Hiatus hernia

A hiatus hernia describes the herniation of part of the stomach above the diaphragm.

There are two types:

 sliding: accounts for 95% of hiatus hernias, the gastroesophageal junction
moves above the diaphragm
 rolling (paraoesophageal): the gastroesophageal junctions remains below the
diaphragm but a separate part of the stomach herniates through the
oesophageal hiatus

Bladder cancer
Bladder cancer is the second most common urological cancer.

It most commonly affects males aged between 50 and 80 years of age.

Those who are current, or previous (within 20 years), smokers have a 2-5 fold increased risk
of the disease.

Exposure to hydrocarbons such as 2-Naphthylamine increases the risk. Although rare in the
UK, chronic bladder inflammation arising from

Schistosomiasis infection remains a common cause of squamous cell carcinomas, in those

countries where the disease is endemic.

Benign tumours
Benign tumours of the bladder including inverted urothelial papilloma and nephrogenic
adenoma are uncommon.

Bladder malignancies

 Transitional cell carcinoma (>90% of cases)

 Squamous cell carcinoma ( 1-7% -except in regions affected by schistosomiasis)
 Adenocarcinoma (2%)

Transitional cell carcinomas may arise as solitary lesions, or may be multifocal, owing to the
effect of 'field change' within the urothelium.

Up to 70% of TCC's will have a papillary growth pattern.

These tumours are usually superficial in location and accordingly have a better prognosis.
The remaining tumours show either mixed papillary and solid growth or pure solid growths.
- These tumours are typically more prone to local invasion and may be of
higher grade, the prognosis is therefore worse.

Those with T3 disease or worse have a 30% (or higher) risk of regional or distant lymph
node metastasis.

TNM Staging

Stage Description
T0 No evidence of tumour
Ta Non invasive papillary carcinoma
T1 Tumour invades sub epithelial connective tissue
T2a Tumor invades superficial muscularis propria (inner half)
T2b Tumor invades deep muscularis propria (outer half)
T3 Tumour extends to perivesical fat
T4 Tumor invades any of the following: prostatic stroma, seminal vesicles, uterus, vagina
T4a Invasion of uterus, prostate or bowel
T4b Invasion of pelvic sidewall or abdominal wall
N0 No nodal disease
N1 Single regional lymph node metastasis in the true pelvis (hypogastric, obturator, external
iliac, or presacral lymph node)
N2 Multiple regional lymph node metastasis in the true pelvis (hypogastric, obturator, external
iliac, or presacral lymph node metastasis)
N3 Lymph node metastasis to the common iliac lymph nodes
M0 No distant metastasis
M1 Distant disease

Presentation

Most patients (85%) will present with painless, macroscopic haematuria.

In those patients with incidental microscopic haematuria, up to 10% of females aged over 50
will be found to have a malignancy (once infection excluded).

Staging

Most will undergo a cystoscopy and biopsies or TURBT, this provides histological diagnosis
and information relating to depth of invasion.

Locoregional spread is best determined using pelvic MRI and distant disease CT scanning.
Nodes of uncertain significance may be investigated using PET CT.

Treatment

Those with superficial lesions may be managed using TURBT in isolation.

Those with recurrences or higher grade/ risk on histology may be offered intravesical
chemotherapy.

Those with T2 disease are usually offered either surgery (radical cystectomy and ileal
conduit) or radical radiotherapy.

Prognosis

T1 90%
T2 60%
T3 35%
T4a 10-25%
Any T, N1-N2 30%
Next question

Acute urinary retention

Acute urinary retention is when a person suddenly (over a period of hours or less)
becomes unable to voluntarily pass urine.

It is the most common urological emergency and there are several potential causes
that must be investigated for.

Epidemiology

 Whilst acute urinary retention is common in men, it rarely occurs in women

(incidence ratio of 13:1). It occurs most frequently in men over 60 years of age
and incidence increases with age.
 It has been estimated that around a third of men in their 80s will develop
acute urinary retention over a five-year period.

Aetiology
 In men, acute urinary retention most commonly occurs secondary to benign
prostatic hyperplasia; a condition where the prostate becomes enlarged but
non-cancerous. The enlarged prostate presses on the urethra which can make
the bladder wall thicker and less able to empty.
 Other urethral obstructions; including urethral strictures, calculi, cystocele,
constipation or masses.
 Some medications can cause acute urinary retention by affecting nerve signals
to the bladder: these include
o Anticholinergics
o tricyclic antidepressants
 o antihistamines
o opioids
o benzodiazepines.
 Less commonly, there may be a neurological cause for the acute urinary
retention.
 In patients with predisposing causes, a simple urinary tract infection can be
enough to cause acute urinary retention
 Acute urinary retention often occurs postoperatively and in women
postpartum: usually secondary to a combination of the above risk factors.

Patients typically present with a subacute onset of:

 Inability to pass urine
 Lower abdominal discomfort
 Considerable pain or distress

This differs from chronic urinary retention which is typically painless. In a patient with
a background of chronic urinary retention, acute urinary retention may present
instead with overflow incontinence.

Signs:
 Palpable distended urinary bladder either on an abdominal or rectal exam
 Lower abdominal tenderness
 All men and women should have a rectal and neurological examination to
assess for the likely causes above.
 **Women should also have a pelvic examination.

Investigations:
 Patients should all be investigated with a urine sample which should be sent
for urinalysis and culture.
 This might only be possible after urinary catheterisation.
 Serum U&Es and creatinine should also be checked to assess for any kidney
injury.
 A FBC and CRP should also be performed to look for infection
 PSA is not appropriate in acute urinary retention as it is typically elevated

Management
 To confirm the diagnosis of acute urinary retention a bladder ultrasound
should be performed. A volume of >300 cc confirms the diagnosis, but if the
history and examination are consistent, with an inconsistent bladder scan,
there are causes of bladder scan inaccuracies and hence the patient can still
have acute urinary retention.
 Acute urinary retention is managed by decompressing the bladder via
catheterisation
  Urinary catheterisation can be performed in patients with suspected acute
urinary retention, and the volume of urine drained in 15 minutes measured.
A volume of <200 confirms that a patient does not have acute urinary
retention, and a volume over 400 cc means the catheter should be left in
place. In between these volumes, it depends on the case.
 Further investigation should be targeted by the likely cause. In reversible
causes such as UTI, resolution with treatment is sufficient and further
investigation is not necessary. Men not diagnosed by BPH should be further
evaluated by a urologist, Patients with neurological symptoms should be
evaluated by a neurologist and women with gynaecological symptoms by a
gynaecologist. Where no likely cause is identified, patients should be
evaluated by a urologist for anatomical and urodynamic causes.
Following relief of urinary retention patients undergo a physiological diuresis (that
which lasts up to 24hrs), with some patients going on to experience a pathological
diuresis (typically lasting longer than 48hrs). During this polyuric state large volumes
of salt and water are lost, with the risk of patients developing hypovolaemia,
dehydration, and electrolyte imbalances.

Consequently, daily monitoring of urea and electrolytes is required to monitor

patients, with this being the investigation of choice in this context given the patient's
history. This patient likely fell due to a syncopal episode secondary to hypovolaemia.

Post-void volumes of <50 ml are considered physiological in patients aged < 65

years old.

Post-void volumes of < 100ml are considered physiological in patients aged > 65
years old.

Chronic urinary retention is defined by the presence of >500ml within the bladder
after voiding.

Post-catheterisation urine volume of >800 ml suggests acute-on-chronic urinary

retention.

Renal tumours
Renal cell carcinoma
Renal cell carcinoma is an adenocarcinoma of the renal cortex and is believed to
arise from the proximal convoluted tubule.

They are usually solid lesions, up to:

 - 20% may be multifocal
- 20% may be calcified
- 20% may have either a cystic component or be wholly cystic.

They are often circumscribed by a pseudocapsule of compressed normal renal tissue.

Spread may occur either by direct extension into the adrenal gland, renal vein or
surrounding fascia.

More distant disease usually occurs via the haematogenous route to lung, bone or
brain.

Renal cell carcinoma comprise up to 85% of all renal malignancies.

Males are more commonly affected than females and sporadic tumours typically
affect patients in their sixth decade.

Patients may present with a variety of symptoms including; haematuria (50%), loin
pain (40%), mass (30%) and up to 25% may have symptoms of metastasis

Less than 10% have the classic triad of haematuria, pain and mass.

Investigation
Many cases will present as haematuria and be discovered during diagnostic work up.

Benign renal tumours are rare, so renal masses should be investigated with
multislice CT scanning. Some units will add and arterial and venous phase to the
scan to demonstrate vascularity and evidence of caval ingrowth.

CT scanning of the chest and abdomen to detect distant disease should also be
undertaken.

Routine bone scanning is not indicated in the absence of symptoms.

Biopsy should not be performed when a nephrectomy is planned but is

mandatory before any ablative therapies are undertaken.

Assessment of the functioning of the contra lateral kidney.

Management
T1 lesions may be managed by partial nephrectomy and this gives equivalent
oncological results to total radical nephrectomy.
 - Partial nephrectomy may also be performed when there is inadequate
reserve in the remaining kidney.

For T2 lesions and above a radical nephrectomy is standard practice and this may
be performed via a laparoscopic or open approach.

Preoperative embolisation is not indicated nor is resection of uninvolved adrenal

glands.

During surgery early venous control is mandatory to avoid shedding of tumour cells
into the circulation.

Patients with completely resected disease do not benefit from adjuvant

therapy with either chemotherapy or biological agents. These should not be
administered outside the setting of clinical trials.

Patients with transitional cell cancer will require a nephroureterectomy with

disconnection of the ureter at the bladder.

Renal cell cancer

Renal cell cancer is also known as hypernephroma and accounts for 85% of primary
renal neoplasms. It arises from proximal renal tubular epithelium. The most common
histological subtype is clear cell (75 to 85 percent of tumours).

Associations*

 more common in middle-aged men

 smoking
 von Hippel-Lindau syndrome
 tuberous sclerosis

Features

 classical triad: haematuria, loin pain, abdominal mass

 pyrexia of unknown origin
 left varicocele (due to occlusion of left testicular vein)
 endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid
hormone (hypercalcaemia), renin, ACTH
 25% have metastases at presentation
  paraneoplastic hepatic dysfunction syndrome. Also known as Stauffer
syndrome. Typically presents as cholestasis/hepatosplenomegaly. It is thought
to be secondary to increased levels of IL-6

Management

 for confined disease a partial or total nephrectomy depending on the tumour

size
 alpha-interferon and interleukin-2 have been used to reduce tumour size
and also treat patients with metatases
 receptor tyrosine kinase inhibitors (e.g. sorafenib, sunitinib) have been shown
to have superior efficacy compared to interferon-alpha

© Image used on license from Radiopaedia

Coronal CT scan of a middle-aged woman with renal cell cancer. Note the heterogeneously enhancing
mass at the upper pole of the right kidney

Image sourced from Wikipedia© Image used on license from PathoPic

Left: normal kidney. Right: 'clear-cell' pattern of renal cell carcinoma

 © Image used on license from PathoPic

'Clear-cell' pattern of renal cell carcinoma - clear cytoplasm, small nuclei

*incidence of renal cell cancer is only slightly increased in patients with autosomal
dominant polycystic kidney disease

Renal stones
Percentage
Type of stones Features of all calculi
Calcium oxalate Hypercalciuria is a major risk factor (various causes) 85%
Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms
complexes with calcium making it more soluble
Stones are radio-opaque (though less than calcium
phosphate stones)
Hyperuricosuria may cause uric acid stones to which
calcium oxalate binds
Cystine Inherited recessive disorder of transmembrane cystine 1%
transport leading to decreased absorption of cystine from
intestine and renal tubule
Multiple stones may form
Semi-opaque because they contain sulphur
 Percentage
Type of stones Features of all calculi
Uric acid Uric acid is a product of purine metabolism 5-10%
May precipitate when urinary pH low
May be caused by diseases with extensive tissue
breakdown e.g. malignancy
More common in children with inborn errors of
metabolism
Radiolucent
Calcium phosphate May occur in renal tubular acidosis, high urinary pH 10%
increases supersaturation of urine with calcium and
phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone
formation (types 2 and 4 do not)
Radio-opaque stones (composition similar to bone)
Struvite Stones formed from magnesium, ammonium and 2-20%
phosphate
Occur as a result of urease producing bacteria (and are
thus associated with chronic infections)
Under the alkaline conditions produced, the crystals can
precipitate
Slightly radio-opaque

Effect of urinary pH on stone formation

Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as
purine metabolism will produce uric acid. Then the urine becomes more alkaline
(alkaline tide). When the stone is not available for analysis the pH of urine may help
to determine which stone was present.

Stone type Urine acidity Mean urine pH

Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5

Renal stones: management

The British Association of Urological Surgeons (BAUS) published guidelines in 2018 on the
management of acute ureteric/renal colic.

Initial management of renal colic

Medication
 the BAUS recommend an NSAID as the analgesia of choice for renal colic
  whilst diclofenac has been traditionally used the increased risk of cardiovascular
events with certain NSAIDs (e.g. diclofenac, ibuprofen) should be considered when
prescribing
 the CKS guidelines suggest for patients who require admission: 'Administer a
parenteral analgesic (such as intramuscular diclofenac) for rapid relief of severe
pain'

Initial investigations
 urine dipstick and culture
 serum creatinine and electrolytes: check renal function
 FBC / CRP: look for associated infection
 calcium/urate: look for underlying causes
 also: clotting if percutaneous intervention planned and blood cultures if pyrexial or
other signs of sepsis

Imaging
 BAUS now recommend that non-contrast CT KUB should be performed on all
patients, within 14 hours of admission
 if a patient has a fever, a solitary kidney or when the diagnosis is uncertain an
immediate CT KUB should be performed. In the case of an uncertain diagnosis, this is
to exclude other diagnoses such as ruptured abdominal aortic aneurysm
 CT KUB has a sensitivity of 97% for ureteric stones and a specificity of 95%
 ultrasound still has a role but given the wider availability of CT now and greater
accurary it is no longer recommend first-line. The sensitivity of ultrasound for stones
is around 45% and specificity is around 90%

Management of renal stones

Stones < 5 mm will usually pass spontaneously.

 Periureteric fat stranding may indicate recent stone passage

Lithotripsy and nephrolithotomy may be for severe cases.

Most renal stones measuring less than 5mm in maximum diameter will typically pass within
4 weeks of symptom onset. More intensive and urgent treatment is indicated in the presence
of ureteric obstruction, renal developmental abnormality such as horseshoe kidney and
previous renal transplant.

Ureteric obstruction due to stones together with infection is a surgical emergency and the
system must be decompressed
- nephrostomy tube placement
- insertion of ureteric catheters and ureteric stent placement

In the non-emergency setting, the preferred options for treatment of stone disease include
extra corporeal shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, open
surgery remains an option for selected cases. However, minimally invasive options are the
most popular first-line treatment.
Shockwave lithotripsy
 A shock wave is generated external to the patient, internally cavitation bubbles and
mechanical stress lead to stone fragmentation. The passage of shock waves can result
in the development of solid organ injury. Fragmentation of larger stones may result in
the development of ureteric obstruction. The procedure is uncomfortable for patients
and analgesia is required during the procedure and afterwards.

