayed emptying. Whilst this is particularly true of Vagotomy this operation is now rarely performed.
Surgeons are divided on the importance of vagal disruption that occurs during an oesophagectomy and some will
routinely perform a pyloroplasty and other will not.

When a distal gastrectomy is performed the type of anastomosis performed will impact on emptying. When a gastro-
enterostomy is constructed, a posterior, retrocolic gastroenterostomy will empty better than an anterior one.

Diabetic gastroparesis
This is predominantly due to neuropathy affecting the vagus nerve. The stomach empties poorly and patients may have
episodes of repeated and protracted vomiting. Diagnosis is made by upper GI endoscopy and contrast studies, in some
cases a radio nucleotide scan is needed to demonstrate the abnormality more clearly. In treating these conditions drugs
such as metoclopramide will be less effective as they exert their effect via the vagus nerve. One of the few prokinetic
drugs that do not work in this way is the antibiotic erythromycin.

Malignancies
Obviously a distal gastric cancer may obstruct the pylorus and delay emptying. In addition malignancies of the pancreas
may cause extrinsic compression of the duodenum and delay emptying. Treatment in these cases is by gastric
decompression using a wide bore nasogastric tube and insertion of a stent or if that is not possible by a surgical
gastroenterostomy. As a general rule gastroenterostomies constructed for bypass of malignancy are usually placed on
the anterior wall of the stomach (in spite of the fact that they empty less well). A Roux en Y bypass may also be
undertaken but the increased number of anastomoses for this in malignant disease that is being palliated is probably not
justified.

Congenital Hypertrophic Pyloric Stenosis

This is typically a disease of infancy. Most babies will present around 6 weeks of age with projectile non bile stained
vomiting. It has an incidence of 2.4 per 1000 live births and is more common in males. Diagnosis is usually made by
careful history and examination and a mass may be palpable in the epigastrium (often cited seldom felt!). The most
important diagnostic test is an ultrasound that usually demonstrates the hypertrophied pylorus. Blood tests may reveal a
hypochloraemic metabolic alkalosis if the vomiting is long standing. Once the diagnosis is made the infant is resuscitated
and a pyloromyotomy is performed (usually laparoscopically). Once treated there are no long term sequelae.

Gastroperesis
- Occurs due to vagal neuropathy, difference with Pyloric Stenosis is - No obstruction or stricture found
in gastroperesis, otherwise rest are same features
- Prokinetics (Metochlopramide) is used
● Coffee ground vomitus – gastric ulceration
● epigastric pain relieved by eating; increased ē stress & anxiety; associated ē presence of nocturnal dyspepsia – then
Dx Duodenal Ulcer answer …
● Episode of Haematemesis and collapse – Duodenal Ulcer ans → GDA culprit vessel
● Gastric ulcer – it may invade vessel but they dont tend to major vessel

Upper gastrointestinal bleeding

Patients may present with the following:

• Haematemesis and/ or malaena

30
 • Epigastric discomfort
• Sudden collapse
The extent to which these will occur will depend upon the source. Mortality is higher in patients presenting with
haematemesis than malaena alone.

Oesophageal bleeding

Cause Presenting features

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

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

Mallory Weiss Typically brisk small to moderate volume of bright red blood following bout of repeated vomiting.
Tear Malaena rare. Usually ceases spontaneously.

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

Gastric Bleeding

Cause Presenting features

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

Dilafeuoy Often no prodromal features prior to haematemesis and malaena, but this arteriovenous malformation
Lesion may produce quite considerable haemorrhage and may be difficult to detect endoscopically

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

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

Duodenum
Most common cause of major haemorrhage is a posteriorly sited duodenal ulcer. However, ulcers at any site in the
duodenum may present with haematemesis, malaena and epigastric discomfort. The pain of duodenal ulcer is slightly
different to that of gastric ulcers and often occurs several hours after eating. Peri ampullary tumours may bleed but these
are rare. In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but
important cause of major haemorrhage associated with high mortality.
Management
• Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and Clotting (as a
minimum)
• Patients with on-going bleeding and haemodynamic instability are likely to require O negative blood pending
cross matched blood
31
 • Early control of airway is vital (e.g. Drowsy patient with liver failure)
• Patients with suspected varices should receive terlipressin prior to endoscopy
• Ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper GI endoscopy
within 24 hours of admission. In those who are unstable this should occur immediately after resuscitation or in
tandem with it. The endoscopy department is a potentially dangerous place for unstable patients and it may be
safer to perform the endoscopy in theatre with an anaesthetist present.
• Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active bleeding then a
Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be done with care; gastric
balloon should be inflated first and oesophageal balloon second. Remember the balloon with need deflating
after 12 hours (ideally sooner) to prevent necrosis. Portal pressure should be lowered by combination of
medical therapy +/- TIPSS.
• Patients with erosive oesophagitis / gastritis should receive a proton pump inhibitor.
• Mallory Weiss tears will typically resolve spontaneously
• Identifiable bleeding points should receive combination therapy of injection of adrenaline and either a thermal or
mechanical treatment. All who have received intervention should receive a continuous infusion of a proton
pump inhibitor (IV omeprazole for 72 hours) to reduce the re-bleeding rate.
• Patients with diffuse erosive gastritis who cannot be managed endoscopically and continue to bleed may
require gastrectomy
• Bleeding ulcers that cannot be controlled endoscopically may require laparotomy and ulcer underruning

Indications for surgery

• Patients > 60 years
• Continued bleeding despite endoscopic intervention
• Recurrent bleeding
• Known cardiovascular disease with poor response to hypotension
Surgery
• Duodenal ulcer:

Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then the ulcer is almost always posteriorly
sited and will have invaded the gastroduodenal artery. Large bites using 0 Vicryl are taken above and below the ulcer
base to occlude the vessel. The duodenotomy should be longitudinal but closed transversely to avoid stenosis.
• For gastric ulcer: Partial gastrectomy-antral ulcer
Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left gastric artery)
Total gastrectomy if bleeding persists

Summary of Acute Upper GI bleeding recommendations:

• All patients should have a pre-endoscopic Rockall score
• Consider admission if: - Aged over 60 years
- Witnessed haematemesis
- Systolic BP < 100mmHg or HR > 100 bpm
- Liver disease/known varices

• Resuscitation: - In shock, Give fluid

-Transfuse if 30% circulating volume is lost
- Administration of proton pump inhibitors prior to endoscopy may reduce evidence
of haemorrhage
32
 • Give IV PPI e.g. 80mg Omeprazole bolus then 8mg/h over 72h, if bleeding ulcer identified
• If post endoscopy Rockall score < 3 consider discharge and follow-up

Gastric Ulcer Surgical Rx

- Bilroth I partial gastrectomy
o Benign distal ulcer; Gastric curvature ulcer
rd
o Distal 3 stomach removed & anastomosis ē duodenum

Fig: Billroth I – pylorus is removed and distal stomach is anastomosed directly to the duodenum

- Bilroth II (polya) gastrectomy

o Used for more proximal ulcer
o Removal of distal 2/3rd stomach & gastro-jejunostomy

A, Subtotal gastrectomy with B, Billroth II gastrojejunostomy - lower part of stomach (antrum) is removed and a loop of
small bowel (jejunum) is brought up and joined to it in a (side-to-side manner) for drainage (gastrojejunostomy)

- Vagotomy, pyloroplasty & excision of ulcer

o Used as alternative of Bilroth-I when contraindicated
o If Surgery is not possible then excision of the ulcer.

- Vagotomy. Antrectomy & Roux-en-Y

o Reserved as 2nd operation for bilious vomiting

33
 Figure 23. A, Total gastrectomy; B, Roux-en-Y esophagojejunostomy

Figure 24. A, High subtotal gastrectomy; B, with Roux-en-Y gastrojejunostomy.

** Lesser Omentum needs to be divided to gain access to celiac axis **

● DUODENAL ULCER SURGICAL Rx

- Truncal vagotomy & pyloroplasty
o Both vagal trunks are cut @ abd. Esophagus level
o As stomach is denervated, stasis occurs
o Gastrojejunostomy / pyloroplasty done

- Selective vaotomy & pyloroplasty

o Denervation of stomach with preservation of intact pylorus’ nerve supply
o Preserve celiac & hepatic branches of vagus

- Highly selective / parietal cell/ proximal vaotomy

o Only branches of body & fundus are cut
o Doesn’t interrupt celiac , hepatic & pyloric branches
o No diversion procedure needed

34
 o High recurrence rate
Gastric cancer

Overview. It is more common in men and incidence rises with increasing age. The exact cause of many sporadic cancer
is not known, however, familial cases do occur in HNPCC families. In addition, smoking and smoked or preserved foods
increase the risk. Japanese migrants retain their increased risk (decreased in subsequent generations). The distribution
of the disease in western countries is changing towards a more proximal location (perhaps due to rising obesity).

Pathology
There is some evidence of support a stepwise progression of the disease through intestinal metaplasia progressing to
atrophic gastritis and subsequent dysplasia, through to cancer. The favoured staging system is TNM. The risk of lymph
node involvement is related to size and depth of invasion; early cancers confined to submucosa have a 20% incidence
of lymph node metastasis. Tumours of gastro-oesophageal junction are:

Type 1 True oesophageal cancers and may be associated with Barrett's oesophagus.

Type 2 Carcinoma of the cardia, arising from cardiac type epithelium

or short segments with intestinal metaplasia at the oesophagogastric junction.

Type 3 Sub cardial cancers that spread across the junction. Involve similar nodal stations to gastric cancer.

Groups for close endoscopic monitoring

• Intestinal metaplasia of columnar type
• Atrophic gastritis
• Low to medium grade dysplasia
• Patients who have previously undergone resections for benign peptic ulcer disease (except highly selective
vagotomy).

Referral to endoscopy

Patients of any age with dyspepsia and Patients without dyspepsia Worsening dyspepsia
any of the following

Chronic gastrointestinal bleeding Dysphagia Barretts oesophagus

Dysphagia Unexplained abdominal pain Intestinal metaplasia

or weight loss

Weight loss Vomiting Dysplasia

Iron deficiency anaemia Upper abdominal mass Atrophic gastritis

Upper abdominal mass Jaundice Patient aged over 55 years with

unexplained or persistent dyspepsia

Upper GI endoscopy performed for dyspepsia. The addition of dye spraying may facilitate identification of
smaller tumours
Staging
• CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in most centres.
• Laparoscopy to identify occult peritoneal disease
• PET CT (particularly for junctional tumours)

35
Treatment
• Type 2 junctional tumours (extending into oesophagus) – Oesophagogastrectomy
• <5cm from OG junction – Total gastrectomy
• Proximally sited disease greater than 5-10cm from the OG junction – Subtotal Gastrectomy
• Mid-sector tumors – Total Gastrectomy
th
• Distal tumor – Partial or sub-total (4/5 removed)- entire pylorus also removed
• Confined to mucosa & perhaps sub mucosa (debated!) – Endoscopic submucosal resection (Snare technique)
• Lymphadenectomy should be performed. A D2 lymphadenectomy is widely advocated by the Japanese, the
survival advantages of extended lymphadenectomy have been debated. However, the overall recommendation
is that a D2 nodal dissection be undertaken.
n
o LN, surrounding tissue : D1 op (stomach part ē lesion removal & atleast 5cm clearance + N1 nodes)
o LN, 1st 11LN stations: D2 opn (2nd rank LN removal ē LGA, CHA & Splenic A.)
st n
o LN, 1 16LN stations: D3 op
• Most patients will receive chemotherapy either pre or post operatively.

Figure A, Total gastrectomy; B, subtotal gastrectomy.

Figure. Surgical lymphadenectomy; D1 and D2 indicate the extent of lymph node removal.

Prognosis UK Data

36
Disease extent Percentage 5 year survival

All RO resections 54%

Early gastric cancer 91%

Stage 1 87%

Stage 2 65%

Stage 3 18%

Operative procedure
Total Gastrectomy , lymphadenectomy and Roux en Y anastomosis
General anaesthesia
Prophylactic intravenous antibiotics
Incision: Rooftop.
Perform a thorough laparotomy to identify any occult disease.
Mobilise the left lobe of the liver off the diaphragm and place a large pack over it. Insert a large self retaining retractor
e.g. omnitract or Balfour (take time with this, the set up should be perfect). Pack the small bowel away.
Begin by mobilising the omentum off the transverse colon.
Proceed to detach the short gastric vessels.
Mobilise the pylorus and divide it at least 2cm distally using a linear cutter stapling device.
Continue the dissection into the lesser sac taking the lesser omentum and left gastric artery flush at its origin.
The lymph nodes should be removed en bloc with the specimen where possible.
Place 2 stay sutures either side of the distal oesophagus. Ask the anaesthetist to pull back on the nasogastric tube.
Divide the distal oesophagus and remove the stomach.
The oesphago jejunal anastomosis should be constructed. Identify the DJ flexure and bring a loop of jejunum up to the
oesophagus (to check it will reach). Divide the jejunum at this point. Bring the divided jejunum either retrocolic or
antecolic to the oesophagus. Anastamose the oesophagus to the jejunum, using either interrupted 3/0 vicryl or a stapling
device. Then create the remainder of the Roux en Y reconstruction distally.
Place a jejunostomy feeding tube.
Wash out the abdomen and insert drains (usually the anastomosis and duodenal stump). Help the anaesthetist insert the
nasogastric tube (carefully!)
Close the abdomen and skin.
Enteral feeding may commence on the first post-operative day. However, most surgeons will leave patients on free NG
drainage for several days and keep them nil by mouth.

Post gastrectomy syndromes

Post gastrectomy syndromes may vary slightly depending upon whether a total of partial gastrectomy is performed. A
Roux en Y reconstruction generally gives the best functional outcomes. Where a gastrojejunostomy is performed as
reconstruction following a distal gastrectomy the gastric emptying is generally better if the jejunal limbs are tunneled in
the retrocolic plane. The following may occur following gastrectomy:
• Small capacity (early satiety)
• Dumping syndrome
• Bile gastritis
• Afferent loop syndrome
• Efferent loop syndrome

37
 • Anaemia (B12 deficiency)
• Metabolic bone disease

Spleen

The spleen is the largest lymphoid organ in the body. It is an intraperitoneal organ, the peritoneal attachments condense
at the hilum where the vessels enter the spleen. Its blood supply is from the splenic artery (derived from the coeliac axis)
and the splenic vein (which is joined by the IMV and unites with the SMV).
• Embryology: derived from mesenchymal tissue (Most of the gut is derived endodermally except for the spleen)
• Shape: clenched fist
• Position: below 9th-12th ribs
• Weight: 75-150g

1,3,5,7,9,11 (odd numbers up to 11)

The spleen is: 1 inch thick, 3 inches wide, 5 inches long, weighs 7oz (200g), lies between the 9th and 11th ribs

Relations
• Superiorly- diaphragm
• Anteriorly- gastric impression
• Posteriorly- kidney
• Inferiorly- colon
• Hilum: tail of pancreas and splenic vessels (splenic artery divides here, branches pass to the white pulp
transporting plasma)
• Forms apex of lesser sac (containing short gastric vessels)

Contents
- White pulp: immune function. Contains central trabecular artery. The germinal centres are supplied by arterioles
called penicilliary radicles.

- Red pulp: filters abnormal red blood cells

Function
• Filtration of abnormal blood cells and foreign bodies such as bacteria.
• Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for phagocytosis.
• Haematopoiesis: up to 5th month gestation or in haematological disorders.
• Pooling: storage of 40% platelets.
• Iron reutilisation
• Storage red blood cells-animals, not humans.
• Storage monocytes

Disorders of the spleen- Massive splenomegaly

• Myelofibrosis
• Chronic myeloid leukaemia
• Visceral leishmaniasis (kala-azar)
• Malaria

38
 • Gaucher's syndrome

Other causes (as above plus)

• Portal hypertension e.g. secondary to cirrhosis
• Lymphoproliferative disease e.g. CLL, Hodgkin's
• Haemolytic anaemia
• Infection: hepatitis, glandular fever
• Infective endocarditis
• Sickle-cell*, thalassaemia
• Rheumatoid arthritis (Felty's syndrome)

Accessory spleens

- 10% population
- 1 cm size
- locations: hilum of the spleen, tail of the pancreas, along the splenic vessels, in the gastrosplenic
ligament, the splenorenal ligament, the walls of the stomach or intestines, the greater omentum, the
mesentery, the gonads

*the majority of adults patients with sickle-cell will have an atrophied spleen due to repeated infarction

Splenic trauma
• The spleen is one of the more commonly injured intra abdominal organs
• In most cases the spleen can be conserved. The management is dictated by the associated injuries,
haemodynamic status and extent of direct splenic injury.

Management of splenic trauma

Conservative Small subcapsular haematoma

Minimal intra abdominal blood
No hilar disruption

Laparotomy with conservation Increased amounts of intraabdominal blood

Moderate haemodynamic compromise
Tears or lacerations affecting <50%

Resection Hilar injuries

Major haemorrhage
Major associated injuries

Splenectomy

Indications
• Trauma: 1/4 are iatrogenic
• Spontaneous rupture: EBV
• Hypersplenism: hereditary spherocytosis or elliptocytosis etc
• Malignancy: lymphoma or leukaemia
• Splenic cysts, hydatid cysts, splenic abscesses
39
Post splenectomy changes
• Platelets will rise first (therefore in ITP should be given after splenic artery clamped)
• Blood film will change over following weeks, Howell Jolly bodies will appear
• Other blood film changes include target cells and Pappenheimer bodies
• Increased risk of post splenectomy sepsis, therefore prophylactic antibiotics and pneumococcal vaccine should
be given.

Post splenectomy sepsis

• Typically occurs with encapsulated organisms
• Opsonisation occurs but then not recognized

The loss of splenic function renders individuals at increased risk of fulminant sepsis. Young children are at the highest
risk, especially in the first 2 years following surgery. Surgery for trauma is associated with a lower risk than when
splenectomy is performed as a treatment for haematological disorders.

Infection with encapsulated organisms poses the greatest risk, these organisms may be opsonised, but this then goes
undetected at an immunological level due to loss of the spleen.

Prophylactic vaccinations are usually administered to reduce the risk of pneumococcal septicaemia. Since the vaccine
only covers up to 80% of pneumococcal infections, patients will usually recieve long term, low dose penicillin prophylaxis
in addition to vaccination.

Organisms causing post splenectomy sepsis:

Streptococcus pneumoniae
Haemophilus influenzae
Meningococci

Encapsulated organisms carry the greatest pathogenic risk following splenectomy. The effects of sepsis following
splenectomy are variable. This may be the result of small isolated fragments of splenic tissue that retain some function
following splenectomy. These may implant spontaneously following splenic rupture (in trauma) or be surgically implanted
at the time of splenectomy.

Post splenectomy blood film changes

The loss of splenic tissue results in the inability to readily remove immature or abnormal red blood cells from the
circulation. The red cell count does not alter significantly. However, cytoplasmic inclusions may be seen e.g. Howell-Jolly
bodies.
In the first few days after splenectomy target cells, siderocytes and reticulocytes will appear in the circulation.
Immediately following splenectomy a granulocytosis (mainly composed of neutrophils) is seen, this is replaced by a
lymphocytosis and monocytosis over the following weeks.
The platelet count is usually increased and this may be persistent, oral antiplatelet agents may be needed in some
patients.

Blood film in hyposplenism: Howell-Jolly bodies

Pappenheimer bodies
Poikilocytes (Target cells)

40
 Erythrocyte containing siderotic granules (Irregular contracted erythrocytes)
Heinz bodies

Splenectomy Technique Trauma

• GA
• Long midline incision
• If time permits insert a self retaining retractor (e.g. Balfour/ omnitract)
• Large amount of free blood is usually present. Pack all 4 quadrants of the abdomen. Allow the anaesthetist to
'catch up'
• Remove the packs and assess the viability of the spleen. Hilar injuries and extensive parenchymal lacerations
will usually require splenectomy.
• Divide the short gastric vessels and ligate them.
• Clamp the splenic artery and vein. Two clamps on the patient side are better and allow for double ligation and
serve as a safety net if your assistant does not release the clamp smoothly.
• Be careful not to damage the tail of the pancreas, if you do then this will need to be formally removed and the
pancreatic duct closed.
• Wash out the abdomen and place a tube drain to the splenic bed.
• Some surgeons implant a portion of spleen into the omentum, whether you decide to do this is a matter of
personal choice.
• Post operatively the patient will require prophylactic penicillin V and pneumococcal vaccine.

Elective
Elective splenectomy is a very different operation from that performed in the emergency setting. The spleen is often
large (sometimes massive). Most cases can be performed laparoscopically. The spleen will often be macerated inside a
specimen bag to facilitate extraction.

Complications
• Haemorrhage (may be early and either from short gastrics or splenic hilar vessels
• Pancreatic fistula (from iatrogenic damage to pancreatic tail)
• Thrombocytosis: prophylactic aspirin
• Encapsulated bacteria infection e.g. Strep. pneumoniae, Haemophilus influenzae andNeisseria meningitides

Splenic vein thrombosis

Thrombosis of the splenic vein may complicate pancreatitis, pancreatic carcinoma, iatrogenic trauma and
hypercoagulable diseases. The condition may predispose to the development of gastric varices, oesophageal varices
are uncommon in splenic vein thrombosis alone. Diagnosis is made by CT angiography. Treatment is with splenectomy.

● Gastrosplenic ligament – short gastric artery chance । (N-281)

● Pancreas splenorenal ligament ।

n
● Lt. radical nephrectomy via a transabd. route, tract on splenorenal and splenocolic may produce significant injury2
spleen

41
● ACCESSORY SPLEENS
- 10% population
- 1 cm size
- locations: Hilum of the spleen,
Tail of the pancreas,
Along the splenic vessels,
In the gastrosplenic ligament,
The splenorenal ligament,
The walls of the stomach or intestines,
The greater omentum,
The mesentery,
The gonads
● SPLENIC TRAUMA
• The spleen is one of the more commonly injured intra abdominal organs
• In most cases the spleen can be conserved. The management is dictated by the associated injuries,
haemodynamic status and extent of direct splenic injury.

Management of splenic trauma

Conservative Small subcapsular haematoma

Minimal intra abdominal blood
No hilar disruption

Laparotomy with conservation Increased amounts of intraabdominal blood

Moderate haemodynamic compromise
Tears or lacerations affecting <50%

Resection Hilar injuries

Major haemorrhage
Major associated injuries

● Young man ē halitosis, regurgitation & flatulence is most likely to have hiatus hernia. These are also found in
pharyngeal pouch, but this is more commonly found in elderly patients,

● Medial Umbilical fold is the obliterated Umbilical Arteries (N-244)

Retroperitoneal Structures List: Sad Pucker: (N-257)

st
- Suprarenal glands - Aorta & IVC - Duodenum (except 1 part)
- Pancreas
- Ureters
- Colon (ascending & descending)
- Kidneys
- Esophagus (anterior & left covered)
- Rectum
**Spleen is the only organ which is completely covered with visceral peritoneum**

Epiploic Foramen (N-256, 327)

42
 Boundary
• Anteriorly : Free border lesser omentum / hepatoduodenal ligament, containing CBD, HA, hepatic PV.
• Posteriorly : IVC; Diaphragm; Rt. Suprarenal gland; T12 vertebra body
• Superiorly : Caudate lobe
• Inferiorly : Duodenum 1st part; HA.; (BD & PV also)
• Left lateral : Gastrosplenic and splenorenal ligament

During liver surgery bleeding may be controlled using a Pringles manoeuvre, this involves placing a vascular clamp
across the anterior aspect of the epiploic foramen. Thereby occluding:
• Common bile duct
• Hepatic artery
• Portal vein

Ischiorectal Fossa (N-364, 368)

Base : Skin

Apex : Meeting point of Ob. Fascia + inf. Fascia pelvic diaphragm

Anterior : Perineal membrane (post. border)

Posterior : G. max.
Sacrotuberous ligament

Lateral : Ischial tuberosity

O.I. muscle ē fascia
Pudendal canal with its contents

Medial : Levator ani ē anal fascia

Ext. Anal sphincter

● Contents (N-364)
 Pad of fat
 Inferior rectal nerve & vessels
 Pudendal canal ē its contents (Internal pudendal vessels & pudendal nerve, Perineal Nerve)
 Post. Scrotal nerves & vessels
 S4 perineal branch
 S2,3 cutaneous branch

● DUKES CLASSIFICATION
Dukes' A : Confined to bowel wall
Dukes' B : Through the bowel wall ; Not involving LN
Dukes' C : LN Involved; no other metastasis
Dukes' C2 : Highest nodes involved
Dukes' D : Distant metastasis; long term survival rare without liver resection

Caecum
43
Location • Proximal right colon below the ileocaecal valve
• Intraperitoneal

Posterior relations • Psoas

• Iliacus
• Femoral nerve
• Genitofemoral nerve
• Gonadal vessels

Anterior relations Greater omentum

Arterial supply Ileocolic artery

Lymphatic drainage Mesenteric nodes accompany the venous drainage

• The caecum is the most distensible part of the colon and in complete large bowel obstruction with a competent
ileocaecal valve the most likely site of eventual perforation.