Ureteroscopy
 A ureteroscope is passed retrograde through the ureter and into the renal pelvis. It is
indicated in individuals (e.g. pregnant females) where lithotripsy is contraindicated
and in complex stone disease. In most cases a stent is left in situ for 4 weeks after the
procedure.

Percutaneous nephrolithotomy
 In this procedure, access is gained to the renal collecting system. Once access is
achieved, intra corporeal lithotripsy or stone fragmentation is performed and stone
fragments removed.

Therapeutic selection

Disease Option
Stone burden of less than 2cm in aggregate Lithotripsy
Stone burden of less than 2cm in pregnant females Ureteroscopy
Complex renal calculi and staghorn calculi Percutaneous nephrolithotomy
Ureteric calculi less than 5mm Manage expectantly

Prevention of renal stones

Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general
population.
 high fluid intake
 low animal protein, low salt diet
 thiazides diuretics (increase distal tubular calcium resorption)

Oxalate stones
 cholestyramine reduces urinary oxalate secretion
 pyridoxine reduces urinary oxalate secretion

Uric acid stones

 allopurinol
 urinary alkalinization e.g. oral bicarbonate
Hydronephrosis
Causes of hydronephrosis include:

Unilateral: PACT Bilateral: SUPER

 Pelvic-ureteric obstruction (congenital or acquired)  Stenosis of the urethra
 Aberrant renal vessels  Urethral valve
 Calculi  Prostatic enlargement
 Tumours of renal pelvis  Extensive bladder tumour
 Retro-peritoneal fibrosis

Investigation

 ultrasound - first-line: identifies presence of hydronephrosis and can assess

the kidneys
 IVU- assess the position of the obstruction
 Antegrade or retrograde pyelography- allows treatment
 if suspect renal colic: CT scan (majority of stones are detected this way)

Management

 Remove the obstruction and drainage of urine

 Acute upper urinary tract obstruction: nephrostomy tube
 Chronic upper urinary tract obstruction: ureteric stent or a pyeloplasty
 © Image used on license from Radiopaedia

The CT shows massive hydronephrosis and a small calculus in the left kidney. A single large calculus is
present distally in the left ureter with accompanying hydroureter.

Lower urinary tract symptoms in men

Lower urinary tract symptoms (LUTS) in men are very common and are present in the
majority of men aged > 50 years. They are most commonly secondary to benign
prostatic hyperplasia but other causes should be considered including prostate
cancer.

It is useful to classify the symptoms into 3 broad groups.

Voiding Storage Post-micturition

Hesitancy Urgency Post-micturition dribbling
Poor or intermittent stream Frequency Sensation of incomplete emptying
Straining
 Voiding Storage Post-micturition
Incomplete emptying Nocturia
Terminal dribbling Urinary incontinence

Examination

 urinalysis: exclude infection, check for haematuria

 digital rectal examination: size and consistency of prostate
 a PSA test may be indicated, but the patient should be properly counselled
first

It is useful to get the patient to complete the following to guide management:

 urinary frequency-volume chart: distinguish between urinary frequency,

polyuria, nocturia, and nocturnal polyuria.
 International Prostate Symptom Score (IPSS): assess the impact on the
patient's life. This classifies the symptoms as mild, moderate or severe

Management

Predominately voiding symptoms

 conservative measures include: pelvic floor muscle training, bladder training,

prudent fluid intake and containment products
 if 'moderate' or 'severe' symptoms offer an alpha-blocker
 if the prostate is enlarged and the patient is 'considered at high risk of
progression' then a 5-alpha reductase inhibitor should be offered
 if the patient has an enlarged prostate and 'moderate' or 'severe' symptoms
offer both an alpha-blocker and 5-alpha reductase inhibitor
 if there are mixed symptoms of voiding and storage not responding to an
alpha blocker then a antimuscarinic (anticholinergic) drug may be added

Predominately overactive bladder

 conservative measures include moderating fluid intake

 bladder retraining should be offered
  antimuscarinic drugs should be offered if symptoms persist. NICE recommend
oxybutynin (immediate release), tolterodine (immediate release), or
darifenacin (once daily preparation)
 mirabegron may be considered if first-line drugs fail

Nocturia

 advise about moderating fluid intake at night

 furosemide 40mg in late afternoon may be considered
 desmopressin may also be helpful

Lower genitourinary tract trauma

Basics

 Most bladder injuries occur due to blunt trauma

 85% associated with pelvic fractures
 Easily overlooked during assessment in trauma
 Up to 10% of male pelvic fractures are associated with urethral or bladder
injuries

Types of injury

Urethral injury Basics

 Mainly in males
 Blood at the meatus (50% cases)
 There are 2 types:

Bulbar rupture

 most common
 straddle type injury e.g. bicycles
 triad signs: urinary retention, perineal haematoma, blood at the meatus

Membranous rupture

 can be extra or intraperitoneal

 commonly due to pelvic fracture
 Penile or perineal oedema/ hematoma
  PR: prostate displaced upwards (beware co-existing retroperitoneal
haematomas as they may make examination difficult)

Investigation

 ascending urethrogram

Management

 suprapubic catheter (surgical placement, not percutaneously)

External Secondary to injuries caused by penetration, blunt trauma, continence- or sexual
genitalia injuries pleasure-enhancing devices, and mutilation
(i.e., the penis
and the scrotum)
Bladder injury Basics

 rupture is intra or extraperitoneal

 presents with haematuria or suprapubic pain
 history of pelvic fracture and inability to void: always suspect bladder or
urethral injury
 inability to retrieve all fluid used to irrigate the bladder through a Foley
catheter indicates bladder injury
Investigation

 IVU or cystogram

Management

 laparotomy if intraperitoneal, conservative if extraperitoneal

Nephroblastoma
Nephroblastoma (Wilm's tumours)

 Usually present in first 4 years of life

 May often present as a mass associated with haematuria (pyrexia may occur in
50%)
 Often metastasise early (usually to lung)
 Treated by nephrectomy
 Younger children have better prognosis (<1 year of age =80% overall 5 year
survival)

Lower urinary tract symptoms in men

Lower urinary tract symptoms (LUTS) in men are very common and are present in the
majority of men aged > 50 years. They are most commonly secondary to benign
prostatic hyperplasia but other causes should be considered including prostate
cancer.

It is useful to classify the symptoms into 3 broad groups.

Voiding Storage Post-micturition

Hesitancy Urgency Post-micturition
Poor or intermittent Frequency dribbling
stream Nocturia Sensation of
Straining Urinary incomplete emptying
Incomplete emptying incontinence
Terminal dribbling

Examination

 urinalysis: exclude infection, check for haematuria

 digital rectal examination: size and consistency of prostate
 a PSA test may be indicated, but the patient should be properly counselled
first

It is useful to get the patient to complete the following to guide management:

 urinary frequency-volume chart: distinguish between urinary frequency,

polyuria, nocturia, and nocturnal polyuria.
 International Prostate Symptom Score (IPSS): assess the impact on the
patient's life. This classifies the symptoms as mild, moderate or severe

Management

Predominately voiding symptoms

 conservative measures include: pelvic floor muscle training, bladder training,

prudent fluid intake and containment products
 if 'moderate' or 'severe' symptoms offer an alpha-blocker
 if the prostate is enlarged and the patient is 'considered at high risk of
progression' then a 5-alpha reductase inhibitor should be offered
 if the patient has an enlarged prostate and 'moderate' or 'severe' symptoms
offer both an alpha-blocker and 5-alpha reductase inhibitor
 if there are mixed symptoms of voiding and storage not responding to an
alpha blocker then a antimuscarinic (anticholinergic) drug may be added

Predominately overactive bladder

 conservative measures include moderating fluid intake

  bladder retraining should be offered
 antimuscarinic drugs should be offered if symptoms persist. NICE recommend
oxybutynin (immediate release), tolterodine (immediate release), or
darifenacin (once daily preparation)
 mirabegron may be considered if first-line drugs fail

Nocturia

 advise about moderating fluid intake at night

 furosemide 40mg in late afternoon may be considered
 desmopressin may also be helpful

Urethral stricture
Causes

 iatrogenic e.g. traumatic placement of indwelling urinary catheters

 sexually transmitted infections
 hypospadias
 lichen sclerosus

Stoma
A stoma is a surgically created opening in the body between

- the skin
- hollow viscus

Abdominal stomas are mainly used to divert faeces or urine outside the body where it can
be collected in a bag at the skin.

Stomas fall into 3 types:

 Colostomy
 Ileostomy
 Urostomy

Each stoma can also be either permanent or temporary.

A stoma’s position, appearance and contents can point to which type of stoma it is and
provide clues as to the patient’s previous surgical history.

Colostomy
As the name suggests these stomas involve the large bowel (or colon).
One of the hallmarks of colostomies is that they are found in the LIF.
The content of a colostomy bag should be solid as the faeces have had time to travel through the
colon undergoing water absorption.
 Colostomies can also be identified because they will be flush to the skin, not sticking out like
ileostomies. This is because the enzymes are less alkali so should not damage the skin.

Permanent end colostomy vs temporary end colostomy

You cannot differentiate between permanent end colostomies and temporary end
colostomies clinically, so in this case you’d have to ask the patient or check the notes.
 Permanent end colostomies are often done in cases of abdominoperineal resection of large
rectal cancers leading to the removal of the entire rectum.

 Temporary end colostomies are done to such as in

 diverticulitis
 obstruction by a tumour
As part of a two stage Hartmann’s procedure the rectum and bowel will be re-anastomosed at a
later date.

Loop colostomy
Loop colostomies are done to protect distal anastomoses after recent surgery.

A loop of bowel will be brought to the surface and half opened, this allows the faecal matter to
drain into the stoma bag without reaching the distal anastomoses, a supporting rod is used to
secure the two parts to the skin.
The two parts are still attached as this is a temporary procedure which will be reversed.

Ileostomy
Formed of small bowel.
Usually located in the right iliac fossa (RIF).

Not as much water absorbed in the small bowel so the contents of the stoma bag are liquid
and lighter.

Because the enzymes in the faeces are toxic to the skin, the bowel is not secured flush to the skin
but has a spout sticking out from the abdominal wall.

This allows faeces to drain without touching the skin.

 Temporary vs
permanent end
ileostomy
Permanent ileostomies are done after a panproctocolectomy for ulcerative colitis or FAP

Once again a temporary end ileostomy cannot be distinguished from a permanent end
ileostomy but is used instead in emergency bowel resection where it is considered unsafe to form
an anastomosis with the remaining bowel at that time (e.g. intra-abdominal sepsis or bleeding).

Loop ileostomy
Temporary loop ileostomies are done in the same way as in temporary loop colostomies, so you
will see two openings instead of one but they will be connected and are used to protect distal
anastomoses.

Urostomies
Used after a cystectomy (bladder removal).

Located in right iliac fossa (RIF).

Bag contains urine not faces, this is the only way to differentiate from ileostomy.

An ileal conduit is used to route the urine out of the abdomen into the bag.

This involves a piece of ileum being resected then attached to the skin with a spout protruding.

The ureters are then attached to the other end of the tube of bowel.
The urine then drains via the piece of bowel into the stoma bag.

Stoma following surgery

- low rectal cancer involves anus therefore need to remove anus; this means nothing
left to anastamose and thus the patient is left with an end colostomy
- upper rectal cancer spares the anus and thus you can remove the affected bowel and
be left with a colo-rectal anastamosis BUT this needs time to heal so create a de-
functioning loop ileostomy
- hartmans is an emergency procedure (often perforated diverticulitis) and thus they
have an end colostomy but the rectal stump is left inside with a view to creating an
anastamosis later

Surgical jaundice
Liver function tests (for
classification)
- pre hepatic
- hepatic
- post hepatic

Location Bilirubin ALT/ AST Alkaline phosphatase

Pre hepatic Normal or Normal Normal
high
Hepatic High Elevated (often very Elevated but seldom to very high
high) levels
Post High-very Moderate elevation High- very high
hepatic high

In post hepatic jaundice the stools are often of pale colour and this feature should be
specifically addressed in the history.

Modes of presentation
 These are addressed in the table below:
Diagnosis Typical features
Gallstones Typically history of biliary colic or Usually small calibre gallstones which can pass
episodes of chlolecystitis.
Obstructive type history and test
results.
Cholangitis Usually obstructive
Charcots triad
Pancreatic cancer Typically painless jaundice with
palpable gallbladder
(Courvoisier's Law)
TPN associated Usually follows long term use and
jaundice is usually painless with non
obstructive features
Bile duct injury Depending upon the type of injury
may be of sudden or gradual onset
and is usually of obstructive type
Cholangiocarcinoma Gradual onset obstructive pattern
Septic surgical patient Usually hepatic features
Metastatic disease Mixed hepatic and post hepatic
Diagnosis
An ultrasound of the liver and biliary tree is the most commonly used first
line test.
Pancreatic neoplasia => CT scan
Liver tumours and cholangiocarcinoma => MRI/ MRCP
Pathogenesis
through the cystic duct.
In Mirizzi syndrome the stone in cystic duct
compress the common hepatic duct duct directly
E. coli
A pool of stagnant bile
Direct occlusion of distal bile duct or pancreatic
duct by tumour.
Often due to hepatic dysfunction and fatty liver
which may occur with long term TPN usage.
Often due to a difficult cholecystectomy when
anatomy in Calots triangle is not appreciated.
In the worst scenario the bile duct is excised and
jaundice offers rapidly post operatively.
More insidious is that of bile duct stenosis which
may be caused by clips or diathermy injury.
Direct occlusion by disease and also extrinsic
compression by nodal disease at the porta hepatis.
Combination of impaired biliary excretion and
drugs such as ciprofloxacin which may cause
cholestasis.
Combination of liver synthetic failure (late) and
extrinsic compression by nodal disease and
anatomical compression of intra hepatic structures
(earlier)
PET scans may be used to stage a number of malignancies but do not routinely form part of
first line testing.

Where MRCP fails => ERCP

- In many cases this may form part of patient management.
- It is however, invasive and certainly not without risk and highly operator dependent.

Management

1. Screen for and address any clotting irregularities

2. With malignancy -> stent

These come in two main types;

- metal
o Expensive
o Compromise surgical resection
o Less prone to displacement + blockage
- plastic.
o Cheap
o Easy to replace
o Prone to displacement + blockage

Failed stenting (in cholangiocarcinoma/pancreatic Ca) => percutaneous drainage via

trranshepatic route

With bile duct injury surgery => repair the defect

- If the bile duct has been inadvertently excised => hepatico-jejunostomy needed

If gallstones are the culprit => ERCP and a cholecystectomy performed.

- When the bile duct has been formally opened the options are between
- closure over a T tube,
- a choledochoduodenostomy
- choledochojejunostomy.

Patients with cholangitis should receive IV high dose broad spectrum antibiotics via

Biliary decompression should follow soon afterwards, instrumenting the bile duct of these
patients will often provoke a septic episode (but should be done anyway).

Laparoscopy: complications

Complications of laparoscopy include:

 general risks of anaesthetic

 vasovagal reaction (e.g. bradycardia) in response to abdominal distension
 extra-peritoneal gas insufflation: surgical emphysema
 injury to gastro-intestinal tract
  injury to blood vessels e.g. common iliacs, deep inferior epigastric artery
 You can see the striations of pec major lateral to the right lung field. Pec major is only
visible if there is subcut emphysema.