Appendix
• Location: Base of caecum.
• Up to 10cm long.
• Mainly lymphoid tissue (Hence mesenteric adenitis may mimic appendicitis).
• Caecal taenia coli converge at base of appendix and form a longitudinal muscle cover over the appendix. This
convergence should facilitate its identification at surgery if it is retrocaecal and difficult to find (which it can be
when people start doing appendicectomies!)
• Arterial supply: Appendicular artery (branch of the ileocolic).
• It is intra peritoneal.
McBurney's point
• 1/3 of the way along a line drawn from the Anterior Superior Iliac Spine to the Umbilicus

6 Positions:
• Retrocaecal 74%
• Pelvic 21%
• Postileal
• Subcaecal
• Paracaecal
• Preileal
Appendicitis
History
• Peri umbilical abdominal pain (visceral stretching of appendix lumen and appendix is mid gut structure)
radiating to the right iliac fossa due to localised parietal peritoneal inflammation.
• Vomit once or twice but marked and persistent vomiting is unusual.
• Diarrhoea is rare. However, pelvic appendicitis may cause localised rectal irritation of some loose stools. A
pelvic abscess may also cause diarrhoea.
o
• Mild pyrexia is common - temperature is usually 37.5 -38 C. Higher temperatures are more typical of conditions
like mesenteric adenitis.
• Anorexia is very common. It is very unusual for patients with appendicitis to be hungry.

44
Examination
• Generalised peritonitis if perforation has occurred or localised peritonism.
• Retrocaecal appendicitis may have relatively few signs.
• Digital rectal examination may reveal boggy sensation if pelvic abscess is present, or even tenderness with a
pelvic appendix.

Diagnosis
• Typically raised inflammatory markers coupled with compatible history and examination findings should be
enough to justify appendicectomy.
• Urine analysis may show mild leucocytosis but no nitrites.
• Ultrasound is useful if females where pelvic organ pathology is suspected. Although it is not always possible to
visualise the appendix on ultrasound the presence of free fluid (always pathological in males) should raise
suspicion.
Ultrasound examination may show evidence of lumenal obstruction and thickening of the appendiceal wall
Treatment
• Appendicectomy which can be performed via either an open or laparoscopic approach.
• Administration of metronidazole reduces wound infection rates.
• Patients with perforated appendicitis require copious abdominal lavage.
• Patients without peritonitis who have an appendix mass should receive broad spectrum antibiotics and
consideration given to performing an interval appendicectomy.
• Be wary in the older patients who may have either an underlying caecal malignancy or perforated sigmoid
diverticular disease.

Colon anatomy

The colon is about 1.5m long although this can vary considerably.
Components:
• Ascending colon
• Transverse colon
• Descending colon
• Sigmoid colon

Arterial supply
Superior mesenteric artery and inferior mesenteric artery: linked by the marginal artery.
Ascending colon: ileocolic and right colic arteries
Transverse colon: middle colic artery
Descending and sigmoid colon: inferior mesenteric artery

Venous drainage
From regional veins (that accompany arteries) to superior and inferior mesenteric vein

Lymphatic drainage
Initially along nodal chains that accompany supplying arteries, then para-aortic nodes.

Embryology

45
Midgut- Second part of duodenum to 2/3 transverse colon
Hindgut- Distal 1/3 transverse colon to anus

Peritoneal location
The right and left colon are part intraperitoneal and part extraperitoneal. The sigmoid and transverse colon are generally
wholly intraperitoneal. This has implications for the sequelae of perforations, which will tend to result in generalised
peritonitis in the wholly intra peritoneal segments.

Left colon

Position

• As the left colon passes inferiorly its posterior aspect becomes extraperitoneal, and the ureter and gonadal
vessels are close posterior relations that may become involved in disease processes
• At a level of L3-4 (variable) the left colon becomes the sigmoid colon and wholly intraperitoneal once again
• The sigmoid colon is a highly mobile structure and may even lie of the right side of the abdomen
• It passes towards the midline, the taenia blend and this marks the transition between sigmoid colon and upper
rectum.

Blood supply

• Inferior mesenteric artery

However, the marginal artery (from the right colon) contributes and this contribution becomes clinically significant when
the IMA is divided surgically (e.g. During AAA repair)

Right colon

Ileocaecal valve
• Entry point of the terminal ileum to the caecum
• An important colonoscopic landmark
• The ileocaecal valve is not always competent and this may allow partial decompression of an obstructed colon

Appendix
• At the base of the caecum the taenia coalesce to mark the base of the appendix
• This is a reliable way of locating the appendix surgically and is a constant landmark
• The appendix has a small mesentery (the mesoappendix) and in this runs the appendiceal artery, a branch of
the ileocolic artery.

The posterior aspect of the right colon is extra peritoneal and the anterior aspect intraperitoneal.

Relations
• Posterior

Iliacus, Iliolumbar ligament, Quadratus lumborum, Transverse abdominis, Diaphragm at the tip of the last rib; Lateral
cutaneous, ilioinguinal, and iliohypogastric nerves; the iliac branches of the iliolumbar vessels, the fourth lumbar artery,
gonadal vessels, ureter and the right kidney.

46
 • Superior

Right kidney which is embedded in the perinephric fat

• Medial

Mesentery which contains the ileocolic artery that supplies the right colon and terminal ileum. A further branch , the right
colic artery, also contributes to supply the hepatic flexure and proximal transverse colon. Medially these pass through
the mesentery to join the SMA. This occurs near to the head of the pancreas and care has to be taken when ligating the
ileocolic artery near to its origin in cancer cases for fear of impinging on the SMA.

- Anterior
Coils of small intestine, the right edge of the greater omentum, and the anterior abdominal wall.

Nerve supply
• Parasympathetic fibres of the vagus nerve (CN X)

Arterial supply
• Ileocolic artery and right colic artery, both branches of the SMA. While the ileocolic artery is almost always
present, the right colic can be absent in 5-15% of individuals.

Transverse colon
• The right colon undergoes a sharp turn at the level of the hepatic flexure to become the transverse colon.
• At this point it also becomes intraperitoneal.
• It is connected to the inferior border of the pancreas by the transverse mesocolon.
• The greater omentum is attached to the superior aspect of the transverse colon from which it can easily be
separated. The mesentery contains the middle colic artery and vein. The greater omentum remains attached to
the transverse colon up to the splenic flexure. At this point the colon undergoes another sharp turn.

Relations

Superior Liver and gall-bladder, the greater curvature of the stomach, and the lower end of the spleen

Inferior Small intestine

Anterior Greater omentum

Posterior From right to left with the descending portion of the duodenum, the head of the pancreas, convolutions of the
jejunum and ileum, spleen

Colonic pseudo-obstruction
Colonic pseudo-obstruction is characterised by the progressive and painless dilation of the colon. The abdomen may
become grossly distended and tympanic. Unless a complication such as impending bowel necrosis or perforation occurs,
there is usually little pain.
Diagnosis involves excluding a mechanical bowel obstruction with a plain film and contrast enema. The underlying
cause is usually electrolyte imbalance and the condition will resolve with correction of this and supportive care.
Patients who do not respond to supportive measures should be treated with attempted colonoscopic decompression
and/ or the drug neostigmine. In rare cases surgery may be required.

47
Colonic obstruction

Cause Features Treatment

Cancer • Usually insidious onset Establish diagnosis (e.g. contrast

• History of progressive constipation enema/ endoscopy)

Laparotomy and resection, stenting,
• Systemic features (e.g. anaemia)
defunctioning colostomy or bypass
• Abdominal distension
• Absence of bowel gas distal to site of obstruction

Diverticular • Usually history of acute diverticulitis Once diagnosis established, usually

stricture • Long history of altered bowel habit surgical resection
Colonic stenting should not be
• Evidence of diverticulosis on imaging or endoscopy
performed for benign disease

Volvulus • Twisting of bowel around its mesentery Initial treatment is to untwist the

• Sigmoid colon affected in 76% cases loop, a flexible sigmoidoscopy may

be needed
• Patients usually present with abdominal pain,
Those with clinical evidence of
bloating and constipation
ischaemia should undergo surgery
• Examination usually shows asymmetrical distension
Patient with recurrent volvulus
• Plain X-rays usually show massively dilated sigmoid
should undergo resection
colon, loss of haustra and "U" shape are typical, the
loop may contain fluid levels

Acute colonic • Symptoms and signs of large bowel obstruction with Colonoscopic decompression
pseudo- no lesion Correct metabolic disorders
obstruction • Usually associated with metabolic disorders IV neostigmine
Surgery
• Usually a cut off in the left colon (82% cases)
• Although abdomen tense and distended, it is usually
not painful
• All patients should undergo contrast enema (may be
therapeutic!)

Colonic lesions - DALM

• The term DALM lesion refers to a Dysplasia Associated Lesion or Mass.
• They may complicate dysplasia occurring in patients with longstanding ulcerative colitis.
• They have a high incidence of invasive foci.
• When they complicate longstanding ulcerative colitis, they should be treated by panproctocolectomy.

Colonic polyps

May occur in isolation of greater numbers as part of the polyposis syndromes. In FAP greater than 100 polyps are
typically present. The risk of malignancy in association with adenomas is related to size and is the order of 10% in a 1cm
adenoma. Isolated adenomas seldom give risk of symptoms (unless large and distal). Distally sited villous lesions may
produce mucous and if very large electrolyte disturbances may occur.

48
Follow up of colonic polyps
Low risk
• 1 or 2 adenomas <1cm. No follow up or re-colonoscopy at 5 years.

Moderate risk
• 3 or 4 small adenomas or 1 adenoma >1cm. Re-scope at 3 years.

High risk
• >5 small adenomas or >3 with 1 of them >1cm. Re scope at 1 year.
From Atkins and Saunders Gut 2002 51 (suppl V:V6-V9). It is important to stratify patients appropriately and ensure that
a complete colonoscopy with good views was performed.

Segmental resection or complete colectomy should be considered when:

1. Incomplete excision of malignant polyp
2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli

-Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy

-Panproctocolectomy and Ileostomy or Restorative Panproctocolectomy.

Rectal polypoidal lesions may be amenable to trans anal endoscopic microsurgery.

Colorectal cancer screening and diagnosis

Overview
• Most cancers develop from adenomatous polyps. Screening for colorectal cancer has been shown to reduce
mortality by 16%
• The NHS now has a national screening programme offering screening every 2 years to all men and women
aged 60 to 69 years. Patients aged over 70 years may request screening
• Eligible patients are sent faecal occult blood (FOB) tests through the post
• Patients with abnormal results are offered a colonoscopy

At colonoscopy, approximately:
• 5 out of 10 patients will have a normal exam
• 4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
• 1 out of 10 patients will be found to have cancer

Diagnosis
Essentially the following patients need referral:
- Altered bowel habit for more than six weeks
- New onset of rectal bleeding
- Symptoms of tenesmus

Colonoscopy is the gold standard, provided it is complete and good mucosal visualisation is achieved. Other options
include double contrast barium enema and CT colonography.
49
Staging
Once a malignant diagnosis is made patients with colonic cancer will be staged using chest / abdomen and pelvic CT.
Patients with rectal cancer will also undergo evaluation of the mesorectum with pelvic MRI scanning. For examination
purposes the Dukes and TNM systems are preferred.

Tumour markers
Carcinoembryonic antigen (CEA) is the main tumour marker in colorectal cancer. Not all tumours secrete this, and it may
be raised in conditions such as IBD. However, absolute levels do correlate (roughly) with disease burden and whilst this
marker may not be used extensively in follow up, it can be useful for investigation of patients with cancer of unknown
primary.

Colorectal cancer treatment

Essentially this is surgical. Patients undergoing elective colonic resection are increasingly being operated on
laparoscopically and many centres now utilise enhanced recovery programmes. These encourage prompt recovery by:
• Early mobilisation
• Judicious administration of fluid
• Carbohydrate loading drinks on day of surgery
• Early resumption of normal diet
• Avoidance of mechanical bowel preparation

In many elective cases mechanical bowel preparation can be avoided; this is universally true for right sided colonic
surgery. Controversy exists as to whether it is needed for left sided surgery.

Which operation is best?

The operations for cancer are segmental resections based on blood supply and lymphatic drainage. In the elective
situation the following operations are recommended:

Site of cancer Type of resection Anastomosis Risk of leak

Right colon Right hemicolectomy Ileo-colic Low <5%

Transverse Extended right hemicolectomy Ileo-colic Low <5%

Splenic flexure Extended right hemicolectomy Ileo-colic Low <5%

Splenic flexure Left hemicolectomy Colo-colon 2-5%

Left colon Left hemicolectomy Colo-colon 2-5%

Sigmoid colon High anterior resection Colo-rectal 5%

Upper rectum Anterior resection (TME) Colo-rectal 5%

Low rectum Anterior resection (Low TME) Colo-rectal 10%

(+/- Defunctioning stoma)

Anal verge Abdomino-perineal excision of colon and rectum None n/a

In the emergency setting where the bowel has perforated the risk of an anastomosis is much greater, particularly when
the anastomosis is colon-colon. In this situation an end colostomy is often safer and can be reversed later. When
resection of the sigmoid colon is performed and an end colostomy is fashioned the operation is referred to as a
50
Hartmans procedure. Whilst left sided resections are more risky, ileo-colic anastomoses are relatively safe even in the
emergency setting and do not need to be defunctioned.