Gastrectomy: complications
Dumping syndrome

 early: food of high osmotic potential moves into small intestine causing fluid
shift
 late (rebound hypoglycaemia): surge of insulin following food of high glucose
value in small intestine - 2-3 hours later the insulin 'overshoots' causing
hypoglycaemia

Weight loss, early satiety

Iron-deficiency anaemia

Osteoporosis/osteomalacia

Vitamin B12 deficiency

Other complications

 increased risk of gallstones

 increased risk of gastric cancer

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 (>500ml) or low output
(<250ml) 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 inflammatory bowel disease.
 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.
 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.

Ano rectal disease

Condition Notes
Haemorrhoids Location: 3, 7, 11 o'clock position
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:
 Condition Notes
- 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
Pruritus ani Systemic and local causes
Anal neoplasm Squamous cell carcinoma commonest unlike adenocarcinoma in rectum
Solitary rectal Associated with chronic straining and constipation.
ulcer
Histology shows mucosal thickening, lamina propria replaced with collagen and
smooth muscle (fibromuscular obliteration)

Rectal prolapse
 Common especially in multiparous women.
 May be internal or external.
 Internal rectal prolapse can present insidiously.
 External prolapse can ulcerate and in long term impair continence.
 Diagnostic work up includes colonoscopy, defecating proctogram, ano rectal
manometry studies and if doubt exists and examination under anaesthesia.

Treatments for prolapse

 In the acute setting reduce it (covering it with sugar may reduce swelling.
 Delormes procedure which excises mucosa and plicates the rectum (high recurrence
rates) may be used for external prolapse.
 Altmeirs procedure which resects the colon via the perineal route has lower
recurrence rates but carries the risk of anastamotic leak.
 Rectopexy is an abdominal procedure in which the rectum is elevated and usually
supported at the level of the sacral promontory. Post operative constipation may be
reduced by limiting the dissection to the anterior plane (laparoscopic ventral mesh
rectopexy).
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.

Fissure in ano

 Typically painful PR bleeding (bright red).

 Nearly always in the posterior midline.
 Usually solitary.

Treatment
 Stool softeners (i.e. bulking – ispaghula husk)
 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.

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 where vessels pierce the muscle to supply the mucosa. For this reason, the
rectum, which lacks taenia, is often spared.

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, CT cologram
or barium enema as part of their diagnostic work up. All tests can identify diverticular
disease. It can be far more difficult to confidently exclude cancer, particularly in
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 (not a CT cologram) 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.

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.

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.
 Type of
Cause bleeding Features in history Examination findings
Fissure in Bright red Painful bleeding that occurs post Muco-epithelial defect usually in the
ano rectal defecation in small volumes. midline posteriorly
bleeding (anterior fissures more likely to be
Usually antecedent features of due to underlying disease)
constipation
Haemorroids Bright red Post defecation bleeding noted Normal colon and rectum.
rectal both on toilet paper and drips
bleeding into pan. Proctoscopy may show internal
haemorrhoids.
May be alteration of bowel habit
and history of straining. Internal haemorrhoids are usually
impalpable.
No blood mixed with stool.

No local pain.
Crohns Bright red or Bleeding that is accompanied by Perineal inspection may show
disease mixed blood other symptoms such as altered fissures or fistulae. Proctoscopy may
bowel habit, malaise, history of demonstrate indurated mucosa and
fissures (especially anterior) and possibly strictures. Skip lesions may
abscesses. be noted at colonoscopy.
Ulcerative Bright red Diarrhoea, weight loss, Proctitis is the most marked finding.
colitis bleeding nocturnal incontinence, passage Peri anal disease is usually absent.
often mixed of mucous PR. Colonoscopy will show continuous
with stool mucosal lesion.
Rectal cancer Bright red Alteration of bowel habit. Usually obvious mucosal
blood mixed abnormality.
volumes Tenesmus may be present.
Lesion may be fixed or mobile
Symptoms of metastatic disease. depending upon disease extent.

Surrounding mucosa often normal,

although polyps may be present.

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 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
bowel disease (setons).
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.

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 where vessels pierce the muscle to supply the mucosa. For this reason, the
rectum, which lacks taenia, is often spared.
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, CT cologram
or barium enema as part of their diagnostic work up. All tests can identify diverticular
disease. It can be far more difficult to confidently exclude cancer, particularly in
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 (not a CT cologram) 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.

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.

Diverticulitis
Diverticulitis is the infection of a diverticulum, an out-pouching of the intestinal
mucosa. The presence of diverticula is called diverticulosis and if these cause
symptoms then it is referred to as diverticular disease. Diverticula are thought to be
due to increased intra-colonic pressure and usually occur along the weaker areas of
the wall such as where the penetrating arteries enter the colonic wall; almost all
diverticula are found in the sigmoid colon, although they may be found in the right
colon in Asian patients. Diverticula are incredibly common and it is thought that 30%
of Westerners will have diverticula by the age of 60. Only about 25% of people with
diverticulosis will experience symptoms but 75% of these will experience an episode
of diverticulitis.

Epidemiology

 Average age of presentation is 50-70 and 80% of those who present are over
50y.

Risk factors

 Age
 Lack of dietary fibre
 Obesity: especially in younger patients
 Sedentary lifestyle
 Smoking
 NSAID use

Patients with diverticular disease typically present with a chronic history of:

 Intermittent abdominal pain: particularly in the left lower quadrant

 Bloating
 Change in bowel habit: constipation or diarrhoea

Patients with acute diverticulitis typically present with an acute onset of:

 Severe abdominal pain in the left lower quadrant: this may be in the right
lower quadrant in some Asian patients
 Nausea and vomiting (20-60%): this may be due to ileus or complicated
diverticulitis with colonic obstruction
  Change in bowel habit: constipation is more common (seen in 50%) but
diarrhoea is also reported (25%)
 Urinary frequency, urgency or dysuria (10-15%): this is due to irritation of the
bladder by the inflamed bowel.
 PR bleeding (in some cases).
 Symptoms such as pneumaturia or faecaluria may suggest colovesical fistula
while vaginal passage of faeces or flatus may suggest a colovaginal fistula.

Signs:

 Low grade pyrexia

 Tachycardia
 Tender LIF: in 20% there will be a tender palpable mass due to inflammation
or an abscess
 Possibly reduced bowel sounds
 Guarding, rigidity and rebound tenderness may suggest complicated
diverticulitis with perforation
 Lack of improvement with treatment in seemingly uncomplicated diverticulitis
may suggest the presence of an abscess.

Investigations:

 FBC: raised WCC

 CRP: raised
 Erect CXR: may show pneumoperitoneum in cases of perforation
 AXR: may show dilated bowel loops, obstruction or abscesses
 CT: this is the best modality in suspected abscesses
 Colonoscopy: should be avoided initially due to increased risk of perforation
in diverticulitis

Management

 mild cases of acute diverticulitis may be managed with oral antibiotics, liquid
diet and analgesia
 if the symptoms don't settle within 72 hours, or the patient intiially presents
with more severe symptoms, the patient should be admitted to hospital for IV
antibiotics

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
disease diverticular bleeds often occur 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
bleeding patients may give graphic 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.
  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 the source of colonic bleeding is 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

Laparoscopy: complications
Complications of laparoscopy include:

 general risks of anaesthetic

 vasovagal reaction (e.g. bradycardia) in response to abdominal distension
 extra-peritoneal gas insufflation: surgical emphysema
 injury to gastro-intestinal tract
  injury to blood vessels e.g. common iliacs, deep inferior epigastric artery

Genetics of colorectal cancer

The lifetime risk of colorectal cancer in the UK population is 5%. Up to 5% of newly
diagnosed bowel cancers will be in those individuals who have a high genetically
acquired risk of bowel cancer. Cancers arising in the low-moderate genetic risk group
comprise approximately 30% of newly diagnosed bowel cancer.

Genetics of inherited colorectal cancer syndromes

Genes
Syndrome Features implicated
FAP More than 100 adenomatous APC (over
polyps affecting the colon and 90%)
rectum. Duodenal and fundic
glandular polyps
Gardner As FAP but with desmoid APC
syndrome tumours and mandibular
osteomas
Turcots Polyposis and colonic tumours APC +MLH1
syndrome and CNS tumours and PMS2
HNPCC Colorectal cancer without MSH2,
extensive polyposis. MLH1, PMS2
Endometrial cancer, renal and and GTBP
CNS
Peutz- Hamartomatous polyps in GI LKB1
Jeghers tract and increased risk of GI andSTK11 (in
syndrome malignancy up to 70%)
Cowden Multiple hamartomas (see PTEN (85%)
disease below)
MYH Autosomal recessive, multiple MYH
associated adenomatous polyps in GI
polyposis tract, those in colon having
somatic KRAS mutations

FAP
Autosomal dominant condition, affects 1 in 12,000. Accounts for 0.5% of all CRCs.
Lifetime incidence of colorectal cancer in untreated FAP =100%. Up to 25% cases are
caused by de-novo germ line mutations and show no prior family history. The APC
tumour suppressor gene is affected in most cases.

APC in non inherited colorectal cancer

Up to 80% of sporadic colorectal cancers will have somatic mutations that inactivate
APC[1]. Both alleles are usually affected. Although the APC protein more than likely
has multiple critical cellular functions, the best-established role for APC in the cancer
process is as a major binding partner and regulator of the β- catenin protein in the
so-called canonical or β- catenin dependent Wnt signaling pathway.

HNPCC (Lynch syndrome)

HNPCC cancers differ from conventional tumours in a number of respects. In the
colon the tumours are more likely to be right sided, histologically they are more
likely to be mucinous and have dense lymphocytic infiltrates. To be diagnosed as
having HNPCC individuals must show typically HNPCC tumours in at least three
individuals, (one of whom must be a first degree relative to the other two). In at least
two successive generations. At least one cancer must be diagnosed under the age of
50. FAP must be excluded and tumours should be verified by pathological
identification (Amsterdam criteria). The genetic changes in HNPCC stem primarily
from microsatellite instability affecting DNA mismatch repair genes. In HNPCC the
mismatch repair genes most commonly implicated include; MSH2 and MLH1 and
these occur in up to 70% of people with HNPCC. The finding of microsatellite
instability is unusual in sporadic colorectal cancers. Approximately 60% of individuals
who fulfill the Amsterdam criteria will not be found to have evidence of mismatch
repair gene defects on genetic testing. The risk of developing colorectal cancer in
those who have not demonstrated mutation of the mis match repair genes is
increased if they fulfill the Amsterdam criteria, but not
the extent that it is increased in those who fulfill the criteria AND have evidence of
mis match repair gene defects.

KRAS Mutations
The RAS family of small G proteins act as molecular switches downstream of growth
factor receptors. KRAS and the other two members of the family; HRAS and NRAS,
are the site of mutation in approximately 40% of colorectal cancers. When adenomas
are examined the proportion of adenomas less than 1cm showing KRAS mutations
was only 10% which contrasts with 50% in those lesions greater than 1cm.

p53 mutations
The p53 protein functions as a key transcriptional regulator of genes that encode
proteins with functions in cell-cycle checkpoints at the G1/S and G2/M boundaries, in
promoting apoptosis, and in restricting angiogenesis . As such, selection for p53
defects at the adenoma-carcinoma transition may reflect the fact that stresses on
tumor cells activate cell-cycle arrest, apoptotic, and antiangiogenic pathways in cells
with wild-type p53 function. Many colonic tumours will demonstrate changes in the
p53 gene that may facilitate tumour progression through from adenoma to
carcinoma.

Cowden syndrome
Also known as multiple hamartoma syndrome. Rare autosomal dominant condition
with incidence of 1 in 200,000.. It is characterised by multiple mucocutaneous lesions,
trichilemmomas, oral papillomas and acral keratosis. Most often diagnosed in third
decade of life. Breast carcinoma may occur in up to 50% of patients and conditions
such as fibrocystic disease of the breast may occur in 75% of women. Thyroid disease
occurs in 75% and may include malignancy. Endoscopic screening will identify
disease in up to 85% although the small bowel is rarely involved. There is a 15-20%
risk of developing colorectal cancer and regular colonoscopic screening from age 45
is recommended.

Terminology
Oncogene Oncogenes are genes which have the
potential to induce cellular proliferation and
avoid apoptosis. Oncogene mutations are
general gain of function and are therefore
dominant. Increased expression of oncogenes
are found in most tumours
Tumour These genes generally inhibit cellular
suppressor proliferation or induce apoptosis. Mutations
gene in tumour suppressor genes are generally loss
of function mutations, and are therefore
recessive. Mutations in both tumour
suppressor gene alleles allow cells to
proliferate without restraint

References
1. Fearon, E.R. and B. Vogelstein, A genetic model for colorectal tumorigenesis. Cell,
1990. 61(5): p. 759-67.

Polyposis syndromes

Screening and Associated

Syndrome Genetic defect Features management disorders
Familial Mutation of APC Typically over 100 If known to be at risk Gastric fundal
adenomatous gene (80%) cases, colonic adenomas then predictive polyps (50%).
polyposis dominant Cancer risk of 100% genetic testing as Duodenal polyps
20% are new teenager 90%.
mutations Annual flexible If severe duodenal
sigmoidoscopy from polyposis cancer
15 years risk of 30% at 10
If no polyps found years.
then 5 yearly Abdominal
colonoscopy started at desmoid tumours.
age 20
Polyps found =
resectional surgery
(resection and pouch
 Screening and Associated
Syndrome Genetic defect Features management disorders
Vs sub total
colectomy and IRA)
MYH Biallelic mutation Multiple colonic Once identified Duodenal
associated of mut Y human polyps resection and ileoanal polyposis in 30%
polyposis homologue (MYH) Later onset right pouch reconstruction Associated with
on chromosome 1p, sided cancers more is recommended increased risk of
recessive common than in FAP Attenuated phenotype breast cancer (self
100% cancer risk by - regular colonoscopy examination)
age 60
Peutz -Jeghers STK11 (LKB1) Multiple benign Annual examination Malignancies at
syndrome mutation on intestinal hamartomas Pan intestinal other sites
chromosome 19 in Episodic obstruction endoscopy every 2-3 Classical
some (but not all) and intussusception years pigmentation
cases, dominant Increased risk of GI pattern
cancers (colorectal
cancer 20%, gastric
5%)
Increased risk of
breast, ovarian,
cervical pancreatic
and testicular cancers
Cowden Mutation of PTEN Macrocephaly Targeted Breast cancer
disease gene on Multiple intestinal individualised (81% risk)
chromosome hamartomas screening Thyroid cancer
10q22, dominant Multiple and non toxic
trichilemmomas goitre
89% risk of cancer at Uterine cancer
any site
16% risk of
colorectal cancer
HNPCC Germline mutations Colo rectal cancer Colonoscopy every 1- Extra colonic
(Lynch of DNA mismatch 30-70% 2 years from age 25 cancers
syndrome) repair genes Endometrial cancer Consideration of
30-70% prophylactic surgery
Gastric cancer 5-10% Extra colonic
Scanty colonic surveillance
polyps may be recommended
present
Colonic tumours
likely to be right
sided and mucinous

Save my notes
Colorectal Polyps
Osmosis - YouTube 25

Colorectal cancer: screening

Overview

 most cancers develop from adenomatous polyps. Screening for colorectal

cancer has been shown to reduce mortality by 16%
 the NHS offers home-based, Faecal Immunochemical Test (FIT) screening to
older adults
 another type of screening is also being rolled out - a one-off flexible
sigmoidoscopy

Faecal Immunochemical Test (FIT) screening

Key points

 the NHS now has a national screening programme offering screening every 2
years to all men and women aged 60 to 74 years in England, 50 to 74 years in
Scotland. Patients aged over 74 years may request screening
 eligible patients are sent Faecal Immunochemical Test (FIT) tests through the
post
 a type of faecal occult blood (FOB) test which uses antibodies that specifically
recognise human haemoglobin (Hb)
 used to detect, and can quantify, the amount of human blood in a single stool
sample
  advantages over conventional FOB tests is that it only detects human
haemoglobin, as opposed to animal haemoglobin ingested through diet
 only one faecal sample is needed compared to the 2-3 for conventional FOB
tests
 whilst a numerical value is generated, this is not reported to the patient or GP,
who will instead be informed if the test is normal or abnormal
 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

Flexible sigmoidoscopy screening

Key points

 screening for bowel cancer using sigmoidoscopy is being rolled out as part of
the NHS screening program
 the aim (other than to detect asymptomatic cancers) is to allow the detection
and treatment of polyps, reducing the future risk of colorectal cancer
 this is being offered to people who are 55-years-old
 NHS patient information leaflets refer to this as 'bowel scope screening'
 patients can self-refer for bowel screening with sigmoidoscopy up to the age
of 60, if the offer of routine one-off screening at age 55 had not been taken
up

Dukes' classification
Dukes' classification describes the extent of spread of colorectal cancer.

Stage Description 5-year survival

Dukes' Tumour confined to the 95%
A mucosa
Dukes' B Tumour invading bowel wall 80%
Dukes' Lymph node metastases 65%
C
Dukes' Distant metastases 5%
D (20% if
resectable)
Colorectal cancer: referral guidelines
NICE updated their referral guidelines in 2015. The following patients should be
referred urgently (i.e. within 2 weeks) to colorectal services for investigation:

 patients >= 40 years with unexplained weight loss AND abdominal pain
 patients >= 50 years with unexplained rectal bleeding
 patients >= 60 years with iron deficiency anaemia OR change in bowel habit
 tests show occult blood in their faeces (see below)

An urgent referral (within 2 weeks) should be 'considered' if:

 there is a rectal or abdominal mass

 there is an unexplained anal mass or anal ulceration
 patients < 50 years with rectal bleeding AND any of the following
unexplained symptoms/findings:
 -→ abdominal pain
 -→ change in bowel habit
 -→ weight loss
 -→ iron deficiency anaemia

Faecal Occult Blood Testing (FOBT)

This was one of the main changes in 2015. Remember that the NHS now has a
national screening programme offering screening every 2 years to all men and
women aged 60 to 74 years. Patients aged over 74 years may request screening.

In addition FOBT should be offered to:

 patients >= 50 years with unexplained abdominal pain OR weight loss

 patients < 60 years with changes in their bowel habit OR iron deficiency
anaemia
 patients >= 60 years who have anaemia even in the absence of iron deficiency

Colorectal cancer treatment

Patients diagnosed as having colorectal cancer should be completely staged using CT of the
chest/ abdomen and pelvis. Their entire colon should have been evaluated with colonoscopy
or CT colonography. Patients whose tumours lie below the peritoneal reflection should have
their mesorectum evaluated with MRI.

Once their staging is complete patients should be discussed within a dedicated colorectal
MDT meeting and a treatment plan formulated.
Treatment of colonic cancer
* Stents, surgical bypass and diversion stomas may all be used as palliative adjuncts.

The lymphatic drainage of the colon follows the arterial supply

- most resections tailored around the resection of particular lymphatic chains (e.g.
ileo-colic pedicle for right sided tumours).

Some with confounding factors

- HNPCC family may be better served with a panproctocolectomy > segmental
resection.

Following resection the decision has to be made regarding restoration of continuity.

For an anastomosis to heal the key technical factors include
- adequate blood supply
- mucosal apposition
- no tissue tension

Surrounding sepsis, unstable patients and inexperienced surgeons may compromise these key
principles => end stoma rather than attempting an anastomosis.

When a colonic cancer presents with an obstructing lesion; the options are to either stent it or
resect

Following resection patients with risk factors for disease recurrence are usually offered
chemotherapy, a combination of 5FU and oxaliplatin is common.

Treatment of rectal cancer

The management of rectal cancer is slightly different to that of colonic cancer. \

Anterior resection
Abdomino-perineal excision of rectum (APER)
- involvement of the sphincter complex
- very low tumours require

In the rectum a 2cm distal clearance margin is required and this may also impact on the
procedure chosen.

In addition to excision of the rectal tube an integral part of the procedure is a meticulous
dissection of the mesorectal fat and lymph nodes (total mesorectal excision/ TME).

Rectum is an extraperitoneal =>possible to irradiate hence neoadjuvent radiotherapy (both

long and short course) prior to resectional surgery.

T1 and 2 /N0 disease on imaging do not require irradiation => should proceed straight to
surgery.

T4 disease => long course chemo radiotherapy

Those with T3 , N0 tumours => short course radiotherapy prior to surgery.

Patients presenting with large bowel obstruction from rectal cancer should not undergo
resectional surgery without staging as primary treatment (very different from colonic
cancer).
- rectal surgery is more technically demanding
- the anastomotic leak rate is higher and the danger of a positive resection margin in an
unstaged patient is high.
Therefore patients with obstructing rectal cancer should have a defunctioning loop
colostomy.

Summary of procedures

The operations for cancer are segmental resections based on blood supply and lymphatic
drainage.

Site of cancer Type of resection Anastomosis

Caecal, ascending or proximal Right hemicolectomy Ileo-colic
transverse colon
Distal transverse, descending colon Left hemicolectomy Colo-colon
Sigmoid colon High anterior resection Colo-rectal
Upper rectum Anterior resection (TME) Colo-rectal
Low rectum Anterior resection (Low TME) Colo-rectal
(+/- Defunctioning
stoma)
Anal verge Abdomino-perineal excision of None
rectum

In the emergency setting where the bowel has perforated the risk of an anastomosis is much
greater, particularly when the anastomosis is colon-colon.
- 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 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.

https://www.cancercouncil.com.au/bowel-cancer/treatment/surgery/

Surgery for inflammatory bowel disease

Ulcerative colitis may be cured by surgical resection (Proctocolectomy)

It’s not the case in Crohns disease which may recur and affect other areas of the
gastrointestinal tract.
Ulcerative colitis

 Elective indications
o requiring maximal therapy
o prolonged courses of steroids.
 Proctocolectomy indication
o Longstanding UC (risk of malignant transformation)
 Dysplastic transformation of the colonic epithelium with associated
mass lesions
 Emergency presentations of poorly controlled colitis that fails to respond to medical
therapy should usually be managed with => 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.

o only be performed if the rectum is in situ and cannot usually be undertaken as
a delayed procedure following proctectomy.

Ileoanal pouch complications

- anastomotic dehiscence
- pouchitis
- poor physiological function with seepage and soiling

Crohns disease

 Surgical resection of Crohns disease => symptomatic improvement (NOT for cure)
 Indications for surgery
o complications
 fistulae
 abscess formation
 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 =>
o long term draining seton suture
o complex attempts at fistula closure e.
 Severe perianal and / or rectal Crohns => proctectomy.
 Ileoanal pouch reconstruction is not recommended
o High risk of fistula
 o
High risk of pouch failure
 Terminal ileal Crohns (commonest) => limited ileocaecal resections.
o Terminal ileal Crohns may affect enterohepatic bile salt recycling and
increase the risk of gallstones.

Paralytic ileus
Paralytic ileus is a common complication after surgery involving the bowel, especially
surgeries involving handling of the bowel. There is no peristalsis resulting in pseudo-
obstruction.

Paralytic ileus can also occur in association with chest infections, myocardial infarction,
stroke and acute kidney injury.

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.

Type of
Cause bleeding
Features in history Examination findings
Fissure in Bright red
Painful bleeding that Muco-epithelial defect
ano rectaloccurs post defecation usually in the midline
bleeding
in small volumes. posteriorly (anterior
Usually antecedent fissures more likely to
features of be due to underlying
constipation disease)
Haemorroids Bright red Post defecation Normal colon and
rectal bleeding noted both on rectum. Proctoscopy
bleeding toilet paper and drips may show internal
into pan. May be haemorrhoids. Internal
alteration of bowel haemorrhoids are
habit and history of usually impalpable.
straining. No blood
mixed with stool. No
local pain.
 Type of
Cause bleeding Features in history Examination findings
Crohn's Bright red Bleeding that is Perineal inspection may
disease or mixed accompanied by other show fissures or
blood symptoms such as fistulae. Proctoscopy
altered bowel habit, may demonstrate
malaise, history of indurated mucosa and
fissures (especially possibly strictures. Skip
anterior) and lesions may be noted at
abscesses. colonoscopy.
Ulcerative Bright red Diarrhoea, weight loss, Proctitis is the most
colitis bleeding nocturnal marked finding.
often incontinence, passage Perianal disease is
mixed of mucous PR. usually absent.
with stool Colonoscopy will show
continuous mucosal
lesion.
Rectal Bright red Alteration of bowel Usually obvious
cancer blood habit. Tenesmus may mucosal abnormality.
mixed be present. Symptoms Lesion may be fixed or
volumes of metastatic disease. mobile depending upon
disease extent.
Surrounding mucosa
often normal, although
polyps may be present.

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 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
bowel disease may be needed for fistulating Crohns
(setons).
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.
Save my notes

Anal cancer
Anal cancer is defined as a malignancy which lies exclusively in the anal canal, the
borders of which are the anorectal junction and the anal margin (area of pigmented
skin surrounding the anal orifice). 80% of anal cancers are squamous cell carcinomas
(SSCs). Other types include melanomas, lymphomas, and adenocarcinomas. The
lymphatic drainage, and therefore, tumour spread, varies in different parts of the
canal: anal margin tumours spread to the inguinal lymph nodes and those which are
more proximal spread to the pelvic lymph nodes.1

Epidemiology

 Anal cancer is relatively rare, with an annual incidence in the UK of about 1.5
in 100,000. However, its incidence is rising, especially amongst men who have
sex with men, due to widespread infection by human papillomavirus (HPV).2
 1:2 male:female ratio.3
 The average age of presentation in the UK is 85-89 years.3
 30-40% of patients present with lymph node involvement at diagnosis,
however, distant spread is uncommon, with 5-8% of cases presenting with
extrapelvic metastases at time of diagnosis.1

Risk factors1

 HPV infection causes 80-85% of SSCs of the anus (usually HPV16 or HPV18
subtypes).
 Anal intercourse and a high lifetime number of sexual partners increases the
risk of HPV infection. 4
 Men who have sex with men have a higher risk of anal cancer.
 Those with HIV and those taking immunosuppressive medication for HIV are
at a greater risk of anal carcinoma.
 Women with a history of cervical cancer or cervical intraepithelial neoplasia
(CIN) are also at greater risk of anal cancer.5
 Immunosuppressive drugs used in transplant recipients increase the risk of
anal cancer.
 Smoking is also a risk factor.

Patients typically present with a subacute onset of:

 Perianal pain, perianal bleeding

  A palpable lesion
 Faecal incontinence
 A neglected tumour in a female may present with a rectovaginal fistula.

Investigations1

 T stage assessment: examination, including a digital rectal examination,

anoscopic examination with biopsy, and palpation of the inguinal nodes.
 Imaging modalities: CT, MRI, endo-anal ultrasound and PET.
 The patient should be tested for relevant infections, including HIV.

T staging 4
The following is a T stage system for anal cancer described by the American Joint
Committee on Cancer and the International Union Against Cancer:

TX primary tumour cannot be assessed

T0 no evidence of primary tumour
Tis carcinoma in situ
T1 tumour 2 cm or less in greatest dimension
T2 tumour more than 2 cm but not more than 5 cm in
greatest dimension
T3 tumour more than 5 cm in greatest dimension
T4 tumour of any size that invades adjacent organ(s) - for
example, vagina, urethra, bladder (direct invasion of the
rectal wall, perirectal skin, subcutaneous tissue, or the
sphincter muscle(s) - is not classified as T4)

Ano rectal disease

Condition Notes
Haemorrhoids Location: 3, 7, 11 o'clock position
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
Condition Notes
Rectal prolapse Associated with childbirth and rectal intussceception. May be internal or
external
Pruritus ani Systemic and local causes
Anal neoplasm Squamous cell carcinoma commonest unlike adenocarcinoma in rectum
Solitary rectal Associated with chronic straining and constipation. Histology shows mucosal
ulcer thickening, lamina propria replaced with collagen and smooth muscle
(fibromuscular obliteration)

Rectal prolapse

 Common especially in multiparous women.

 May be internal or external.
 Internal rectal prolapse can present insidiously.
 External prolapse can ulcerate and in long term impair continence.
 Diagnostic work up includes colonoscopy, defecating proctogram, ano rectal
manometry studies and if doubt exists and examination under anaesthesia.

Treatments for prolapse

 In the acute setting reduce it (covering it with sugar may reduce swelling.
 Delormes procedure which excises mucosa and plicates the rectum (high
recurrence rates) may be used for external prolapse.
 Altmeirs procedure which resects the colon via the perineal route has lower
recurrence rates but carries the risk of anastamotic leak.
 Rectopexy is an abdominal procedure in which the rectum is elevated and
usually supported at the level of the sacral promontory. Post operative
constipation may be reduced by limiting the dissection to the anterior plane
(laparoscopic ventral mesh rectopexy).

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.

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.