Large bowel obstruction

Colonic obstruction remains a common surgical problem. It is most commonly due to malignancy (60%) and diverticular
disease (20%). Volvulus affecting the colon accounts for 5% of cases. Acute colonic pseudo-obstruction remains a
potential differential diagnosis in all cases. Intussceception affecting the colon (most often due to tumours in the adult
population) remains a rare but recognised cause.
The typical patient will present with gradual onset of progressive abdominal distension, colicky abdominal pain and
either obstipation or absolute constipation.
On examination abdominal distension is present, the presence of caecal tenderness (assuming no overt evidence of
peritonitis) is a useful sign to elicit. A digital rectal examination and rigid sigmoidoscopy should be performed.
A plain abdominal x-ray is the usual first line test and; the caecal diameter and ileocaecal valve competency should be
assessed on this film.

Imaging modalities
Debate long surrounds the use of CT versus gastrograffin enemas. The latter investigation has always been the
traditional method of determining whether a structural lesion is indeed present. However, in the UK the use of this
technique has declined and in most units a CT scan will be offered as the first line investigation by the majority of
radiologists (and is advocated by the ACPGBI). In most cases this will provide sufficient detail to allow operative
planning, and since malignancy accounts for most presentations may also stage the disease. In the event that the
radiologist cannot provide a clear statement of lesion site, the surgeon should have no hesitation in requesting a contrast
enema.

Surgical options
The decision as to when to operate or not is determined firstly by the patients physiological status. Unstable patients
require resuscitation prior to surgery and admission to a critical care unit for invasive monitoring and potential inotropic
support may be needed. In patients who are otherwise stable the decision then rests on the radiological and clinical
findings. As a general rule the old adage that the sun should not rise and set on unrelieved large bowel obstruction still
holds true. A caecal diameter of 12cm or more in the presence of complete obstruction with a competent ileocaecal
valve and caecal tenderness is a sign of impending perforation and a relative indication for prompt surgery.

Right sided and transverse lesions

Right sided lesions producing large bowel obstruction should generally be treated by right hemicolectomy or its extended
variant if the lesion lies in the distal transverse colon or splenic flexure. In these cases an ileocolic anastomosis may be
easily constructed and even in the emergency setting has a low risk of anastomotic leak.

Left sided lesions

The options here lie between sub total colectomy and anastomosis, left hemicolectomy with on table lavage and primary
anastomosis, left hemicolectomy and end colostomy formation and finally colonic stent insertion.
The usefulness of colonic stents was the subject of a Cochrane review in 2011. The authors concluded that on the basis
of the data that they reviewed, there was no benefit from the use of colonic stents over conventional surgical resection
with a tendency to better outcomes seen in the surgical group (1). A more recently conducted meta analysis met with the
same conclusion (2). There remains some enthusiasm for use of stents as a bridge to surgery but this may too pass with
the passage of time. They do remain an option in selected cases such as patients who are unfit for anaesthesia.
However, in this group the development of complications at the time of stent insertion would have dire consequences.

Rectosigmoid lesions
51
Lesions below the peritoneal reflection that are causing obstruction should generally be treated with a loop colostomy.
Primary resection of unstaged rectal cancer would most likely carry a high CRM positivity rate and cannot be condoned.
Where the lesion occupies the distal sigmoid colon the usual practice would be to perform a high anterior resection. The
decision surrounding restoration of intestinal continuity would lie with the operating surgeon.
Scaphoid fractures in children will usually involve the distal pole and are easily missed. The initial clinical examination
(and sometimes x-rays) may be normal and repeated clinical examination and imaging is advised for this reason. Whilst
the other injuries may be sustained from a fall onto an outstretched hand they are less likely to be overlooked on clinical
examination. In the case of a Bennetts fracture, the injury mechanism is less compatible with this type of injury.

Lower Gastrointestinal bleeding

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

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

Cause Presenting features

Colitis Bleeding may be brisk in advanced cases, diarrhoea is commonly present. Abdominal x-ray may
show featureless colon.

Diverticular Acute diverticulitis often is not complicated by major bleeding and diverticular bleeds often occur
disease sporadically. 75% all will cease spontaneously within 24-48 hours. Bleeding is often dark and of
large volume.

Cancer Colonic cancers often bleed and for many patients this may be the first sign of the disease. Major
bleeding from early lesions is uncommon

Haemorrhoidal Typically bright red bleeding occurring post defecation. Although patients may give graphic
bleeding descriptions bleeding of sufficient volume to cause haemodynamic compromise is rare.

Angiodysplasia Apart from bleeding, which may be massive, these arteriovenous lesions cause little in the way of
symptoms. The right side of the colon is more commonly affected.

Management
• Prompt correction of any haemodynamic compromise is required. Unlike upper gastrointestinal bleeding the
first line management is usually supportive. This is because in the acute setting endoscopy is rarely helpful.
• When haemorrhoidal bleeding is suspected a proctosigmoidoscopy is reasonable as attempts at full
colonoscopy are usually time consuming and often futile.
• In the unstable patient the usual procedure would be an angiogram (either CT or percutaneous), when these
are performed during a period of haemodynamic instability they may show a bleeding point and may be the
only way of identifying a patch of angiodysplasia.
• In others who are more stable the standard procedure would be a colonoscopy in the elective setting. In
patients undergoing angiography attempts can be made to address the lesion in question such as coiling.
Otherwise surgery will be necessary.

52
 • In patients with ulcerative colitis who have significant haemorrhage the standard approach would be a sub total
colectomy, particularly if medical management has already been tried and is not effective.
Indications for surgery
Patients > 60 years
Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known cardiovascular disease with poor response to hypotension

Surgery
Selective mesenteric embolisation if life threatening bleeding. This is most helpful if conducted during a period of relative
haemodynamic instability. If all haemodynamic parameters are normal then the bleeding is most likely to have stopped
and any angiography normal in appearance. In many units a CT angiogram will replace selective angiography but the
same caveats will apply.

If source of colonic bleeding unclear perform a laparotomy, on table colonic lavage and following this attempt a
resection. A blind sub total colectomy is most unwise, for example bleeding from an small bowel arterio-venous
malformation will not be treated by this manoeuvre.

Summary of Acute Lower GI bleeding recommendations Consider admission if:

* Over 60 years
* Haemodynamically unstable/profuse PR bleeding
* On aspirin or NSAID
* Significant co morbidity
Management
• All patients should have a history and examination, PR and proctoscopy
• Colonoscopic haemostasis aimed for in post polypectomy or diverticular bleeding

Irritable bowel syndrome

The diagnosis of irritable bowel syndrome is made according to the ROME III diagnostic criteria which state:

Recurrent abdominal pain or discomfort at 3 days per month for the past 3 months associated with two or more
of the following:
• Improvement with defecation.
• Onset associated with a change in the frequency of stool.
• Onset associated with a change in the form of the stool.

Features such as lethargy, nausea, backache and bladder symptoms may also support the diagnosis

Red flag features should be inquired about:

• Rectal bleeding
• Unexplained/unintentional weight loss
• Family history of bowel or ovarian cancer
• Onset after 60 years of age

Suggested investigations are:

• Full blood count

53
 • ESR/CRP
• Coeliac disease screen (tissue transglutaminase antibodies)
• Colonoscopy (if worrying symptoms, positive family history)
• Thyroid function tests
• Glucose (ensure not diabetic)

The NICE criteria state that blood tests alone will suffice in people fulfilling the diagnostic criteria. We would point out
that luminal colonic studies should be considered early in patients with altered bowel habit referred to hospital and a
diagnosis of IBS should still be largely one of exclusion.

Treatment
• Usually reduce fibre intake.
• Tailored prescriptions of laxatives or loperamide according to clinical picture.
• Dietary modification (caffeine avoidance, less carbonated drinks).
• Consider low dose tricyclic antidepressants if pain is a dominant symptom.
• Biofeedback may help.

● Basic :
Rt. colon ca --- commonly shows
Pain @ RIF
Mass rt side, per abd. Exam
Anaemia ± wt. loss

Lt. colon ca + Tr.colon ca --- commonly shows

Bowel habit change
Abd. Distensn
Abdominal Pain (relieved with flatus… ☺)
Tenesmus
Early morning diarrhoea
Mass in DRE

Blood mixed stool ± wt. loss

● FAP Extra intestinal Menifestation(EIM)

- Desmoid tumor

- Hamartomatous polyp stomach

- Adenoma duodenum
- Dental cyst
- Supernumerary teeth
- Epidermoid cyst
- Osteoma Jaw
- Retinal pigmentation
** FAP with the presence of EIM is called Gardener’s Syndrome

Ulcerative colitis

54
Ulcerative colitis is a form of inflammatory bowel disease. Inflammation always starts at rectum, never spreads beyond
ileocaecal valve and is continuous. The peak incidence of ulcerative colitis is in people aged 15-25 years and in those
aged 55-65 years. It is less common in smokers.

The initial presentation is usually following insidious and intermittent symptoms. Features include:

• bloody diarrhoea
• urgency
• tenesmus
• abdominal pain, particularly in the left lower quadrant
• extra-intestinal features (see below)

Questions regarding the 'extra-intestinal' features of inflammatory bowel disease are common. Extra-intestinal features
include sclerosing cholangitis, iritis and ankylosing spondylitis.

{Common to both Crohn's disease (CD) and {Notes}

Ulcerative colitis (UC)}

{Related to disease Arthritis: pauciarticular, asymmetric Arthritis is the most common extra-intestinal
activity} Erythema nodosum feature in both CD and UC
Episcleritis Episcleritis is more common in CD
Osteoporosis

{Unrelated to disease Arthritis: polyarticular, symmetric Primary sclerosing cholangitis is much more
activity} Uveitis common in UC
Pyoderma gangrenosum Uveitis is more common in UC
Clubbing
Primary sclerosing cholangitis

Pathology
• red, raw mucosa, bleeds easily
• no inflammation beyond submucosa (unless fulminant disease)
• widespread superficial ulceration with preservation of adjacent mucosa which has the appearance of polyps
('pseudopolyps')
• inflammatory cell infiltrate in lamina propria
• neutrophils migrate through the walls of glands to form crypt abscesses
• depletion of goblet cells and mucin from gland epithelium
• granulomas are infrequent

Barium enema
• loss of haustrations
• superficial ulceration, 'pseudopolyps'
• long standing disease: colon is narrow and short -'drainpipe colon'

Endoscopy
• Superficial inflammation of the colonic and rectal mucosa
55
 • Continuous disease from rectum proximally
• Superifical ulceration, mucosal islands, loss of vascular definition and continuous ulceration pattern.

Management
• Patients with long term disease are at increased risk of development of malignancy
• Acute exacerbations are generally managed with steroids, in chronic patients agents such as azathioprine and
infliximab may be used
• Individuals with medically unresponsive disease usually require surgery- in the acute phase a sub total
colectomy and end ileostomy. In the longer term a proctectomy will be required. An ileoanal pouch is an option
for selected patients

Crohns disease

Crohns disease is a chronic transmural inflammation of a segment(s) of the gastrointestinal tract and may be associated
with extra intestinal manifestations. Frequent disease patterns observed include ileal, ileocolic and colonic disease. Peri-
anal disease may occur in association with any of these. The disease is often discontinuous in its distribution.
Inflammation may cause ulceration, fissures, fistulas and fibrosis with stricturing. Histology reveals a chronic
inflammatory infiltrate that is usually patchy and transmural.

Extraintestinal manifestations of Crohns with %

Related to disease extent Unrelated to disease extent

Aphthous ulcers (10%) Sacroiliiitis (10-15%)

Erythema nodosum (5-10%) Ankylosing spondylitis (1-2%)

Pyoderma gangrenosum (0.5%) Primary sclerosing cholangitis (Rare)

Acute arthropathy (6-12%) Gallstones (up to 30%)

Ocular complications (up to 10%) Renal calculi (up to 10%)

Extraintestinal manifestation of inflammatory bowel disease: A PIE SAC

Aphthous ulcers
Pyoderma gangrenosum
Iritis
Erythema nodosum
Sclerosing cholangitis
Arthritis
Clubbing

Surgery for inflammatory bowel disease

Patients with inflammatory bowel disease (UC and Crohns) frequently present in surgical practice. Ulcerative colitis may
be cured by surgical resection (Proctocolectomy), this is not the case in Crohns disease which may recur and affect
other areas of the gastrointestinal tract.

Ulcerative colitis In short – main place for surgery is when medical treatment has failed, in the emergency setting
this will be a sub total colectomy, end ileostomy and a mucous fistula. Electively it will be a pan

56
 proctocolectomy, an ileoanal pouch may be a selected option for some. Remember that
longstanding UC increases colorectal cancer risk.
• Elective indications for surgery include disease that is requiring maximal therapy, or prolonged courses of
steroids.
• Longstanding UC is associated with a risk of malignant transformation. Dysplastic transformation of the colonic
epithelium with associated mass lesions is an absolute indication for a proctocolectomy.
• Emergency presentations of poorly controlled colitis that fails to respond to medical therapy should usually be
managed with a sub total colectomy. Excision of the rectum is a procedure with a higher morbidity and is not
generally performed in the emergency setting. An end ileostomy is usually created and the rectum either
stapled off and left in situ, or, if the bowel is very oedematous, may be brought to the surface as a mucous
fistula.
• Patients with IBD have a high incidence of DVT and appropriate thromboprophylaxis is mandatory.
• Restorative options in UC include an ileoanal pouch. This procedure can only be performed whilst the rectum is
in situ and cannot usually be undertaken as a delayed procedure following proctectomy.
• Ileoanal pouch complications include, anastomotic dehiscence, pouchitis and poor physiological function with
seepage and soiling.