Anal fissure
Anal fissures are longitudinal or elliptical tears of the squamous lining of the distal anal
canal. If present for less than 6 weeks they are defined as acute, and chronic if present for
more than 6 weeks. Around 90% of anal fissures occur on the posterior midline

Risk factors

 constipation
 inflammatory bowel disease
 sexually transmitted infections e.g. HIV, syphilis, herpes

Features

 painful, bright red, rectal bleeding

Management of an acute anal fissure (< 6 weeks)

 dietary advice: high-fibre diet with high fluid intake

 bulk-forming laxatives are first line - if not tolerated then lactulose should be tried
 lubricants such as petroleum jelly may be tried before defecation
 topical anaesthetics
-analgesia

 topical steroids do not provide significant relief

Management of a chronic anal fissure (> 6 weeks)

 the above techniques should be continued

 topical glyceryl trinitrate (GTN) is first line treatment for a chronic anal fissure
 if topical GTN is not effective after 8 weeks then secondary referral should be
considered for surgery or botulinum toxin

Haemorrhoids
Haemorrhoidal tissue is part of the normal anatomy which contributes to anal
continence. These mucosal vascular cushions are found in the left lateral, right
posterior and right anterior portions of the anal canal (3 o'clock, 7'o'clock and 11
o'clock respectively). Haemorrhoids are said to exist when they become enlarged,
congested and symptomatic

Clinical features

 painless rectal bleeding is the most common symptom

 pruritus
 pain: usually not significant unless piles are thrombosed
 soiling may occur with third or forth degree piles

Types of haemorrhoids

External

 originate below the dentate line

 prone to thrombosis, may be painful

Internal

 originate above the dentate line

 do not generally cause pain

Grading of internal haemorrhoids

Grade I Do not prolapse out of the anal canal

Grade II Prolapse on defecation but reduce spontaneously
Grade III Can be manually reduced
Grade IV Cannot be reduced

Management

 soften stools: increase dietary fibre and fluid intake

 topical local anaesthetics and steroids may be used to help symptoms
 outpatient treatments: rubber band ligation is superior to injection
sclerotherapy
 surgery is reserved for large symptomatic haemorrhoids which do not
respond to outpatient treatments
 newer treatments: Doppler guided haemorrhoidal artery ligation, stapled
haemorrhoidopexy
Acutely thrombosed external haemorrhoids

 typically present with significant pain

 examination reveals a purplish, oedematous, tender subcutaneous perianal
mass
 if patient presents within 72 hours then referral should be considered for
excision. Otherwise patients can usually be managed with stool softeners, ice
packs and analgesia. Symptoms usually settle within 10 days

Abdominal incisions
Midline incision  Commonest approach to the abdomen
 Structures divided: linea alba, transversalis fascia,
extraperitoneal fat, peritoneum (avoid falciform ligament
above the umbilicus)
 Bladder can be accessed via an extraperitoneal approach
through the space of Retzius
Paramedian  Parallel to the midline (about 3-4cm)
incision  Structures divided/retracted: anterior rectus sheath,
rectus (retracted), posterior rectus sheath, transversalis
fascia, extraperitoneal fat, peritoneum
 Incision is closed in layers
Battle  Similar location to paramedian but rectus displaced
medially (and thus denervated)
 Now seldom used
Kocher's Incision under right subcostal margin e.g. Cholecystectomy
(open)
Lanz Incision in right iliac fossa e.g. Appendicectomy
Gridiron Oblique incision centered over McBurneys point- usually
appendicectomy (less cosmetically acceptable than Lanz
Gable Rooftop incision
Pfannenstiel's Transverse supra pubic, primarily used to access pelvic organs
McEvedy's Groin incision e.g. Emergency repair strangulated femoral
hernia
Rutherford Extraperitoneal approach to left or right lower quadrants. Gives
Morrison excellent access to iliac vessels and is the approach of choice for
first time renal transplantation.
Volvulus
Volvulus may be defined as torsion of the colon around it's mesenteric axis resulting
in compromised blood flow and closed loop obstruction.

Sigmoid volvulus (around 80% of cases) describes large bowel obstruction caused by
the sigmoid colon twisting on the sigmoid mesocolon. A similar problem may also
occur at the caecum (20% of cases). In most people (around 80%) the caecum is a
retroperitoneal structure so not at risk of twisting. In the remaining minority there is
however developmental failure of peritoneal fixation of the proximal bowel putting
these patients at risk of caecal volvulus.

Caecal volvulus
Sigmoid volvulus associations associations
 older patients  all ages
 chronic constipation  adhesions
 Chagas disease  pregnancy
 neurological conditions e.g.
Parkinson's disease, Duchenne
muscular dystrophy
 psychiatric conditions e.g.
schizophrenia

Features
  constipation
 abdominal bloating
 abdominal pain
 nausea/vomiting

Diagnosis

 usually diagnosed on the abdominal film

 sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often
with air-fluid levels) + coffee bean sign
 caecal volvulus: small bowel obstruction may be seen

Management

 sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion

 caecal volvulus: management is usually operative. Right hemicolectomy is
often needed
© Image used on license from Radiopaedia

Abdominal film from a patient with sigmoid volvulus. Note the signs of large bowel obstruction
alongside the coffee bean sign
© Image used on license from Radiopaedia

Abdominal film from a patient with caecal volvulus. Small bowel obstruction is clearly visible on this
film (note the valvulae conniventes, mucosal folds, that cross the full width of the bowel).

Perianal abscess

A perianal abscess is a collection of pus within the subcutaneous tissue of the anus
that has tracked from the tissue surrounding the anal sphincter.
Epidemiology

 They are the most common form of anorectal abscess, making up around 60%
of cases;
 They are more common in men (M:F 2:1);
 The average age of patients is around 40 years.

Signs and Symptoms

 Patients may describe pain around the anus, which may be worse on sitting;
 They may have also discovered some hardened tissue in the anal region;
 There may be pus-like discharge from the anus;
 If the abscess is longstanding, the patient may have features of systemic
infection.

Causes

 They are generally colonised by gut flora such as E. coli;

 Those caused by organisms such as Staph. aureus are more likely to be an
infection of the skin rather than originating from the digestive tract.

Investigations

 Most perianal abscesses can be detected through inspection of the anus and
digital rectal examination;
 When querying the underlying cause, colonoscopy and blood tests such as
cultures and inflammatory markers may be of use;
 Imaging such as MRI and transperineal ultrasound can be useful tools, with
the former being the gold standard in imaging anorectal abscesses. They are
however rarely used except for cases where the abscess has complications or
is part of a more serious underlying process such as IBD.

Associated Conditions

 Any anorectal abscess can be caused by an underlying inflammatory bowel

disorder, especially Crohn's;
 Diabetes mellitus is a risk factor due to its ability to affect wound healing;
 Underlying malignancy can cause these abscesses as well as other anorectal
lesions due to the risk of bowel perforation.

Treatment
  Treatment is usually surgical, with incision and drainage being first line,
usually under local anaesthetic. The wound can then either be packed or left
open, in which case it will heal in around 3-4 weeks;
 Antibiotics can be of use, but are only usually employed if there is systemic
upset secondary to the abscess, as they do not seem to help with healing of
the wound after drainage.

As stated above 'perianal abscess' refers to a simple abscess of the subcutaneous

tissue. There are numerous other anorectal abscesses which can be classified by the
layers and planes that they occupy.

 Ischiorectal abscesses are found between the obturator internus muscles and
the external anal sphincter;
 Supralevator abscesses form when infection tracks superiorly from the peri-
sphincteric area to above the levator ani;
 Intersphincteric abscesses are rare (2-5% of cases) and as their name suggests
are sited between the internal and external anal sphincters;
 The pelvis is notorious for the presence of potential spaces, which can become
sites of infection. One such incidence of this is the formation of a horseshoe
abscess, a reference to their shape. These are found in a potential space
between the coccyx and the anal canal, and can be the result of complication
of another type of anorectal abscess, such as a supralevator abscess.

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Pilonidal sinus
- Occur as a result of hair debris creating sinuses in the skin (Bascom theory).
 Usually in the natal cleft of male patients after puberty.
 It is more common in Caucasians related to their hair type and growth
patterns.
 The opening of the sinus is lined by squamous epithelium, but most of its wall
consists of granulation tissue. Up to 50 cases of squamous cell carcinoma
have been described in patients with chronic pilonidal sinus disease.
 Hairs become trapped within the sinus.
 Clinically the sinus presents when acute inflammation occurs, leading to an
abscess. Patients may describe cycles of being asymptomatic and periods of
pain and discharge from the sinus.
  Treatment is difficult and opinions differ. Definitive treatment should never be
undertaken when acute infection or abscess is present as this will result in
failure.
 Definitive treatments include the Bascom procedure with excision of the pits
and obliteration of the underlying cavity. The Karydakis procedure involves
wide excision of the natal cleft such that the surface is recontoured once the
wound is closed. This avoids the shearing forces that break off the hairs and
has reasonable results.

Pilonidal sinuses are most commonly located in the midline of the natal cleft, as
illustrated below

Image sourced from Wikipedia

Wound healing
Surgical wounds are either incisional or excisional and either clean, clean
contaminated or dirty. Although the stages of wound healing are broadly similar
their contributions will vary according to the wound type.

The main stages of wound healing include:

Haemostasis

 Minutes to hours following injury

 Vasospasm in adjacent vessels, platelet plug formation and generation of
fibrin rich clot.

Inflammation

 Typically days 1-5

 Neutrophils migrate into wound (function impaired in diabetes).
 Growth factors released, including basic fibroblast growth factor and vascular
endothelial growth factor.
 Fibroblasts replicate within the adjacent matrix and migrate into wound.
 Macrophages and fibroblasts couple matrix regeneration and clot substitution.

Regeneration

 Typically days 7 to 56
 Platelet derived growth factor and transformation growth factors stimulate
fibroblasts and epithelial cells.
 Fibroblasts produce a collagen network.
 Angiogenesis occurs and wound resembles granulation tissue.

Remodeling

 From 6 weeks to 1 year

 Longest phase of the healing process and may last up to one year (or longer).
 During this phase fibroblasts become differentiated (myofibroblasts) and
these facilitate wound contraction.
 Collagen fibres are remodeled.
 Microvessels regress leaving a pale scar.

The above description represents an idealised scenario. A number of diseases may

distort this process. Neovascularisation is an important early process. Endothelial
cells may proliferate in the wound bed and recanalise to form a vessel. Vascular
disease, shock and sepsis can all compromise microvascular flow and impair healing.
Conditions such as jaundice will impair fibroblast synthetic function and immunity
with a detrimental effect in most parts of the healing process.

Problems with scars:

Hypertrophic scars
Excessive amounts of collagen within a scar. Nodules may be present histologically
containing randomly arranged fibrils within and parallel fibres on the surface. The
tissue itself is confined to the extent of the wound itself and is usually the result of a
full thickness dermal injury. They may go on to develop contractures.

Image of hypertrophic scarring. Note that it remains confined to the boundaries of

the original wound:

Image sourced from Wikipedia

Keloid scars
Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond
the boundaries of the original injury. They do not contain nodules and may occur
following even trivial injury. They do not regress over time and may recur following
removal.

Image of a keloid scar. Note the extension beyond the boundaries of the original
incision:

Image sourced from Wikipedia

Drugs which impair wound healing:

 Non steroidal anti inflammatory drugs

 Steroids
 Immunosupressive agents
 Anti neoplastic drugs

Closure
Delayed primary closure is the anatomically precise closure that is delayed for a few
days but before granulation tissue becomes macroscopically evident.

Secondary closure refers to either spontaneous closure or to surgical closure after

granulation tissue has formed.

Blood loss in surgery

Whilst there is clearly a large degree of variation in terms of blood loss during the same
procedure it is important to have some knowledge about the likely amount as this will
determine whether a group and save is adequate or whether a patient needs to be cross-
matched, and if so how much.

Chance of Example of
transfusion action Example of operations
Unlikely Group and Hysterectomy (simple), appendicectomy, thyroidectomy, elective
save lower segment caesarean section, laparoscopic cholecystectomy
Likely Cross-match 2 Salpingectomy for ruptured ectopic pregnancy, total hip
units replacement
Definite Cross-match Total gastrectomy, oophorectomy, oesophagectomy
4-6 units Elective AAA repair, cystectomy, hepatectomy

Please note that guidelines vary depending on both hospital and surgeon.

Intracranial haemorrhage
An intracranial haemorrhage describes a collection of blood or active process of bleeding
within the skull. There are several types that are divided by the anatomical compartment in
which they are found:

Extradural An extradural haematoma is a collection of blood between the skull and the dura. It is
haematoma caused by low-impact trauma and classically presents with a loss of consciousness, a
lucid interval and then a rapid decline in consciousness. Mass effect on the brain will
cause uncal herniation and a fixed, dilated pupil due to third cranial nerve
compression. CT imaging features are a hyperdense (bright), biconvex (or lentiform)
collection around the surface of the brain. Definitive management is craniotomy and
evacuation of the haematoma.
Acute subdural An acute subdural haematoma is a fresh collection of blood that is under the layer of
haematoma the dura mater of the meninges. It is most commonly caused by trauma but can be
caused by vascular lesions (e.g. arteriovenous malformations). It is typically caused
by high-speed injuries or acceleration-deceleration injuries and is therefore commonly
associated with other brain injuries. There is a spectrum of severity of clinical
presentation from an asymptomatic patient to those who are severely comatose. CT
imaging will show a hyperdense (bright), crescenteric collection surrounding the
brain that is not limited by suture lines. Definitive treatment is a decompressive
craniectomy.
Chronic subdural A chronic subdural haematoma is an old collection of blood that is under the layer of
haematoma the dura mater of the meninges. It is more common in elderly patients, alcoholics,
people on anticoagulation or in infants due to the fragility and/or predisposition of the
bridging veins to bleed. Patients typically present several weeks after a mild head
injury with progressive confusion, loss of consciousness, weakness or higher cortical
function. CT imaging will show a hypodense (dark), crescenteric collection around
the surface of the brain that is not limited by suture lines. In symptomatic patients,
definitive treatment is burr hole drainage.
Intracerebral An intracerebral (or intraparenchymal) haemorrhage is a collection of blood within
haematoma the substance of the brain. Causes / risk factors include: hypertension, vascular lesion
(e.g. aneurysm or arteriovenous malformation), cerebral amyloid angiopathy, brain
 tumour or infarct (particularly in stroke patients undergoing thrombolysis). Patients
will present similarly to an ischaemic stroke (which is why it is crucial to obtain a CT
in head in all stroke patients prior to thrombolysis) or with a decrease in
consciousness. CT imaging will show a hyperdensity (bright lesion) within the
substance of the brain. Treatment is often conservative under the care of stroke
physicians, but large clots in patients with impaired consciousness may warrant
surgical evacuation.
Subarachnoid A subarachnoid haemorrhage is a bleed into the subarachnoid space which is deep to
haemorrhage the subarachnoid layer of the meninges. The most common cause is trauma. In non-
traumatic (‘spontaneous) subarachnoid haemorrhage, the most common cause is a
ruptured aneurysm, but can be caused by an arteriovenous malformation, mycotic
aneurysm, pituitary apoplexy or can be idiopathic. The classical presentation of
sponataneous subarachnoid haemorrahge is a sudden-onset and severe headache, neck
stiffness and photophobia. CT imaging will show hyperdensity within the cisterns or
the brain and the sulci. In cases where the clinical diagnosis is certain but the CT
imaging is inconclusive, a lumbar puncture should be performed after 12 hours to
look for xanthocrhomia. Treatment is directed at the cause of the bleed.
Intraventricular An intraventricular haemorrahge is a collection of blood within the ventricular system
haemorrhage of the brain. In children it can occur due to the prematurity of the periventricular
vascular structures. In adults it may be caused by an extension of subarachnoid
haemorrhage, vascular lesions (e,g. aneurysms or arteriovenous malformations) or
tumours. On CT imaging it appears as hyperdensity within the dark CSF spaces
within the ventricles. Patients with intraventricular haemorrhage at risk of obstructive
hydrocephalus and this would required surgical CSF diversion.

In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the
aetiology is not well understood and it is suggested to occur as a result of birth trauma
combined with cellular hypoxia, together the with the delicate neonatal CNS.

Groin hernias: comparision

Direct inguinal hernia Indirect inguinal hernia Femoral hernia

Anatomy Protrudes through Protrudes through the Protrudes below the inguinal
Hesselback triangle inguinal ring ligament, lateral to the pubic
Passes medial to the Passes lateral to the tubercle
inferior epigastric artery inferior epigastric artery
Cause Defect or weakness in the Failure of the processus
transversalis fascia area vaginalis to close
of the Hesselbach triangle
Risk of Low risk of strangulation Low risk of strangulation High risk of strangulation
strangulation
Age Seen in adults May occur in infants Seen in adults
Gender Much more common in Much more common in More common in females
males males
Groin masses clinical
Groin masses are common and include:

 Herniae
 Lipomas
 Lymph nodes
 Undescended testis
 Femoral aneurysm
 Saphena varix (more a swelling than a mass!)

In the history features relating to systemic illness and tempo of onset will often give
a clue as to the most likely underlying diagnosis.

Groin lumps- some key questions

 Is there a cough impulse

 Is it pulsatile AND is it expansile (to distinguish between false and true
aneurysm)
 Are both testes intra scrotal
 Any lesions in the legs such as malignancy or infections (?lymph nodes)
 Examine the ano rectum as anal cancer may metastasise to the groin
 Is the lump soft, small and very superficial (?lipoma)

Scrotal lumps - some key questions

 Is the lump entirely intra scrotal

 Does it transilluminate (?hydrocele)
 Is there a cough impulse (?hernia)

In most cases a diagnosis can be made clinically. Where it is not clear an ultrasound
scan is often the most convenient next investigation.

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
disease often occur 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
bleeding graphic 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.
 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 the source of colonic bleeding is 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

References
http://www.sign.ac.uk/guidelines/fulltext/105/index.html

Venous thromboembolism: prophylaxis in patients admitted to

hospital
VTEs can cause severe morbidity and mortality, but they are preventable. Current NICE
guidelines (updated for 2018) outline recommendations for assessment and management of
patients at risk of VTE in hospital.

Risk factors

All patients admitted to hospital should be individually assessed to identify risk factors for
VTE development and bleeding risk. For medical and surgical patients the recommended risk
proforma is the department of healths VTE risk assessment tool.

The following inpatients would be deemed at increased risk of developing a VTE:

Medical patients:
  significant reduction in mobility for 3 days or more (or anticipated to have
significantly reduced mobility)

Surgical/trauma patients:

 hip/knee replacement
 hip fracture
 general anaesthetic and a surgical duration of over 90 minutes
 surgery of the pelvis or lower limb with a general anaesthetic and a surgical duration
of over 60 minutes
 acute surgical admission with an inflammatory/intra-abdominal condition
 surgery with a significant reduction in mobility

General risk factors:

 active cancer/chemotherapy
 aged over 60
 known blood clotting disorder (e.g. thrombophilia)
 BMI over 35
 dehydration
 one or more significant medical comorbidities (e.g. heart disease; metabolic/endocrine
pathologies; respiratory disease; acute infectious disease and inflammatory
conditions)
 critical care admission
 use of hormone replacement therapy (HRT)
 use of the combined oral contraceptive pill
 varicose veins
 pregnant or less than 6 weeks post-partum

After a patients VTE risk has been assessed, this should be compared to their risk of bleeding
to decide whether VTE prophylaxis should be offered. If indicated VTE prophylaxis should
be started as soon as possible.

Types of VTE prophylaxis

Mechanical:

 Correctly fitted anti-embolism (aka compression) stockings (thigh or knee height)

 An Intermittent pneumatic compression device

Pharmacological:

 Fondaparinux sodium (SC injection)

 Low molecular weight heparin (LMWH) - e.g. enoxaparin (brand name = Clexane)
 Unfractionated heparin (UFH) - used in patients with chronic kidney disease

Management
In general, all medical patients deemed at risk of VTE after individual assessment are started
on pharmacological VTE prophylaxis. This is providing the risk of VTE outweighs the risk of
bleeding (this is often a clinical judgement) and there are no contraindications. Those at very
high risk may be offered anti-embolic stockings alongside the pharmacological methods.

For surgical patients at low risk of VTE first-line treatment is anti-embolism stockings. If a
patient is at high risk these stockings are used in conjunction with pharmacological
prophylaxis.

Advice for patients

Pre-surgical interventions:

 Advise women to stop taking their combined oral contraceptive pill/hormone

replacement therapy 4 weeks before surgery.

Post-surgical interventions:

 Try to mobilise patients as soon as possible after surgery

 Ensure the patient is hydrated

Post procedure prophylaxis

For certain surgical procedures (hip and knee replacements) pharmacological VTE
prophylaxis is recommended for all patients to reduce the risk of a VTE developing post-
surgery. NICE make the following recommendations:

Procedure Prophylaxis
Elective hip LMWH for 10 days followed by aspirin (75 or 150
mg) for a further 28 days

or

LMWH for 28 days combined with anti-embolism

stockings until discharge

or

Rivaroxaban
Elective knee Aspirin (75 or 150 mg) for 14 days

or

LMWH for 14 days combined with anti-embolism

stockings until discharge

or
 Procedure Prophylaxis

Rivaroxaban
Fragility fractures of the LMWH or fondaparinux
pelvis, hip and proximal
femur 'Continue until the person no longer has significantly
reduced mobility relative to their normal or
anticipated mobility'

Benign liver lesions

Benign liver lesions

Cause Notes
Haemangioma  Most common benign tumours of mesenchymal origin
 Incidence in autopsy series is 8%
 Cavernous haemangiomas may be enormous
 Clinically they are reddish purple hypervascular lesions
 Lesions are normally separated from normal liver by ring of fibrous tissue
 On ultrasound they are typically hyperechoic
Liver cell  90% develop in women in their third to fifth decade
adenoma  Linked to use of oral contraceptive pill
 Lesions are usually solitary
 They are usually sharply demarcated from normal liver although they usually
lack a fibrous capsule
 On ultrasound the appearances are of mixed echoity and heterogeneous
texture. On CT most lesions are hypodense when imaged prior to
administration of IV contrast agents
 In patients with haemorrhage or symptoms removal of the adenoma may be
required
Mesenchymal Congential and benign, usually present in infants. May compress normal liver
hamartomas
Liver abscess  Biliary sepsis is a major predisposing factor
 Structures drained by the portal venous system form the second largest
source
 Common symptoms include fever, right upper quadrant pain. Jaundice may
be seen in 50%
 Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be
seen in chronic abscesses
Amoebic abscess  Liver abscess is the most common extra intestinal manifestation of
amoebiasis
 Between 75 and 90% lesions occur in the right lobe
 Presenting complaints typically include fever and right upper quadrant pain
Cause Notes
 Ultrasonography will usually show a fluid filled structure with poorly defined
boundaries
 Aspiration yield sterile odourless fluid which has an anchovy paste
consistency
 Treatment is with metronidazole
Hyatid cysts  Seen in cases of Echinococcus infection
 Typically an intense fibrotic reaction occurs around sites of infection
 The cyst has no epithelial lining
 Cysts are commonly unilocular and may grow to 20cm in size. The cyst wall
is thick and has an external laminated hilar membrane and an internal
enucleated germinal layer
 Typically presents with malaise and right upper quadrant pain. Secondary
bacterial infection occurs in 10%.
 Liver function tests are usually abnormal and eosinophilia is present in 33%
cases
 Ultrasound may show septa and hyatid sand or daughter cysts.
 Percutaneous aspiration is contra indicated
 Treatment is by sterilisation of the cyst with mebendazole and may be
followed by surgical resection. Hypertonic swabs are packed around the cysts
during surgery
Polycystic liver  Usually occurs in association with polycystic kidney disease
disease  Autosomal dominant disorder
 Symptoms may occur as a result of capsular stretch
Cystadenoma  Rare lesions with malignant potential
 Usually solitary multiloculated lesions
 Liver function tests usually normal
 Ultrasonography typically shows a large anechoic, fluid filled area with
irregular margins. Internal echos may result from septa
 Surgical resection is indicated in all cases

Liver tumours
Primary liver tumours
The most common primary tumours are cholangiocarcinoma and hepatocellular carcinoma.
Overall metastatic disease accounts for 95% of all liver malignancies making the primary
liver tumours comparatively rare.

Primary liver tumours include:

 Cholangiocarcinoma
 Hepatocellular carcinoma
 Hepatoblastoma
 Sarcomas (Rare)
 Lymphomas
 Carcinoids (most often secondary although primary may occur)

Hepatocellular carcinoma
These account for the bulk of primary liver tumours (75% cases). Its worldwide incidence
reflects its propensity to occur on a background of chronic inflammatory activity. Most cases
arise in cirrhotic livers or those with chronic hepatitis B infection, especially where viral
replication is actively occurring. In the UK it accounts for less than 5% of all cancers,
although in parts of Asia its incidence is 100 per 100,000.
The majority of patients (80%) present with existing liver cirrhosis, with a mass discovered
on screening ultrasound.

Diagnosis

 CT/ MRI (usually both) are the imaging modalities of choice

 a-fetoprotein is elevated in almost all cases
 Biopsy should be avoided as it seeds tumours cells through a resection plane.
 In cases of diagnostic doubt serial CT and αFP measurements are the preferred
strategy.

Treatment

 Patients should be staged with liver MRI and chest, abdomen and pelvic CT scan.
 The testis should be examined in males (testicular tumours may cause raised AFP).
PET CT may be used to identify occult nodal disease.
 Surgical resection is the mainstay of treatment in operable cases. In patients with a
small primary tumour in a cirrhotic liver whose primary disease process is controlled,
consideration may be given to primary whole liver resection and transplantation.
 Liver resections are an option but since most cases occur in an already diseased liver
the operative risks and post-operative hepatic dysfunction are far greater than is seen
following metastectomy.
 These tumours are not particularly chemo or radiosensitive however, both may be
used in a palliative setting. Tumour ablation is a more popular strategy.

Survival
Poor, overall survival is 15% at 5 years.

Cholangiocarcinoma
This is the second most common type of primary liver malignancy. As its name suggests
these tumours arise in the bile ducts. Up to 80% of tumours arise in the extra hepatic biliary
tree. Most patients present with jaundice and by this stage the majority will have disease that
is not resectable.
Primary sclerosing cholangitis is the main risk factor. In deprived countries typhoid and liver
flukes are also major risk factors.

Diagnosis

 Patients will typically have an obstructive picture on liver function tests.

 CA 19-9, CEA and CA 125 are often elevated
 CT/ MRI and MRCP are the imaging methods of choice.

Treatment
  Surgical resection offers the best chance of cure. Local invasion of peri hilar tumours
is a particular problem and this coupled with lobar atrophy will often contra indicate
surgical resection.
 Palliation of jaundice is important, although metallic stents should be avoided in those
considered for resection.

Survival
Is poor, approximately 5-10% 5 year survival.

Hydatid cysts
Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are
caused by the tapeworm parasite Echinococcus granulosus. An outer fibrous capsule
is formed containing multiple small daughter cysts. These cysts are allergens which
precipitate a type 1 hypersensitivity reaction.

Clinical features are as follows:

 Up to 90% cysts occur in the liver and lungs

 Can be asymtomatic, or symptomatic if cysts > 5cm in diameter
 Morbidity caused by cyst bursting, infection and organ dysfunction (biliary,
bronchial, renal and cerebrospinal fluid outflow obstruction)
 In biliary ruputure there may be the classical triad of; biliary colic, jaundice,
and urticaria

CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic
cysts.
Surgery is the mainstay of treatment (the cyst walls must not be ruptured during
removal and the contents sterilised first).
© Image used on license from Radiopaedia

CT scan showing a hydatid cyst of the l

Acute pancreatitis
Acute pancreatitis is usually due to alcohol or gallstones.

Pathophysiology:
- autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis

Features:

 Severe epigastric pain that may radiate through to the back

 Vomiting is common
  Examination may reveal tenderness, ileus and low-grade fever
 Periumbilical discolouration (Cullen's sign) and flank discolouration (Grey-
Turner's sign) is described but rare

Rare features associated with pancreatitis include:

 ischaemic (Purtscher) retinopathy - may cause temporary or permanent

blindness

Investigations:

 raised amylase is seen in 75% of patients.

Scoring systems

There are several scoring systems used to identify cases of severe pancreatitis which
may require intensive care management. These include the Ranson score, Glasgow
score and APACHE II.

Some common factors indicating severe pancreatitis include:

 age > 55 years

 hypocalcaemia
 hyperglycaemia
 hypoxia
 neutrophilia
 elevated LDH and AST

Note that the actual amylase level is not of prognostic value.

Acute pancreatitis: complications

Local complications

Peripancreatic fluid collections

 Occur in 25% cases

 Located in or near the pancreas and lack a wall of granulation or fibrous tissue
 May resolve or develop into pseudocysts or abscesses
 Since most resolve aspiration and drainage is best avoided as it may
precipitate infection
Pseudocysts

 In acute pancreatitis result from organisation of peripancreatic fluid collection.

They may or may not communicate with the ductal system.
 The collection is walled by fibrous or granulation tissue and typically occurs 4
weeks or more after an attack of acute pancreatitis
 Most are retrogastric
 75% are associated with persistent mild elevation of amylase
 Investigation is with CT, ERCP and MRI or endoscopic USS
 Symptomatic cases may be observed for 12 weeks as up to 50% resolve
 Treatment is either with endoscopic or surgical cystogastrostomy or aspiration

Pancreatic necrosis

 Pancreatic necrosis may involve both the pancreatic parenchyma and

surrounding fat
 Complications are directly linked to extent of parenchymal necrosis and extent
of necrosis overall
 Early necrosectomy is associated with a high mortality rate (and should be
avoided unless compelling indications for surgery exist)
 Sterile necrosis should be managed conservatively (at least initially)
 Some centres will perform fine-needle aspiration sampling of necrotic tissue if
infection is suspected. False negatives may occur and the extent of sepsis and
organ dysfunction may be a better guide to surgery

Pancreatic abscess

 Intraabdominal collection of pus associated with pancreas but in the absence

of necrosis
 Typically occur as a result of infected pseudocyst
 Transgastric drainage is one method of treatment, endoscopic drainage is an
alternative

Haemorrhage

 Infected necrosis may involve vascular structures with resultant haemorrhage

that may occur de novo or as a result of surgical necrosectomy.
 When retroperitoneal haemorrhage occurs Grey Turner's sign may be
identified

Systemic complications
Acute respiratory distress syndrome

 associated with a high-mortality rate of around 20%

Acute pancreatitis: management

Management of Acute Pancreatitis in the UK

Diagnosis

 Traditionally hyperamylasaemia has been utlilised with amylase being elevated

three times the normal range.
 However, amylase may give both false positive and negative results.
 Serum lipase is both more sensitive and specific than serum amylase. It also
has a longer half life.
 Serum amylase levels do not correlate with disease severity.

Differential causes of hyperamylasaemia

Acute pancreatitis
Pancreatic pseudocyst
Mesenteric infarct
Perforated viscus
Acute cholecystitis
Diabetic ketoacidosis

Assessment of severity

 Glasgow, Ranson scoring systems and APACHE II

 Biochemical scoring e.g. using CRP

Features that may predict a severe attack within 48 hours of admission to hospital
Initial assessment  Clinical impression of severity
 Body mass index >30
 Pleural effusion
 APACHE score >8
24 hours after  Clinical impression of severity
admission  APACHE II >8
 Glasgow score of 3 or more
 Persisting multiple organ failure
 CRP>150
48 hours after  Glasgow Score of >3
admission  CRP >150
 Persisting or progressive organ failure

Management

Nutrition

 There is reasonable evidence to suggest that the use of enteral nutrition does
not worsen the outcome in pancreatitis
 Most trials to date were underpowered to demonstrate a conclusive benefit.
 The rationale behind feeding is that it helps to prevent bacterial translocation
from the gut, thereby contributing to the development of infected pancreatic
necrosis.