Crohns disease Unlike UC, Crohn's patients need to avoid surgeons, minimal resections are the rule. They should
not have ileoanal pouches as they will do poorly with them. Management of Crohn's ano rectal
sepsis is with a minimal approach, simply drain sepsis and use setons to facilitate drainage.
Definitive fistula surgery should be avoided
• Surgical resection of Crohns disease does not equate with cure, but may produce substantial symptomatic
improvement.
• Indications for surgery include complications such as fistulae, abscess formation and strictures.
• Extensive small bowel resections may result in short bowel syndrome and localised stricturoplasty may allow
preservation of intestinal length.
• Staging of Crohns will usually involve colonoscopy and a small bowel study (e.g. MRI enteroclysis).
• Complex perianal fistulae are best managed with long term draining seton sutures, complex attempts at fistula
closure e.g. advancement flaps, may be complicated by non healing and fistula recurrence.
• Severe perianal and / or rectal Crohns may require proctectomy, ileoanal pouch reconstruction in Crohns
carries a high risk of fistula formation and pouch failure and is not recommended.
• Terminal ileal Crohns remains the commonest disease site and these patients may be treated with limited
ileocaecal resections.
• Terminal ileal Crohns may affect enterohepatic bile salt recycling and increase the risk of gallstones.

● UC + CD EIM same. EIM is more in UC; if both options are given then answer UC . but anything in orally and
anus then answer will be CD.
● Fistula(specially enterovesical); Fissure; Mass; Infection; Stricture → CD’s Unique features
● Pseudopolyp; Crypt Abscess; Crypt distortion; Malignancy → UC’s Unique features

● Perforation can occur in both cases; but bleeding is UC > CD

● Incidence of GB stone & Kidney stone --- CD

UC & CD Difference

57
 FEATURES CD UC
Sex FM are more sufferer Equal
Site Only large bowel; occasional “backwash
Mouth to anus, anywhere… ileitis”
Lesion type Skip Lesion No skip lesion; continuous
Histology Whole thickness wall affected- hose pipe Limited to mucosa-not affecting muscularis
thickening, luminal narrowing; fibrosis propria
MUCOSA: cobblestone appearance MUCOSA: Atrophic- inflammatory
SEROSA : fatty encroachment pseudopolyps

Deep Ulcer; rose thorn ulcer SEROSA: is not affected until Toxic
Megacolon
Small & shallow ulcer

C/F Tenesmas absent Tenesmas + incontinence present

Pain is relieved by bowel movement
n
Inflam Spread Trans mural Confined to Lamina propria
Malignancy Chance less More chance --- Metaplasia , dysplasia
occurs
Granuloma Non-caseating Caseating

n
Lymphoid Found … Lymphocyte infiltrat of Lamina Not found
follicle propria present

Ba enema Kantor’s string sign found None

Blood picture Platelet raised None

Unique Fistula(specially enterovesical); Fissure Pseudopolyp;

Mass; Crypt Abscess & distortion;
features
Infection; Goblet cell mucous depletion
Stricture; Hge;
Skin tags Toxic megacolon (but Large bowel
obstruction is not a feature of UC)
Surgical RX Benefit less Diseased segment removed so beneficial
● Anti TNF-α antibody – Infliximab is given as a single infusion for clinical improvement in steroid resistant CD

Principles of Surgery IBD

*Proctocolectomy ē ileostomy : Traditional, Common procedure for UC

*Proctocolectomy ē ileal / ileo-anal pouch
(Sphincter preserving)
Procedure of choice among Middle aged and Elderly
Leaves the pt. ē permanent colostomy
n
: Best opr for UC
Procedure of choice among young
n
Rectum excised, Anal canal reserved ē intact sphincter act
Pouch is anastomosed @ dentate line

*Colectomy ē ileo-rectal anastomosis : Used in Both UC + CD

Used when rectum isn’t or mildly affected

58
 Used rarely bcz- (recurrent disease, risk of ca, good outcome
in pouch surgery)
Proctectomy is used, in failed cases.

Sub-total colectomy ē end ileostomy : Perforation

± mucous fistula Severe hemorrhage
Toxic Megacolon
Fistulation leading to sepsis
Severe acute colitis resistant to medical management
Obstruction due to stricture

Large bowel obstruction resulting from carcinoma should be resected, stented or defunctioned. Colonic resections with
an anastomosis below the peritoneal reflection may have an anastomotic leak rate (both clinical and radiological) of up
to 15%. End ileostomy & End colostomy typically apply to tumours above the peritoneal reflection. Lower tumours should
be defunctioned with a loop colostomy and then formal staging undertaken prior to definitive surgery.

Fig: Rx of UC Fig: Restorative proctocolectomy (ileoanal pouch procedure)

Fig: Ileal pouch anal anastomosis (mucosal lining left intact) Fig: ileal pouch anastomosis with distal rectal mucosal stripping

59
 Fig: low ant- resection-j-pouch

Fig: low ant- resection

60
 Fig: APR

Fig: Total proctocolectomy with Brooke ileostomy

Fig: colectomy vs total proctocolectomy

Fig: Colectomy with ileorectal anastomosis

61
 Fig: ex-rt-hemicolectomy

Abdominal Stomas

Name of stoma Use Common sites

Gastrostomy • Gastric decompression or fixation Epigastrium

• Feeding

Loop jejunostomy • Seldom used as very high output Any location according to

• May be used following emergency laparotomy with need

planned early closure

Percutaneous • Usually performed for feeding purposes and site in Usually left upper quadrant
jejunostomy the proximal bowel

Loop ileostomy • Defunctioning of colon e.g. following rectal cancer Usually right iliac fossa
surgery
• Does not decompress colon (if ileocaecal valve
competent)

End ilestomy • Usually following complete excision of colon or Usually right iliac fossa
where ileo-colic anastomosis is not planned
• May be used to defunction colon, but reversal is
more difficult

End colostomy Where a colon is diverted or resected and anastomosis is Either left or right iliac fossa
not primarily achievable or desirable

Loop colostomy • To defunction a distal segment of colon May be located in any

• Since both lumens are present the distal lumen region of the abdomen,

acts as a vent depending upon colonic

segment used

Caecostomy Stoma of last resort where loop colostomy is not possible Right iliac fossa

62
 Mucous fistula • To decompress a distal segment of bowel May be located in any
following colonic division or resection region of the abdomen

• Where closure of a distal resection margin is not according to clinical need

safe or achievable

** End ileostomy + End Colostomy usually applied for tumors above peritoneal reflection.
Lower tumors should be defunctioned with a Loop Colostomy**

● In fulminant UC, total colectomy with an end ileostomy is performed, usually in the Rt. iliac fossa.(RIF)

● In Crohn’s disease, Proximal small bowel strictures can be treated with segmental resection if only isolated areas

are affected, otherwise Stricturoplasty done if multiple segments involved.

● Pt. having large tumours not immediately resectable (peritoneal seeding, fixed to lateral pelvic wall ) may be

suitable for pre-operative radiotherapy to downsize the lesion. These cases require Loop Colostomy to divert the
faecal stream – commonly performed @ transverse or sigmoid colon

rd n
● Abd. Perineal resection - Middle & lower 3 of rectal ca – Its use when adequate distal resect margin not
achievable. If MRI shows resectable lesion present, then Total Mesorectal Excision (TME) done.(Waldeyer’s Fascia
is cut to mobilize)
● Below 5 cm of anal verge there will be not enough bowel left for an anastomosis, so APR is performed with a
permanent LIF end colostomy

● High Anterior Resection – Left Ureter is in high risk (of injury)

Which operation is best?

The operations for cancer are segmental resections based on blood supply and lymphatic drainage. In the elective
situation the following operations are recommended:

Site of cancer Type of resection Anastomosis Risk of leak

Right colon Right hemicolectomy Ileo-colic Low <5%

Transverse Extended right hemicolectomy Ileo-colic Low <5%

Splenic flexure Extended right hemicolectomy Ileo-colic Low <5%

Splenic flexure Left hemicolectomy Colo-colic 2-5%

Left colon Left hemicolectomy Colo-colic 2-5%

Sigmoid colon High anterior resection Colo-rectal 5%

Upper rectum Anterior resection (TME) Colo-rectal 5%

Low rectum Anterior resection (Low TME) Colo-rectal 10%

(+/- Defunctioning stoma)

Anal verge Abdomino-perineal excision of colon and rectum None n/a

● Young person,, bright red rectal bleed without other symptoms. Investigation of choice – Flexible Sigmoidoscopy

63
● Young person,, maroon rectal bleed without other symptoms, both UGI endoscopy & Colonoscopy normal.

Investigation of choice – Technetium -99m scanning

● Young person,, maroon rectal bleed without other symptoms, both UGI endoscopy & Colonoscopy normal.

Diagnosis is Meckel’s Diverticulam

● Aged person, bright red rectal bleed without other symptoms, Fresh blood on rectal exam gloves --- commonest
nd
cause? Ans:- Diverticular disease, 2 option Angiodysplasia

● Aged person, bright red rectal bleed without other symptoms; Gastroscopy & Colonoscopy normal i.e. don’t think

about Diverticular disease; ans will be Angiodysplasia. Mesenteric Angiography Or Radionucleotide Scan may be
used. But maximum cases cant be identified. In case of continued bleeding, with negative invx - RX – Total Colectomy

Angiodysplasia

- Small, submucosal vascular swelling of unknown etiology

- Associated with Aortic Stenosis
- Common sites are – ascending colon; caecum
- PR bleed may present as Anemia; (+)ve FOBT; Recurrent small bleed or torrential acute bleed
- Association ē hereditary telangiectasia skin & mouth in Osler- Weber- Rendu disease.
st nd
- Investigation : 1 choice Colonoscopy; 2 choice Meseteric Angiography – if all fails,
Technetium-99m labeled RBC can localize source of haemorrage.
Colonoscopy shows spider naevi like lesion

Diverticular disease

Diverticular disease is a common surgical problem. It consists of herniation of colonic mucosa through the muscular wall
of the colon. The usual site is between the taenia coli which vessels pierce the muscle to supply the mucosa.

● Symptoms
• Altered bowel habit
• Bleeding
• Abdominal pain

● Complications
• Diverticulitis
• Haemorrhage
• Development of fistula
• Perforation and faecal peritonitis
• Perforation and development of abscess
• Development of diverticular phlegmon

● Diagnosis
Patients presenting in clinic will typically undergo either a colonoscopy or barium enema as part of their diagnostic work
up. Both tests will identify diverticular disease. It can be far more difficult to confidently exclude cancer, particularly in

64
diverticular strictures.

Acutely unwell surgical patients should be investigated in a systematic way. Plain abdominal films and an erect chest x-
ray will identify perforation. An abdominal CT scan with oral and intravenous contrast will help to identify whether acute
inflammation is present but also the presence of local complications such as abscess formation.

● Suspected Diverticular Mass suitable investigation USG

Diverticular Abscess suitable investigation CT abd. & pelvis
Diverticular disease suitable investigation Enema

● Severity Classification- Hinchey

I - Para-colonic abscess
II - Pelvic abscess
III - Purulent peritonitis
IV - Faecal peritonitis

● Treatment
• Increase dietary fibre intake.
• Mild attacks of diverticulitis may be managed conservatively with antibiotics.
• Peri colonic abscesses should be drained either surgically or radiologically.
• Recurrent episodes of acute diverticulitis requiring hospitalisation are a relative indication for a segmental
resection.
• Hinchey IV perforations (generalised faecal peritonitis) will require a resection and usually a stoma. This group
have a very high risk of post operative complications and usually require HDU admission. Less severe
perforations may be managed by laparoscopic washout and drain insertion.

● Aged person, Constipation requires perineal massage requires to defaecate, female paitent complains vagina bulging
during defaecation (rectocele)---- outlet obstruction constipation
● Aged person, psychogenic, Constipation & abd.distension-- supine Abd Xray is to be done, but if this option is not
there, colonoscopy will be the 2nd option.

● Maximum center use CT in ≥ 80yrs group with primary colorectal ca.

● Suspected, acutely obstructing large bowel ca--- suitable investigation Gastrografin enema
● Rectal ca. Tissue invasion within the pelvis is best assessed with MRI

● Suspected Psoas abscess suitable investigation CT abd.

● Suspected colovesical fistula suitable investigation double contrast Ba enema

Coeliac disease typical histological features

Villous atrophy (‘gold standard’)
Crypt hyperplasia / hypertrophy,
Inflammatory infiltrate of the lamina propria
Intra-epithelial lymphocytes
Anti TTG antibody present in >90% cases.