Use of antibiotic therapy

 Many UK surgeons administer antibiotics to patients with acute pancreatitis.

 A recent Cochrane review highlights the potential benefits of administering
Imipenem to patients with established pancreatic necrosis in the hope of
averting the progression to infection.
 There are concerns that the administration of antibiotics in mild attacks of
pancreatitis will not affect outcome and may contribute to antibiotic
resistance and increase the risks of antibiotic associated diarrhoea.

Surgery

 Patients with acute pancreatitis due to gallstones should undergo early

cholecystectomy.
 Patients with obstructed biliary system due to stones should undergo early
ERCP.
 Patients who fail to settle with necrosis and have worsening organ dysfunction
may require debridement, fine needle aspiration is still used by some.
 Patients with infected necrosis should undergo either radiological drainage or
surgical necrosectomy. The choice of procedure depends upon local expertise.

Chronic pancreatitis
Chronic pancreatitis is an inflammatory condition which can ultimately affect both
the exocrine and endocrine functions of the pancreas. Around 80% of cases are due
to alcohol excess with up to 20% of cases being unexplained.
Other than alcohol, causes include:

 genetic: cystic fibrosis, haemochromatosis

 ductal obstruction: tumours, stones, structural abnormalities
including pancreas divisum and annular pancreas

Features

 pain is typically worse 15 to 30 minutes following a meal

 steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5
and 25 years after the onset of pain
 diabetes mellitus develops in the majority of patients. It typically occurs more
than 20 years after symptom begin

Investigation

 abdominal x-ray shows pancreatic calcification in 30% of cases

 CT is more sensitive at detecting pancreatic calcification. Sensitivity is 80%,
specificity is 85%
 functional tests: faecal elastase may be used to assess exocrine function if
imaging inconclusive

Management

 pancreatic enzyme supplements

 analgesia
 antioxidants: limited evidence base - one study suggests benefit in early
disease
© Image used on license from Radiopaedia

Multiple small calcific foci projected in the pancreas consistent with chronic pancreatitis
© Image used on license from Radiopaedia

CT showing an irregular shaped pancreas with the typical calcification of chronic pancreatitis

Hydrocephalus
Hydrocephalus is defined as a condition in which there is an excessive volume of
cerebrospinal (CSF) fluid within the ventricular system of the brain and is caused by
an imbalance between CSF production and absorption.

Patients with hydrocephalus present with symptoms due to raised intracranial

pressure, which include:

 Headache (typically worse in the morning, when lying down and during
valsalva)
  Nausea and vomiting
 Papilloedema
 Coma (in severe cases)

Since infants have skull sutures that are not yet fused, the pathological rise in
intracranial pressure that is caused by hydrocephalus will cause an increase in head
circumference. The open anterior fontanelle will bulge and become tense. Children
with severe hydrocephalus also classically present with failure of upward gaze
(‘sunsetting’ eyes) due to compression of the superior colliculus of the midbrain.

Hydrocephalus can be broadly divided into two categories

 Obstructive (‘non-communicating’) hydrocephalus

 Non-obstructive (‘communicating’) hydrocephalus

Obstructive hydrocephalus is due to a structural pathology blocking the flow of

cerebrospinal fluid. Dilatation of the ventricular system is seen superior to site of
obstruction. Causes include: tumours, acute haemorrhage (e.g. subarachnoid
haemorrhage or intraventricular haemorrhage) and developmental abnormalities
(e.g. aqueduct stenosis).

Non-obstructive hydrocephalus is due to an imbalance of CSF production

absorption. It is either caused by an increased production of CSF (e.g. choroid plexus
tumour (very rare)) or more commonly a failure of reabsorption at the arachnoid
granulations (e.g. meningitis or post-haemorrhagic).

Normal pressure hydrocephalus is a unique form of non-obstructive hydrocephalus

characterised by large ventricles but normal intracranial pressure. The classic triad of
symptoms is dementia, incontinence and disturbed gait.

Investigation

 CT head is used as a first line imaging investigation since it is fast and shows
adequate resolution of the brain and ventricles
 MRI may be used to investigate hydrocephalus in more detail, particularly if
there is a suspected underlying lesion
 Lumbar puncture* is both diagnostic and therapeutic since it allows you to
sample CSF, measure the opening pressure, but also to drain CSF to reduce
the pressure

Treatment
  An external ventricular drain (EVD) is used in acute, severe hydrocephalus and
is typically inserted into the right lateral ventricle and drains into a bag at the
bedside
 A ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique that
drains CSF from the ventricles to the peritoneum
 In obstructive hydrocephalus, the treatment may involve surgically treating
the obstructing pathology

*Lumbar puncture must not be used in obstructive hydrocephalus since the

difference of cranial and spinal pressures induced by the drainage of CSF will cause
brain herniation.

Head injury: NICE guidance on investigation

NICE has strict and clear guidance regarding which adult patients are safe to
discharge and which need further CT head imaging. The latter group are also divided
into two further cohorts, those who require an immediate CT head and those
requiring CT head within 8 hours of injury:

CT head immediately

 GCS < 13 on initial assessment

 GCS < 15 at 2 hours post-injury
 suspected open or depressed skull fracture.
 any sign of basal skull fracture (haemotympanum, 'panda' eyes, cerebrospinal
fluid leakage from the ear or nose, Battle's sign).
 post-traumatic seizure.
 focal neurological deficit.
 more than 1 episode of vomiting

CT head scan within 8 hours of the head injury - for adults with any of the following
risk factors who have experienced some loss of consciousness or amnesia since the
injury:

 age 65 years or older

 any history of bleeding or clotting disorders
 dangerous mechanism of injury (a pedestrian or cyclist struck by a motor
vehicle, an occupant ejected from a motor vehicle or a fall from a height of
greater than 1 metre or 5 stairs)
 more than 30 minutes' retrograde amnesia of events immediately before the
head injury
Post-operative pyrexia
Early causes of post-op pyrexia (0-5 days) include:

 Blood transfusion
 Cellulitis
 Urinary tract infection
 Physiological systemic inflammatory reaction (usually within a day following
the operation)
 Pulmonary atelectasis - this if often listed but the evidence base to support
this link is limited

Late causes (>5 days) include:

 Venous thromboembolism
 Pneumonia
 Wound infection
 Anastomotic leak

When considering causes of post-op pyrexia, it is helpful to consider the memory aid
of 'the 4 W's' (wind, water, wound, what did we do? (iatrogenic).
Abdominal aortic aneurysm

Abdominal aortic aneurysms occur primarily as a result of the failure of elastic

proteins within the extracellular matrix. Aneurysms 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
- connective tissues diseases such as Ehlers Danlos type 1 and Marfans
syndrome

Abdominal aortic aneursym: management of unruptured aneurysms

Low rupture risk

 asymptomatic, aortic diameter <5.5cm

 treat with abdominal US surveillance and optimise cardiovascular risk factors (e.g.
stop smoking)

High rupture risk

 symptomatic, aortic diameter >=5.5cm or rapidly enlarging (>1cm/year)

 treat with elective endovascular repair (EVAR) or open repair if unsuitable.
o In EVAR a stent is placed into the abdominal aorta via the femoral artery to
prevent blood from collecting in the aneurysm.
o A complication of EVAR is an endo-leak, where the stent fails to exclude
blood from the aneurysm, and usually presents without symptoms on routine
follow-up.

Peripheral arterial disease: acute limb-threatening ischaemia

Three main patterns of presentation may be seen in patients with peripheral arterial
disease:

 intermittent claudication
 critical limb ischaemia
 acute limb-threatening ischaemia

Acute limb-threatening ischaemia

Features - 1 or more of the 6 P's

 pale
 pulseless
 painful
 paralysed
 paraesthetic
 'perishing with cold'

Peripheral arterial disease: critical limb ischaemia

Critical limb ischaemia

Features should include 1 or more of:

 rest pain in foot for more than 2 weeks
 ulceration
 gangrene

Patients often report hanging their legs out of bed at night to ease the pain.

An ankle-brachial pressure index (ABPI) of < 0.5 is suggestive of critical limb

ischaemia.

Interpretation of ABPI

Result Usual clinical correlation

1 Normal
0.6-0.9 Claudication
0.3-0.6 Rest pain
<0.3 Impending

Peripheral arterial disease: intermittent claudication

Intermittent claudication
Features
 intermittent claudication: aching or burning in the leg muscles following
walking
 patients can typically walk for a predictable distance before the symptoms
start
 usually relieved within minutes of stopping
 not present at rest

Assessment
 check the femoral, popliteal, posterior tibialis and dorsalis pedis pulses
 check ankle brachial pressure index (ABPI)
 duplex ultrasound is the first line investigation
 magnetic resonance angiography (MRA) should be performed prior to any
intervention

Interpretation of ABPI

Result Usual clinical correlation

1 Normal
0.6-0.9 Claudication
0.3-0.6 Rest pain
<0.3 Impending

Peripheral arterial disease: management

Peripheral arterial disease (PAD) is strongly linked to smoking.

Patients who still smoke should be given help to quit smoking.

Comorbidities should be treated, including

 hypertension
 diabetes mellitus
 obesity

As with any patient who has established cardiovascular disease, all patients should be
taking a statin.
- Atorvastatin 80 mg is currently recommended.

In 2010 NICE published guidance suggesting that clopidogrel should be used first-
line in patients with peripheral arterial disease in preference to aspirin.

Exercise training has been shown to have significant benefits.

 - NICE recommend a supervised exercise programme for all patients with
peripheral arterial disease prior to other interventions.

Severe PAD or critical limb ischaemia may be treated by:

 angioplasty
 stenting
 bypass surgery

Amputation should be reserved for patients with critical limb ischaemia who are not
suitable for other interventions such as angioplasty or bypass surgery.

Drugs licensed for use in peripheral arterial disease (PAD) include:

 naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor
quality of life
 cilostazol: phosphodiesterase III inhibitor with both antiplatelet and
vasodilator effects - not recommended by NICE

Ankle-brachial pressure index

The ankle-brachial pressure index (ABPI) is the ratio of the systolic blood pressure in
the lower leg to that in the arms. Lower blood pressure in the legs (result in a ABPI <
1) is an indicator of peripheral arterial disease (PAD). ABPI is therefore useful in
evaluating patients with suspected PAD, for example a male smoker who presents
with intermittent claudication.

It is also important to determine the ABPI in patients with leg ulcers. Venous ulcers
are often treated with compression bandaging. Doing this in a patient with PAD
could however be harmful as it would further restrict the blood supply to the foot.
ABPIs should therefore always be measured in patients with leg ulcers.

Interpretation of ABPI
 > 1.2: may indicate calcified, stiff arteries. This may be seen with advanced age
or PAD
 1.0 - 1.2: normal
 0.9 - 1.0: acceptable
 < 0.9: likely PAD. Values < 0.5 indicate severe disease which should be
referred urgently

The ABPI is a good test, values less than 0.90 have been shown to have a sensitivity
of 90% and a specificity of 98%* for PAD.

Compression bandaging is generally considered acceptable if the ABPI >= 0.8.

Lower leg ulcers

Venous leg ulcers

 Most due to venous hypertension, secondary to chronic venous insufficiency

(other causes include calf pump dysfunction or neuromuscular disorders)
 Ulcers form due to capillary fibrin cuff or leucocyte sequestration
 Features of venous insufficiency include oedema, brown pigmentation,
lipodermatosclerosis, eczema
 Location above the ankle, painless
 Deep venous insufficiency is related to previous DVT and superficial venous
insufficiency is associated with varicose veins
 Doppler ultrasound looks for presence of reflux and duplex ultrasound looks
at the anatomy/ flow of the vein
 Management: 4 layer compression banding after exclusion of arterial disease
or surgery
 If fail to heal after 12 weeks or >10cm2 skin grafting may be needed

Marjolin's ulcer

 Squamous cell carcinoma

 Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-
20 years
 Mainly occur on the lower limb

Arterial ulcers

 Occur on the toes and heel

 Painful
 There may be areas of gangrene
 Cold with no palpable pulses
 Low ABPI measurements

Neuropathic ulcers
  Commonly over plantar surface of metatarsal head and plantar surface of
hallux
 The plantar neuropathic ulcer is the condition that most commonly leads to
amputation in diabetic patients
 Due to pressure
 Management includes cushioned shoes to reduce callous formation

Pyoderma gangrenosum
 Associated with inflammatory bowel disease/RA
 Can occur at stoma sites
 Erythematous nodules or pustules which ulcerate

Vascular disorders of the upper limb

Upper limb arterial disease is less common than lesions causing symptoms in the
lower limb. The upper limb circulation may be affected by embolic events, stenotic
lesions (both internal and extrinsic), inflammatory disorders and venous diseases.
The anatomy of the collateral circulation of the arterial inflow may impact on the
history and nature of disease presentation. In the region of the subclavian and
axillary arteries the collateral vessels passing around the shoulder joint may provide
pathways for flow if the main vessels are stenotic or occluded. During periods of
increased metabolic demand the collateral flow is not sufficient and the vertebral
arteries may have diminished flow. This may result in diminished flow to the brain
with neurological sequelae such as syncope.

Condition Features
Axillary/ brachial  50% of upper limb emboli will lodge in the brachial artery
embolus  30% of upper limb emboli will lodge in the axillary artery
 Sudden onset of symptoms; pain, pallor, paresis, pulselessness,
paraesthesia
 Sources are left atrium with cardiac arrhythmia (mainly AF),
mural thrombus
 Cardiac arrhythmias may cause result in impaired consciousness
in addition to the embolus
Arterial  Those resulting from atheroma are the most common, trauma
occlusions may result in vascular changes and long term occlusion but this is
rare
 Features may include claudication, ulceration and gangrene.
Proximally sited lesions may result in subclavian steal
syndrome
 The progressive nature of the disease allows development of
collaterals, acute ischaemia may occur as a result of acute
thrombosis
Raynaud's disease  Idiopathic condition affecting young females
  Usually affects hands > feet
 Digits become: white →blue →red
 Treatment is with calcium antagonists
Upper limb  Gradual onset of upper limb swelling and discomfort.
venous thrombosis  Sensation and motor function are normal
 Condition may complicate pre-existing malignancy (especially
breast cancer) or arise as a result of repetitive use of the limb in a
task such axs painting a ceiling
 The condition is diagnosed with duplex ultrasound and treatment
is with anticoagulation
Cervical rib  0.2-0.4% incidence
 Consist of an anomalous fibrous band that often originates from
C7 and may arc towards, but rarely reaches the sternum
 Congenital cases may present around the third decade, some
cases are reported to occur following trauma
 Bilateral in up to 70%
 Compression of the subclavian artery may produce absent radial
pulse on clinical examination and in particular may result in a
positive Adsons test (lateral flexion of the neck away from
symptomatic side and traction of the symptomatic arm- leads to
obliteration of radial pulse)
 Treatment is most commonly undertaken when there is evidence
of neurovascular compromise.