65
(However, detection of tissue transglutaminase antibodies has high specificity and sensitivity and is widely used as a
screening test)

Fistulas
• A fistula is defined as an abnormal connection between two epithelial surfaces.
• There are many types ranging from Branchial fistulae in the neck to entero-cutaneous fistulae abdominally.
• In general surgical practice the abdominal cavity generates the majority and most of these arise from
diverticular disease and Crohn's.
• As a general rule all fistulae will resolve spontaneously as long as there is no distal obstruction. This is
particularly true of intestinal fistulae.

The four types of fistulae are:

Enterocutaneous
These link the intestine to the skin. They may be high (>1L) or low output (<1L) depending upon source. Duodenal
/jejunal fistulae will tend to produce high volume, electrolyte rich secretions which can lead to severe excoriation of the
skin. Colo-cutaneous fistulae will tend to leak faeculent material. Both fistulae may result from the spontaneous rupture
of an abscess cavity onto the skin (such as following perianal abscess drainage) or may occur as a result of iatrogenic
input. In some cases it may even be surgically desirable e.g. mucous fistula following sub total colectomy for colitis.
Suspect if there is excess fluid in the drain.

Enteroenteric or Enterocolic
This is a fistula that involves the large or small intestine. They may originate in a similar manner to enterocutaneous
fistulae. A particular problem with this fistula type is that bacterial overgrowth may precipitate malabsorption syndromes.
This may be particularly serious in IBD

Enterovaginal Aetiology as above.

Enterovesicular
This type of fistula goes to the bladder. These fistulas may result in frequent urinary tract infections, or the passage of
gas from the urethra during urination.

Management Some rules relating to fistula management:

• They will heal provided there is no underlying inflammatory bowel disease and no distal obstruction, so
conservative measures may be the best option
• Where there is skin involvement, protect the overlying skin, often using a well fitted stoma bag- skin damage is
difficult to treat
• A high output fistula may be rendered more easily managed by the use of octreotide, this will tend to reduce the
volume of pancreatic secretions.
• Nutritional complications are common especially with high fistula (e.g. high jejunal or duodenal) these may
necessitate the use of TPN to provide nutritional support together with the concomitant use of octreotide to
reduce volume and protect skin.
• When managing perianal fistulae surgeons should avoid probing the fistula where acute inflammation is
present, this almost always worsens outcomes.
• When perianal fistulae occur secondary to Crohn's disease the best management option is often to drain acute
sepsis and maintain that drainage through the judicious use of setons whilst medical management is
implemented.

66
 • Always attempt to delineate the fistula anatomy, for abscesses and fistulae that have an intra abdominal source
the use of barium and CT studies should show a track. For perianal fistulae surgeons should recall Goodsall's
rule in relation to internal and external openings.

Benign proctology

Condition Features Treatment

Fissure in ano Painful, bright red rectal bleeding Stool softeners, topical diltiazem or GTN, botulinum
toxin, Sphincterotomy

Haemorroids Painless, bright red rectal bleeding occurs Stool softeners, avoid straining, surgery (see below)
following defecation and bleeds onto the toilet
paper and into the toilet pan

Fistula in ano May initially present with an abscess and then Lay open if low, no sphincter involvement or IBD, if
persisting discharge onto the perineum, separate complex, high or IBD insert seton and consider other
from the anus options (see below)

Peri anal Peri anal swelling and surrounding erythema Incision and drainage, leave the cavity open to heal by
abscess secondary intention

Pruritus ani Peri anal itching, occasional mild bleeding (if Avoid scented products, use wet wipes rather than
severe skin damage) tissue, avoidance of scratching, ensure no underlying
faecal incontinence

Rectum (N-369, 370)

The rectum is approximately 12 cm long. It is a capacitance organ. It has both intra and extraperitoneal components.
The transition between the sigmoid colon is marked by the disappearance of the tenia coli.The extra peritoneal rectum is
surrounded by mesorectal fat that also contains lymph nodes. This mesorectal fatty layer is removed surgically during
rectal cancer surgery (Total Mesorectal Excision). The fascial layers that surround the rectum are important clinical
landmarks, anteriorly lies the fascia of Denonvilliers. Posteriorly lies Waldeyers fascia.

Extra peritoneal rectum

• Posterior upper third
• Posterior and lateral middle third
• Whole lower third

Relations

Anteriorly (Males) Rectovesical pouch

Bladder
Prostate
Seminal vesicles

Anteriorly (Females) Recto-uterine pouch (Douglas)

Cervix
Vaginal wall

Posteriorly Sacrum

67
 Coccyx
Middle sacral artery

Laterally Levator ani

Coccygeus

Support
- Pelvic floor
- Waldeyer’s fascia with sacrum
- Rectovesical fascia of Denonvilier’s
- Laeral ligament of rectum
- Pelvic peritoneum

Arterial supply
Superior rectal artery ← IMA
Middle rectal artery ← IIA (ant. division)
Median sacral artery ← AA

Venous drainage
Superior rectal vein → IMV
Middle rectal vein → IIV

Nerve supply (thru’ inf. Hypogastric + Inf. Mesenteric / sup. Rectal plexus)
Sympathetic(L1,2):- Vasoconstrictor; Rectal muscle (–); IAS(+); Pain
P. Sympathetic(S2,3,4):- Rectal muscle(+); IAS (–); Rectal distension sense; Pain

Lymphatic drainage
• Mesorectal lymph nodes (superior to dentate line)
• Internal iliac and then para-aortic nodes
• Inguinal nodes (inferior to dentate line)

Rectal bleeding

Rectal bleeding is a common cause for patients to be referred to the surgical clinic. In the clinical history it is useful to try
and localise the anatomical source of the blood. Bright red blood is usually of rectal anal canal origin, whilst dark red
blood is more suggestive of a proximally sited bleeding source. Blood which has entered the GI tract from a gastro-
duodenal source will typically resemble malaena due to the effects of the digestive enzymes on the blood itself.

In the table below we give some typical bleeding scenarios together with physical examination findings and causation.

Cause Type of Features in history Examination findings

bleeding

Fissure in Bright red Painful bleeding that occurs post Muco-epithelial defect usually in the midline
ano rectal bleeding defecation in small volumes. Usually posteriorly (anterior fissures more likely to
antecedent features of constipation be due to underlying disease)

Haemorroids Bright red Post defecation bleeding noted both on Normal colon and rectum. Proctoscopy may

68
 rectal bleeding toilet paper and drips into pan. May be show internal haemorrhoids. Internal
alteration of bowel habit and history of haemorrhoids are usually impalpable.
straining. No blood mixed with stool. No
local pain.

Crohns Bright red or Bleeding that is accompanied by other Perineal inspection may show fissures or
disease mixed blood symptoms such as altered bowel habit, fistulae. Proctoscopy may demonstrate
malaise, history of fissures (especially indurated mucosa and possibly strictures.
anterior) and abscesses. Skip lesions may be noted at colonoscopy.

Ulcerative Bright red Diarrhoea, weight loss, nocturnal Proctitis is the most marked finding. Peri
colitis bleeding often incontinence, passage of mucous PR. anal disease is usually absent.
mixed with Colonoscopy will show continuous mucosal
stool lesion.

Rectal Bright red Alteration of bowel habit. Tenesmus may Usually obvious mucosal abnormality.
cancer blood mixed be present. Symptoms of metastatic Lesion may be fixed or mobile depending
volumes disease. upon disease extent. Surrounding mucosa
often normal, although polyps may be
present.

Image showing a fissure in ano. Typically these are located posteriorly and in the midline. Fissures at other sites may be
associated with underlying disease.

Investigation
• All patients presenting with rectal bleeding require digital rectal examination and procto-sigmoidoscopy as a
minimal baseline.
• Remember that haemorrhoids are typically impalpable and to attribute bleeding to these in the absence of
accurate internal inspection is unsatisfactory.
• In young patients with no other concerning features in the history a carefully performed sigmoidoscopy that
demonstrates clear haemorrhoidal disease may be sufficient. If clear views cannot be obtained then patients
require bowel preparation with an enema and a flexible sigmoidscopy performed.
• In those presenting with features of altered bowel habit or suspicion of inflammatory bowel disease a
colonoscopy is the best test.
• Patients with excessive pain who are suspected of having a fissure may require an examination under general
or local anaesthesia.
• In young patients with external stigmata of fissure and a compatible history it is acceptable to treat medically
and defer internal examination until the fissure is healed. If the fissure fails to heal then internal examination
becomes necessary along the lines suggested above to exclude internal disease.

Special tests
• In patients with a malignancy of the rectum the staging investigations comprise an MRI of the rectum to identify
circumferential resection margin compromise and to identify mesorectal nodal disease. In addition to this CT
scanning of the chest abdomen and pelvis is necessary to stage for more distant disease. Some centres will
still stage the mesorectum with endo rectal ultrasound but this is becoming far less common.

• Patients with fissure in ano who are being considered for surgical sphincterotomy and are females who have an
obstetric history should probably have ano rectal manometry testing performed together with endo anal

69
 ultrasound. As this service is not universally available it is not mandatory but in the absence of such information
there are continence issues that may arise following sphincterotomy.

Management

Disease Management

Fissure in ano GTN ointment 0.2% or diltiazem cream applied topically is the usual first line treatment. Botulinum
toxin for those who fail to respond. Internal sphincterotomy for those who fail with botox, can be
considered at the botox stage in males.

Haemorroids Lifestyle advice, for small internal haemorrhoids can consider injection sclerotherapy or rubber band
ligation. For external haemorrhoids consider haemorrhoidectomy. Modern options include HALO
procedure and stapled haemorrhoidectomy.

Inflammatory Medical management- although surgery may be needed for fistulating Crohns (setons).
bowel disease

Rectal cancer Anterior resection or abdomino-perineal excision of the colon and rectum. Total mesorectal excision
is now standard of care. Most resections below the peritoneal reflection will require defunctioning
ileostomy. Most patients will require preoperative radiotherapy.

Anal Canal
• 3.8 cm long
• Upper 1.5 cm; middle 1.5cm; lower 0.8cm

Arterial supply
Above pectinate line : Superior rectal artery ← IMA
Below pectinate line : Inferior rectal artery ← IPA ← IIA (ant. division)

Venous drainage
- Internal rectal venous plexus (haemorrhoidal; lies @ submucosa) →SRV → IMV
(It can freely connect ē External plexus thus ē Middle & Inf. Rectal vein – important site for porto-systemic anastomosis)

- External rectal venous plexus (outside muscular coat) – Inf. Rectal vein → IPV
– Mid. Rectal vein → IIV

Nerve supply (thru’ inf. Hypogastric + Inf. Mesenteric / sup. Rectal plexus)
Above pectinate line : Inf. Hypogastric plexus(Sympathetic L1,2) – Pain
Pelvic splanchnic (S2,3,4) – Pain
Below pectinate line : Inferior rectal S2,3,4 (Somatic)

Lymphatic drainage
Above pectinate line: IIN
Below pectinate line: Superficial IN

Anal sphincter

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 • Internal anal sphincter composed of smooth muscle continuous with the circular muscle of the rectum. It
surrounds the upper two- thirds of the anal canal and is supplied by sympathetic nerves.
• External anal sphincter is composed of striated muscle which surrounds the internal sphincter but extends more
distally.
• The nerve supply of the external anal sphincter is from the inferior rectal branch of the pudendal nerve (S2 and
S3) and the perineal branch of the S4 nerve roots.

Pruritus ani
• Extremely common.
• Check not secondary to altered bowel habits (e.g. Diarrhoea)
• Associated with underlying diseases such as haemorrhoids.
• Examine to look for causes such as worms.
• Proctosigmoidoscopy to identify associated haemorrhoids and exclude cancer.
• Treatment is largely supportive and patients should avoid using perfumed products around the area.

Pruritis Ani is associated with:

Systemic (DM, Hyperbilirubinaemia, aplastic anaemia)
Mechanical (diarrhoea, constipation, anal fissure)
Infections (STDs)
Dermatological
Drugs (quinidine, colchicine)
Topical agents

Fissure in ano
• Typically painful PR bleeding (bright red).
• Nearly always in the posterior midline.
• Usually solitary.

Treatment
• Stool softeners.
• Topical diltiazem (or GTN).
• If topical treatments fail then botulinum toxin should be injected.
• If botulinum toxin fails then males should probably undergo lateral internal sphincterotomy and females and
advancement flap.

Overview of surgical therapies

Haemorroidal disease
The treatment of haemorroids is usually conservative. Acutely thrombosed haemorroids may be extremely painful.
Treatment of this acute condition is usually conservative and consists of stool softeners, ice compressions and topical
GTN or diltiazem to reduce sphincter spasm. Most cases managed with this approach will settle over the 5-7 days. After
this period there may be residual skin tags that merit surgical excision or indeed residual haemorroidal disease that may
necessitate haemorroidectomy.
Patients with more chronic symptoms are managed according to the stage of their disease, small mild internal
haemorroids causing little symptoms are best managed conservatively. More marked symptoms of bleeding and
occasional prolapse, where the haemorroidal complex is largely internal may benefit from stapled haemorroidopexy. This
procedure excises rectal tissue above the dentate line and disrupts the haemorroidal blood supply. At the same time the

71
excisional component of the procedure means that the haemorroids are less prone to prolapse. Adverse effects of this
procedure include urgency, which can affect up to 40% of patients (but settles over 6-12 months) and recurrence. The
procedure does not address skin tags and therefore this procedure is unsuitable if this is the dominant symptom.
Large haemorroids with a substantial external component may be best managed with a Milligan Morgan style
conventional haemorroidectomy. In this procedure three haemorroidal cushions are excised, together with their vascular
pedicle. Excision of excessive volumes of tissue may result in anal stenosis. The procedure is quite painful and most
surgeons prescribe metronidazole post operatively as it decreases post operative pain.

Fissure in ano
Probably the most efficient and definitive treatment for fissure in ano is lateral internal sphincterotomy. The treatment is
permanent and nearly all patients will recover. Up to 30% will develop incontinence to flatus. There are justifiable
concerns about using this procedure in females as pregnancy and pelvic floor damage together with a sphincterotomy
may result in faecal incontinence. The usual first line therapy is relaxation of the internal sphincter with either GTN or
diltiazem (the latter being better tolerated) applied topically for 6 weeks. Treatment failures with topical therapy will
usually go on to have treatment with botulinum toxin. This leads to more permanent changes in the sphincter and this
may facilitate healing.
Typical fissures usually present in the posterior midline, multiple or unusually located fissures should prompt a search for
an underlying cause such as inflammatory bowel disease or internal prolapse.
Refractory cases where the above treatments have failed may be considered for advancement flaps.

Fistula in ano
The most effective treatment for fistula is laying it open (fistulotomy). When the fistula is below the sphincter and
uncomplicated, this is a reasonable option. Sphincter involvement and complex underlying disease should be assessed
both surgically and ideally with imaging (either MRI or endoanal USS). Surgery is then usually staged, in the first
instance a draining seton suture may be inserted. This avoids the development of recurrent sepsis and may allow
resolution. In patients with Crohns disease the seton should be left in situ long term and the patient managed medically,
as in these cases attempts at complex surgical repair nearly always fail. Fistulas not associated with IBD may be
managed by advancement flaps, instillation of plugs and glue is generally unsuccessful. A newer technique of ligation of
intersphincteric tract (LIFT procedure) is reported to have good results in selected centres.

Ano rectal disease

Location: 3, 7, 11 o'clock position

Haemorrhoids Internal or external
Treatment: Conservative, Rubber band ligation, Haemorrhoidectomy

Fissure in ano Location: midline 6 (posterior midline 90%) & 12 o'clock position. Distal to the
dentate line
Chronic fissure > 6/52: triad: Ulcer, sentinel pile, enlarged anal papillae

Proctitis Causes: Crohn's, Ulcerative Colitis, Clostridium difficile

Ano rectal abscess E.coli, staph aureus

Positions: Perianal, Ischiorectal, Pelvirectal, Intersphincteric

Anal fistula Usually due to previous ano-rectal abscess

Intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric.
Goodsalls rule determines location

Rectal prolapse Associated with childbirth and rectal intussceception. May be internal or external

72
 Pruritus ani Systemic and local causes

Anal neoplasm Squamous cell carcinoma commonest unlike adenocarcinoma in rectum

Solitary rectal ulcer Associated with chronic straining and constipation. Histology shows mucosal
thickening, lamina propria replaced with collagen and smooth muscle
(fibromuscular obliteration)

Haemorrhoids Rx
0
1 (confined anal canal) : Bulking agents; tropical anaesthesia > if unresponsive, inj. Sclerotherapy
0 n
2 (prolapse on defaecat &
n
spontaneous/digital reduct ): Rubber band ligation

0
3 (permanent prolapse) : Haemorrhoidectomy

Fistula

● Good sal’s Rule

Goodsall's rule relates the external opening of an anal fistula to its internal opening. It states that the external
opening situated behind the transverse anal line will open into the anal canal in the midline posteriorly. An anterior
opening is usually associated with a radial tract. Or in more direct terms, it means that anterior-opening fistulas
tend to follow a simple direct course while posterior-opening fistulas may follow a devious, curving path with some
even being horseshoe-shaped before opening in the posterior midline

73
 Intersphincteric : Fistulotomy
Dentate line + its above : Seton suture
Rest : Fistulectomy
● Complex anal fistula is best assessed with MRI

● Sphincters destruction suitable investigation endoanal USG . Other investigations anorectal manometry.

Anal Fissure

Most fissures are idiopathic and present mostly as mucocutaneous defect in the posterior midline (90% cases).
Fissures are more likely to be anteriorly located in females, particularly if multiparous. Multiple fissures and those
which are located at other sites are more likely to be due to underlying causes:
Sexually transmitted diseases (syphilis, HIV)
Inflammatory bowel disease (Crohn's up to 50%)
Leukaemia (25% of patients)
Tuberculosis
Previous anal surgery
RX:
1st line : GTN oint. tds X 8wks
nd nd
2 line : If Headache Diltiazem oint, 2 option
Chronic : Botulinum toxin is an effective treatment (73% efficacy)** if it fails –
Lateral internal sphincterotomy (male – but assoc. ē flatus incontinence in 10% later)
Advancement flaps (Female).

Rectal prolapse

74
 • Common especially in multiparous women.
• May be internal or external.
• Patients with internal prolapse
o May present insidiously,
o Have internal intussceception of the rectum
o Present with constipation, obstructed defecation and occasionally faecal incontinence
• Patients with external rectal prolapse
o Have a full thickness external protrusion of the rectum.
o Can ulcerate and in long term impair continence
• Diagnostic work up includes
o Colonoscopy,
o Defecating proctogram,
o Ano rectal manometry studies
o If doubt exists and examination under anaesthesia.
o Sinister pathology should be excluded with endoscopy

Treatment
• In the acute setting reduce it (covering it with sugar may reduce swelling)
• Delormes operation
o Perineal approaches
o may be used for external prolapse
o Excises mucosa and plicates the rectum - this avoids resection and is relatively safe.
o Associated with high recurrence rates.

• Altmeirs procedure
o Resection of colon via the perineal route
o Has lower recurrence rates
o but carries the risk of anastamotic leak
• Rectopexy
o Abdominal procedure.
o The rectum is mobilized, elevated and fixed onto the sacral promotary.
o Post operative constipation may be reduced by limiting the dissection to the anterior plane
(laparoscopic ventral mesh rectopexy).
o The recurrence rates are low and the procedure is well tolerated (particularly if performed
laparoscopically).
• Thirsch tape- this is a largely historical procedure and involves encircling the rectum with tape or wire. It may be
of use in a palliative setting.

● Solitary rectal ulcer syndrome treatment ----Biofeedback

● Perianal hematoma treatment----- 4% Formalin (topical)

● Levator ani (pubococcygeus+puborectalis+iliococcygeus) and Coccygeus muscles form Pelvic Diaphragm(N-363)

● Levator ani arises from Back of Pubis Body; Ischial spineand the tendinous arch of Obturator internus fascia.

● Thrombosed piles can be treated conservatively or by incision and drainage to evacuate clot under LA

75
● Laparoscopic repair is indicated in bilateral inguinal hernia unless there is any contraindicated.

● Emergency appendicectomy --- iliohypogastric nerve (L1) injury, results numbness of pubic region

● Sigmoid colon most likely 2b involved in left-sided indirect inguinal hernia as it is mobile due2 sigmoid mesocolon.

● Fallopian tube lies between the layers of the mesosalpinx

● OSLER WEBER RENDU SYNDROME : TEACH (after OCP use)

T elengiectasia
E pistaxis
A V malformation
C erebral abscess
H aemorrhages-pulmonary,GIT

● Vagus supplies p.symp. fibres 2abdominal organs, which receive blood from coeliac trunk/SMA. Means,up2 last part of
n
transverse colon. End of transverse colon & all GIT structures distal 2that point receive p.symp. innervat from pelvic
splanchnic & blood from IMA.

Mesenteric Vessel Disease

Mesenteric ischaemia accounts for 1 in 1000 acute surgical admissions. It is primarily caused by arterial embolism
resulting in infarction of the colon. It is more likely to occur in areas such as the splenic flexure that are located at
the borders of the territory supplied by the superior and inferior mesenteric arteries.

Acute mesenteric • Sudden onset abdominal pain followed by profuse diarrhoea.

embolus (commonest • May be associated with vomiting.
50%)
• Rapid clinical deterioration.
• Serological tests: WCC, lactate, amylase may all be abnormal particularly in
established disease. These can be normal in the early phases.

Acute on chronic • Usually longer prodromal history.

mesenteric ischaemia
• Post prandial abdominal discomfort and weight loss are dominant features. Patients
will usually present with an acute on chronic event, but otherwise will tend not to
present until mesenteric flow is reduced by greater than 80%.
• When acute thrombosis occurs presentation may be as above. In the chronic setting
the symptoms will often be those of ischaemic colitis (mucosa is the most sensitive
area to this insult).
• O/E diffuse epigastric tenderness & abdominal bruit

Mesenteric vein • Usually a history over weeks.

thrombosis • Overt abdominal signs and symptoms will not occur until venous thrombosis has
reached a stage to compromise arterial inflow.
• Thrombophilia accounts for 60% of cases.

Low flow mesenteric • This occurs in patients with multiple co morbidities in whom mesenteric perfusion is
infarction significantly compromised by overuse of inotropes or background cardiovascular
compromise.

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 • The end result is that the bowel is not adequately perfused and infarcts occur from
the mucosa outwards.

Diagnosis
• Serological tests: WCC, lactate, CRP, amylase (can be normal in early disease).
• Cornerstone for diagnosis of arterial AND venous mesenteric disease is CT angiography scanning in the
arterial phase with thin slices (<5mm). Venous phase contrast is not helpful.
• SMA duplex USS is useful in the evaluation of proximal SMA disease in patients with chronic mesenteric
ischaemia.
• MRI is of limited use due to gut peristalsis and movement artefact.

Management
• Overt signs of peritonism: Laparotomy
• Mesenteric vein thrombosis: If no peritonism: Medical management with IV heparin
• At operation limited resection of frankly necrotic bowel with view to relook laparotomy at 24-48h. In the interim
urgent bowel revascularisation via endovascular (preferred) or surgery.
Prognosis
Overall poor. Best outlook is from an acute ischaemia from an embolic event where surgery occurs within 12h. Survival
may be 50%. This falls to 30% with treatment delay. The other conditions carry worse survival figures

● A 19 year old lady is admitted with lower abdominal pain. On examination she is diffusely tender. A laparoscopy is
performed and at operation multiple fine adhesions are noted between the liver and abdominal wall. Her appendix is
normal.
answer: Pelvic inflammatory disease
This is Fitz Hugh Curtis syndrome in which pelvic inflammatory disease (usually Chlamydia) causes the formation of
fine peri hepatic adhesions.

Pseudomyxoma Peritonei
• Rare mucinous tumour
• Most commonly arising from the appendix (other abdominal viscera are also recognised as primary sites)
• Incidence of 1-2/1,000,000 per year
• The disease is characterised by the accumulation of large amounts of mucinous material in the abdominal
cavity
Treatment
Is usually surgical and consists of cytoreductive surgery (and often peritonectomy c.f Sugarbaker procedure) combined
with intra peritoneal chemotherapy with mitomycin C.
Survival is related to the quality of primary treatment and in Sugarbakers own centre 5 year survival rates of 75% have
been quoted. Patients with disseminated intraperitoneal malignancy from another source fare far worse.
In selected patients a second look laparotomy is advocated and some practice this routinely.

Gastro Intestinal Parasitic Infections

Enterobiasis • Due to organism Enterobius vermicularis

• Common cause of pruritus ani
• Diagnosis usually made by placing scotch tape at the anus, this will trap eggs that

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 can then be viewed microscopically.
• Treatment is with mebendazole.

Ancylostoma • Hookworms that anchor in proximal small bowel.

duodenale • Most infections are asymptomatic although may cause iron deficiency anaemia
• Larvae may be found in stools left at ambient temperature, otherwise infection is difficult
to diagnose.
• Infection occurs as a result of cutaneous penetration, migrates to lungs, coughed up and
then swallowed.
• Treatment is with mebendazole.

Ascariasis • Due to infection with roundworm Ascaris lumbricoides

• Infections begin in gut following ingestion, then penetrate duodenal wall to migrate to
lungs, coughed up and swallowed, cycle begins again.
• Diagnosis is made by identification of worm or eggs within faeces.
• Treatment is with mebendazole

Strongyloidiasis • Due to infection with Strongyloides stercoralis

• Rare in west
• Organism is a nematode living in duodenum of host
• Initial infection is via skin penetration. They then migrate to lungs and are coughed
up and swallowed. Then mature in small bowel are excreted and cycle begins
again. An auto infective cycle is also recognised where larvae will penetrate
colonic wall.
• Individuals may be asymptomatic, although they may also have respiratory disease and
skin lesions.
• Diagnosis is usually made by stool microscopy
• In the UK mebendazole is used for treatment.

Cryptosporidium • Protozoal infection

• Organisms produce cysts which are excreted and thereby cause new infections
• Symptoms consist of diarrhoea and cramping abdominal pains. Symptoms are
worse in immunosuppressed people
• Cysts may be identified in stools.
• Treatment is with metronidazole

Giardiasis • Diarrhoeal infection caused by Giardia lamblia (protozoan)

• Infections occur as a result of ingestion of cysts
• Symptoms are usually gastrointestinal with abdominal pain, bloating and passage of soft
or loose stools.
• Diagnosis is by serology or stool microscopy
• First line treatment is with metronidazole

Malabsorption
Malabsorption is characterised by diarrhoea, steatorrhoea and weight loss. Causes may be broadly divided into
intestinal (e.g. villous atrophy), pancreatic (deficiency of pancreatic enzyme production or secretion) and biliary
(deficiency of bile-salts needed for emulsification of fats) Intestinal causes of malabsorption
• coeliac disease
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 • Crohn's disease
• tropical sprue
• Whipple's disease
• Giardiasis
• brush border enzyme deficiencies (e.g. lactase insufficiency)

Pancreatic causes of malabsorption

• chronic pancreatitis
• cystic fibrosis
• pancreatic cancer

Biliary causes of malabsorption

• biliary obstruction
• primary biliary cirrhosis

Other causes
• bacterial overgrowth (e.g. systemic sclerosis, diverticulae, blind loop)
• short bowel syndrome
• lymphoma

Lymphatic drainage of the uterus and cervix

• The uterine fundus has a lymphatic drainage that runs with the ovarian vessels and may thus drain to the para-
aortic nodes. Some drainage may also pass along the round ligament to the inguinal nodes.
• The body of the uterus drains through lymphatics contained within the broad ligament to the iliac lymph nodes.
• The cervix drains into three potential nodal stations; laterally through the broad ligament to the external iliac
nodes, along the lymphatics of the uterosacral fold to the presacral nodes and posterolaterally along lymphatics
lying alongside the uterine vessels to the internal iliac nodes.

Ferritin

Ferritin is an intracellular protein that binds iron and stores it to be released in a controlled fashion at sites where iron is
required. Because iron and ferritin are bound the total body ferritin levels may be decreased in cases of iron deficiency
anaemia. Measurement of serum ferritin levels can be useful in determining whether an apparently low haemoglobin and
microcytosis is truly caused by an iron deficiency state.
Ferritin is an acute phase protein and may be synthesised in increased quantities in situations where inflammatory
activity is ongoing. Falsely elevated results may therefore be encountered clinically and need to be taken in context of
the clinical picture and full blood count results.

Iron metabolism

Absorption • Duodenum and upper jejunum

• About 10% of dietary iron absorbed
• Fe2+ (ferrous iron) much better absorbed than Fe3+ (ferric iron)
• Ferrous iron is oxidized to form ferric iron, which is combined with apoferritin to form ferritin
• Absorption is regulated according to body's need

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 • Increased by vitamin C, gastric acid
• Decreased by proton pump inhibitors, tetracycline, gastric achlorhydria, tannin (found in tea)

3+
Transport In plasma as Fe bound to transferrin

Storage Ferritin (or haemosiderin) in bone marrow

Excretion Lost via intestinal tract following desquamation

Distribution in body

Total body iron 4g

Haemoglobin 70%

Ferritin and haemosiderin 25%

4%
Myoglobin

Plasma iron 0.1%

Collagen

One of the major connective tissue proteins

• Composed of 3 polypeptide strands that are woven into a helix
• Numerous hydrogen bonds exist within molecule to provide additional strength
• Many sub types but commonest sub type is I (90% of bodily collagen)
• Vitamin c is important in establishing cross links

Collagen Diseases

• Osteogenesis imperfecta
• Ehlers Danlos

Osteogenesis imperfecta:

-8 Subtypes
-Defect of type I collagen
-In type I the collagen is normal quality but insufficient quantity
-Type II- poor quantity and quality
-Type III- Collagen poorly formed, normal quantity
-Type IV- Sufficient quantity but poor quality
Patients have bones which fracture easily, loose joint and multiple other defects depending upon which sub type they
suffer from

Ehlers Danlos:
- Multiple sub types
- Abnormality of types 1 and 3 collagen
- Patients have features of hypermobility.

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 - Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to many other
diseases related to connective tissue defects

Vitamin deficiency

Vitamin Effect of deficiency

A Night blindness
Epithelial atrophy
Infections

C Poor wound healing

Impaired collagen synthesis

D Rickets (Children)
Osteomalacia (Adults)

K Clotting disorders

Vitamin C deficiency

Vitamin C deficiency (scurvy) leads to defective synthesis of collagen resulting in capillary fragility (bleeding tendency)
and poor wound healing
Features
• gingivitis, loose teeth
• poor wound healing
• bleeding from gums, haematuria, epistaxis
• general malaise

B Vitamin Deficiency

Vitamin B12 deficiency

Vitamin B12 is mainly used in the body for red blood cell development and also maintenance of the nervous system. It is
absorbed after binding to intrinsic factor (secreted from parietal cells in the stomach) and is actively absorbed in the
terminal ileum. A small amount of vitamin B12 is passively absorbed without being bound to intrinsic factor.

Causes of vitamin B12 deficiency

• pernicious anaemia
• post gastrectomy
• poor diet
• disorders of terminal ileum (site of absorption): Crohn's, blind-loop etc

Features of vitamin B12 deficiency

• macrocytic anaemia
• sore tongue and mouth
• neurological symptoms: e.g. Ataxia
• neuropsychiatric symptoms: e.g. Mood disturbances
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Management
• if no neurological involvement 1 mg of IM hydroxocobalamin 3 times each week for 2 weeks, then once every 3
months
• if a patient is also deficient in folic acid then it is important to treat the B12 deficiency first to avoid precipitating
subacute combined degeneration of the cord
Vitamin Name DEFICIENCY EFFECTS

Beriberi.
Wernicke's encephalopathy
Korsakoff's syndrome,
B1 Thiamine
( irreversible psychosis
characterized by amnesia
n
confabulat

Cheilosis (cracks in the lips),

Hgh sensitivity to sunlight,
Agular cheilitis,
B2 Riboflavin
Gossitis (inflamnof tongue),
Sborrheic dermatitis
Paryngitis (sore throat),

B3 Niacin Pellagra.

B5 Pantothenic acid Acne & paresthesia,

B6 Pyridoxine Microcytic anemia ,

Multiple carboxylase deficiency,(Inorn

error of metabolism, can lead 2iotin
B7 Biotin
deficiency even when dietary intake
normal)

Macrocytic anemia,
Eevated levels of homocysteine.
B9 Folic acid
Deficiency in pregnant women can
lead to birth defects.

Pernicious anemia.
Macrocytic anemia,
B12 Cobalamin Eevated homocysteine,
Pripheral neuropathy, memory loss &
other cognitive deficits.
Malabsorption
Malabsorption is characterised by diarrhoea, steatorrhoea and weight loss. Causes may be broadly divided into
intestinal (e.g. villous atrophy), pancreatic (deficiency of pancreatic enzyme production or secretion) and biliary
(deficiency of bile-salts needed for emulsification of fats)

Intestinal causes of malabsorption

• coeliac disease
• Crohn's disease
• tropical sprue
• Whipple's disease

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 • Giardiasis
• brush border enzyme deficiencies (e.g. lactase insufficiency)

Pancreatic causes of malabsorption

• chronic pancreatitis
• cystic fibrosis
• pancreatic cancer

Biliary causes of malabsorption

• biliary obstruction
• primary biliary cirrhosis

Other causes
• bacterial overgrowth (e.g. systemic sclerosis, diverticulae, blind loop)
• short bowel syndrome
• lymphoma

Obesity: physiology

Leptin
Leptin is thought to play a key role in the regulation of body weight. It is produced by adipose tissue and acts on satiety
centres in the hypothalamus and decreases appetite. More adipose tissue (e.g. in obesity) results in high leptin levels.
Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH).
Low levels of leptin stimulates the release of neuropeptide Y (NPY)

Ghrelin
Where as leptin induces satiety, ghrelin stimulates hunger. It is produced mainly by the fundus of the stomach and the
pancreas. Ghrelin levels increase before meals and decrease after meals

● BARIATRIC SURGERY
- Wt. reducing surgery.
- body mass index(BMI) exceeding 40, or BMI > 35 with serious co-morbidities (eg sleep apnoea, type 2 DM).
- Post-operative mortality ranges from 0.1 – 2 %.
- Vomiting is a risk associated with bariatric surgery, as is dumping syndrome and nutritional deficiencies. There
is no evidence as yet, that bariatric surgery reduces cardiovascular mortality in patient.

NICE guidelines

Consider surgery for people with severe obesity if:

2 2
• BMI >/= 40 kg/m or between 35-40 kg/m and other significant disease (for example, type 2 diabetes,
hypertension) that could be improved with weight loss.
• All non-surgical measures have failed to achieve or maintain adequate clinically beneficial weight loss for at
least 6 months.
• Will receive intensive specialist management
• They are generally fit for anaesthesia and surgery
• They commit to the need for long-term follow-up

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 2
• First-line option for adults with a BMI > 50 kg/m in whom surgical intervention is considered appropriate;
consider orlistat if there is a long waiting list.

Notes
• After bariatric surgery patents are found to have partial or complete resolution of co morbidities associated with
obesity.
• Bariatric surgery is the only intervention to demonstrate long-term weight loss in randomised controlled trials.
Bariatric surgery

Obesity is a major health problem in the Western world. Surgical solutions to the problem have evolved dramatically over
the past few years. Randomised controlled trials have shown that dramatic weight loss can be achieved following
surgical interventions compared with standard medical therapy. The weight loss process is also more durable following
surgery than with non surgical interventions.

Case selection
2 2
BMI >/= 40 kg/m or between 35-40 kg/m and other significant disease (for example, type 2 diabetes, hypertension) that
could be improved with weight loss.

Pre-requisites to surgery (NICE UK Guidelines

• All non-surgical measures have failed to achieve or maintain adequate clinically beneficial weight loss for at
least 6 months.
• Will receive intensive specialist management
• They are generally fit for anaesthesia and surgery
• They commit to the need for long-term follow-up
• First-line option for adults with a BMI > 50 kg/m2 in whom surgical intervention is considered appropriate;
consider orlistat if there is a long waiting list.

Surgical options

Adjustable gastric • Laparoscopic placement of adjustable band around proximal stomach.

band • Contains an adjustable filling port
• Effective method for lifestyle control
• Reversible
• Takes longer to achieve target weight
• Complications such as band erosion (rare), slippage or loss of efficacy may require
re-intervention

Gastric bypass • Combines changes to reservoir size with malabsorptive procedure for more enduring
weight loss.
• Technically more challenging
• Risks related to anastomoses (2% leak rate)
• Irreversible
• Up to 50% may become B12 deficient

Sleeve gastrectomy • Resection of stomach using stapling devices

• Less popular now as initial promising results not sustained

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Intragastric balloon is really only suitable as a bridge to a more definitive surgical solution. Bariatric surgery: the main
operations
Gastric banding: band applied to upper stomach which can be inflated or deflated with normal saline. This affects
satiety. Over a 5 year period complications requiring further surgery occur in up to 15% cases.

Roux-en-Y gastric bypass: a gastric pouch is formed and connected to the jejunum. Patients achieve greater and more
longterm weight loss than gastric banding.

Sleeve gastrectomy: body and fundus resected to leave a small section of stomach

Biliopancreatic diversion +/- duodenal switch: bypass the small bowel. Greatest weight loss but a very complex
procedure associated with malnutrition and diarrhoea.
.
Vertical banded gastroplasty (stomach stapling): rarely performed due to longterm failure rate

Vomiting

Reflex oral expulsion of gastric (and sometimes intestinal) contents - reverse peristalsis and abdominal contraction
The vomiting centre is in part of the medulla oblongata and is triggered by receptors in several locations:
• Labyrinthine receptors of ear (motion sickness)
• Overdistention receptors of duodenum and stomach
• Trigger zone of CNS - many drugs (e.g., opiates) act here
• Touch receptors in throat
• Sensory innervation rich, both extrinsic and intrinsic

Water absorption

During a 24 hours period the average person will ingest up to 2000ml of liquid orally. In addition a further 8000ml of fluid
will enter the small bowel as gastrointestinal secretions. Intestinal water absorption is a passive process and is related to
solute load. In the jejunum the active absorption of glucose and amino acids will create a concentration gradient that
water will flow across. In the ileum most water is absorbed by a process of facilitated diffusion (with sodium).
Approximately 150ml of water enters the colon daily, most is absorbed, the colon can adapt to, and increase this amount
following resection.

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