- A transaxillary approach is the traditional operative method for

excision

Vascular disease
Aortic dissection  Chest pain (anterior chest pain- ascending aorta, back pain -
descending aorta)
 Widening of aorta on chest x-ray
 Diagnosis made by CT scanning
 Treatment is either medical (Type B disease) or surgical (Type A
disease)
Cervical rib  Supernumery fibrous band arising from seventh cervical vertebra
 Incidence of 1 in 500
 May cause thoracic outlet syndrome
 Treatment involves surgical division of rib
Subclavian steal  Due to proximal stenotic lesion of the subclavian artery
syndrome  Results in retrograte flow through vertebral or internal thoracic
arteries
 The result is that decrease in cerebral blood flow may occur and
produce syncopal symptoms
  A duplex scan and/ or angiogram will delineate the lesion and
allow treatment to be planned
Takayasu's  Large vessel granulomatous vasculitis
arteritis  Results in intimal narrowing
 Most commonly affects young asian females
 Patients present with features of mild systemic illness, followed by
pulseless phase with symptoms of vascular insufficiency
 Systolic murmur
 Treatment is with systemic steroids
Patent ductus  Ductus arteriosus is a normal foetal vessel that closes
arteriosus spontaneously after birth
 Results in high pressure, oxygenated blood entering the pulmonary
circuit
 Untreated patients develop symptoms of congestive cardiac failure
Coarctation of the  Aortic stenosis at the site of the ductus arteriosus insertion
aorta  Most common in boys and girls with Turners syndrome
 Patients may present with symptoms of arterial insufficiency, such
as syncope and claudication
 Blood pressure mismatch may be seen, as may mismatch of pulse
pressure in the upper and lower limbs
 * Collateral flow through the intercostal vessels may produce
notching of the ribs, if the disease is long standing.
 Treatment is either with angioplasty or surgical resection (the
former is the most common)

Trauma management
The cornerstone of trauma management is embodied in the principles of ATLS.

Following trauma there is a trimodal death distribution:

 Immediately following injury. Typically as result of brain or high spinal

injuries, cardiac or great vessel damage. Salvage rate is low.
 In early hours following injury. In this group deaths are due to phenomena
such as splenic rupture, sub dural haematomas and haemopneumothoraces
 In the days following injury. Usually due to sepsis or multi organ failure.

Aspects of trauma management

 ABCDE approach.
 Tension pneumothoraces will deteriorate with vigorous ventilation attempts.
 External haemorrhage is managed as part of the primary survey. As a rule
tourniquets should not be used. Blind application of clamps will tend to
 damage surrounding structures and packing is the preferred method of
haemorrhage control.
 Urinary catheters and naso gastric tubes may need inserting. Be wary of basal
skull fractures and urethral injuries.
 Patients with head and neck trauma should be assumed to have a cervical
spine injury until proven otherwise.

Thoracic injuries

 Simple pneumothorax
 Mediastinal traversing wounds
 Tracheobronchial tree injury
 Haemothorax
 Blunt cardiac injury
 Diaphragmatic injury
 Aortic disruption
 Pulmonary contusion

Management of thoracic trauma

 Simple pneumothorax insert chest drain. Aspiration is risky in trauma as

pneumothorax may be from lung laceration and convert to tension
pneumothorax.
 Mediastinal traversing wounds These result from situations like stabbings.
Exit and entry wounds in separate hemithoraces. The presence of a
mediastinal haematoma indicates the likelihood of a great vessel injury. All
patients should undergo CT angiogram and oesophageal contrast swallow.
Indications for thoracotomy are largely related to blood loss and will be
addressed below.
 Tracheobronchial tree injury Unusual injuries. In blunt trauma most injuries
occur within 4cm of the carina. Features suggesting this injury include
haemoptysis and surgical emphysema. These injuries have a very large air leak
and may have tension pneumothorax.
 Haemothorax Usually caused by laceration of lung vessel or internal
mammary artery by rib fracture. Patients should all have a wide bore 36F chest
drain. Indications for thoracotomy include loss of more than 1.5L blood
initially or ongoing losses of >200ml per hour for >2 hours.
 Cardiac contusions Usually cardiac arrhythmias, often overlying sternal
fracture. Perform echocardiography to exclude pericardial effusions and
tamponade. Risk of arrhythmias falls after 24 hours.
 Diaphragmatic injury Usually left sided. Direct surgical repair is performed.
 Traumatic aortic disruption Commonest cause of death after RTA or falls.
Usually incomplete laceration near ligamentum arteriosum. All survivors will
 have contained haematoma. Only 1-2% of patients with this injury will have a
normal chest x-ray.
 Pulmonary contusion Common and lethal. Insidious onset. Early intubation
and ventilation.

Abdominal trauma

 Deceleration injuries are common.

 In blunt trauma requiring laparotomy the spleen is most commonly injured
(40%)
 Stab wounds traverse structures most commonly liver (40%)
 Gunshot wounds have variable effects depending upon bullet type. Small
bowel is most commonly injured (50%)
 Patients with stab wounds and no peritoneal signs up to 25% will not enter
the peritoneal cavity
 Blood at urethral meatus suggests a urethral tear
 High riding prostate on PR = urethral disruption
 Mechanical testing for pelvic stability should only be performed once

Investigations in abdominal trauma

Diagnostic
Peritoneal Lavage Abdominal CT scan USS
Indication Document bleeding Document organ Document fluid if
if hypotensive injury if normotensive hypotensive
Advantages Early diagnosis and Most specific for Early diagnosis, non
sensitive; 98% localising injury; 92 to invasive and
accurate 98% accurate repeatable; 86 to
95% accurate
Disadvantages Invasive and may Location of scanner Operator dependent
miss retroperitoneal
away from facilities, and may miss
and diaphragmatic time taken for retroperitoneal injury
injury reporting, need for
contrast
 Amylase may be normal following pancreatic trauma
 Urethrography if suspected urethral injury

Thoracic trauma
Types of thoracic trauma

Condition Notes
Tension  Often laceration to lung parenchyma with flap
pneumothorax  Pressure develops in thorax
 Condition Notes
 Most common cause is mechanical ventilation in patient with pleural injury
 Symptoms overlap with cardiac tamponade, hyper-resonant percussion note
is more likely in tension pnemothorax
Flail chest  Chest wall disconnects from thoracic cage
 Multiple rib fractures (at least two fractures per rib in at least two ribs)
 Associated with pulmonary contusion
 Abnormal chest motion
 Avoid over hydration and fluid overload
Pneumothorax  Most common cause is lung laceration with air leakage
 Most traumatic pneumothoraces should have a chest drain
 Patients with traumatic pneumothorax should never be mechanically
ventilated until a chest drain is inserted
Haemothorax  Most commonly due to laceration of lung, intercostal vessel or internal
mammary artery
 Haemothoraces large enough to appear on CXR are treated with large bore
chest drain
 Surgical exploration is warranted if >1500ml blood drained immediately
Cardiac tamponade  Beck's triad: elevated venous pressure, reduced arterial pressure, reduced
heart sounds.
 Pulsus paradoxus
 May occur with as little as 100ml blood
Pulmonary  Most common potentially lethal chest injury
contusion  Arterial blood gases and pulse oximetry important
 Early intubation within an hour if significant hypoxia
Blunt cardiac injury  Usually occurs secondary to chest wall injury
 ECG may show features of myocardial infarction
 Sequelae: hypotension, arrhythmias, cardiac wall motion abnormalities
Aorta disruption  Deceleration injuries
 Contained haematoma
 Widened mediastinum
Diaphragm  Most due to motor vehicle accidents and blunt trauma causing large radial
disruption tears (laceration injuries result in small tears)
 More common on left side
 Insert gastric tube, which will pass into the thoracic cavity
Mediastinal  Entrance wound in one hemithorax and exit wound/foreign body in
traversing wounds opposite hemithorax
 Mediastinal haematoma or pleural cap suggests great vessel injury
 Mortality is 20%

Priapism
Priapism is a persistent penile erection, typically defined as:
 - lasting longer than 4 hours
- not associated with sexual stimulation

Priapism can be described as either ischaemic or non-ischaemic with both

categories having a different pathophysiology.

Ischaemic priapism is typically due to impaired vasorelaxation and therefore

reduced vascular outflow resulting in congestion and trapping of de-oxygenated
blood within the corpus cavernosa.

Non-ischaemic priapism is due to high arterial inflow, typically due to fistula

formation often either as the result of congenital or traumatic mechanisms.

Epidemiology
 Age at presentation has a bimodal distribution, with peaks between 5-10 years
and 20-50 years of age
 incidence has been estimated at up to 5.34 per 100,000 patient-years

Causes
 Idiopathic
 Sickle cell disease or other haemoglobinopathies
 Erectile dysfunction medication (e.g. Sildenafil and other PDE-5 inhibitors),
this also includes intracavernosal injected therapies.
 Other drugs both prescribed (anti-hypertensives, anticoagulants,
antidepressants etc) and recreational (specifically cocaine, cannabis and
ecstasy).
 Trauma

Patients typically present acutely with:

 A persistent erection lasting over 4 hours
 Pain localised to the penis
 Often a history of either known haemoglobinopathy or use of medications
listed above
 Patients may, more rarely, present with either a non-painful erection or an
erection that is not fully rigid: these are both suggestive of non-ischaemic
priapism.
 History of trauma to the genital or perineal region: also suggestive of non-
ischaemic priapism.

Investigations:
  Cavernosal blood gas analysis to differentiate between ischaemic and non-
ischaemic: in ischaemic priapism pO2 and pH would be reduced whilst pCO2
would be increased.
 Doppler or duplex ultrasonography: this can be used as an alternative to
blood gas analysis to assess for blood flow within the penis.
 A full blood count and toxicology screen can be used to assess for an
underlying cause of the priapism.
 Diagnosis of priapism is largely clinical, with investigations helping to
categorise into ischaemic and non-ischaemic as well as assessing for the
underlying cause.

Management

Ischaemic priapism is a medical emergency and delayed treatment can lead to

permanent tissue damage and long-term erectile dysfunction.
 If the priapism has lasted longer than 4 hours, the first-line treatment is
aspiration of blood from the cavernosa, this is often combined with injection
of a saline flush to help clear viscous blood that has pooled.
 If aspiration and injection fails, then intracavernosal injection of a
vasoconstrictive agent such as phenylephrine is used and repeated at 5
minute intervals.
 If medical therapy fails then surgical options can be considered.

Non-ischaemic priapism is not a medical emergency and is normally suitable for

observation as a first-line option.

Scrotal problems
Epididymal cysts

Epididymal cysts are the most common cause of scrotal swellings seen in primary
care.

Features
 separate from the body of the testicle
 found posterior to the testicle

Associated conditions
 polycystic kidney disease
 cystic fibrosis
  von Hippel-Lindau syndrome

Diagnosis may be confirmed by ultrasound.

Management is usually supportive

- larger or symptomatic cysts: surgical removal or sclerotherapy

Hydrocele

A hydrocele describes the accumulation of fluid within the tunica vaginalis.

They can be divided into communicating and non-communicating:

 communicating: caused by patency of the processus vaginalis allowing
peritoneal fluid to drain down into the scrotum.
Communicating hydroceles are common in newborn males (clinically apparent
in 5-10%) and usually resolve within the first few months of life
 non-communicating: caused by excessive fluid production within the tunica
vaginalis

Hydroceles may develop secondary to:

 epididymo-orchitis
 testicular torsion
 testicular tumours

Features
 soft, non-tender swelling of the hemi-scrotum. Usually anterior to and below
the testicle
 the swelling is confined to the scrotum, you can get 'above' the mass on
examination
 transilluminates with a pen torch
 the testis may be difficult to palpate if the hydrocele is large

Diagnosis may be clinical but ultrasound is required if there is any doubt about the
diagnosis or if the underlying testis cannot be palpated.

Management
 infantile hydroceles are generally repaired if they do not resolve
spontaneously by the age of 1-2 years
 in adults a conservative approach may be taken depending on the severity of
the presentation.
Further investigation (e.g. ultrasound) is usually warranted however to exclude
any underlying cause such as a tumour
 Varicocele

A varicocele is an abnormal enlargement of the testicular veins.

They are usually asymptomatic but may be important as they are associated with
infertility.

Varicoceles are much more common on the left side (> 80%). Features:
 classically described as a 'bag of worms'
 subfertility

Diagnosis
 ultrasound with Doppler studies

Management
 usually conservative
 occasionally surgery is required if the patient is troubled by pain. There is
ongoing debate regarding the effectiveness of surgery to treat infertility

Scrotal swelling
Condition Notes
Inguinal hernia If inguinoscrotal swelling; cannot 'get above it' on examination
Cough impulse may be present
May be reducible
Testicular tumours Often discrete testicular nodule (may have associated hydrocele)
Symptoms of metastatic disease may be present
USS scrotum and serum AFP and β HCG required
Acute epididymo- Often history of dysuria and urethral discharge
orchitis Swelling may be tender and eased by elevating testis
Condition Notes

Most cases due to Chlamydia

Infections with other gram negative organisms may be associated with

underlying structural abnormality
Epidiymal cysts Single or multiple cysts
May contain clear or opalescent fluid (spermatoceles)
Usually occur over 40 years of age
Painless
Lie above and behind testis
It is usually possible to 'get above the lump' on examination
Hydrocele Non painful, soft fluctuant swelling
Often possible to 'get above it' on examination
Usually contain clear fluid
Will often transilluminate
May be presenting feature of testicular cancer in young men
Testicular torsion Severe, sudden onset testicular pain
Risk factors include abnormal testicular lie

Typically affects adolescents and young males

On examination testis is tender and pain not eased by elevation

Urgent surgery is indicated, the contralateral testis should also be fixed

Varicocele Varicosities of the pampiniform plexus
Typically occur on left (because testicular vein drains into renal vein)
May be presenting feature of renal cell carcinoma
Affected testis may be smaller and bilateral varicoceles may affect
fertility

Management

 Testicular malignancy is always treated with orchidectomy via an inguinal

approach. This allows high ligation of the testicular vessels and avoids
exposure of another lymphatic field to the tumour.
 Torsion is commonest in young teenagers and the history in older children
can be difficult to elicit. Intermittent torsion is a recognised problem. The
treatment is prompt surgical exploration and testicular fixation.

- This can be achieved using sutures or by placement of the testis in a Dartos

pouch.

 Varicoceles are usually managed conservatively. If there are concerns about

testicular function of infertility then surgery or radiological management can
be considered.
  Epididymal cysts can be excised using a scrotal approach

 Hydroceles are managed differently in children where the underlying

pathology is a patent processus vaginalis and therefore an inguinal approach
is used in children so that the processus can be ligated.

- In adults a scrotal approach is preferred and the hydrocele sac excised or

plicated.

Balanitis
Balanitis is inflammation of the glans penis and sometimes extends to the underside
of the foreskin which is known as balanoposthitis.

There are a number of causes of balanitis and the most common causes are
infective (both bacterial and candidal) although there are a number of other
autoimmune causes that are important to know.

Simple hygiene is a key part of the treatment of balanitis and both improper washing
under the foreskin and the presence of a tight foreskin can make balanitis worse.

The presentation can either be acute or more chronic and children and adults are
affected by the causes differently.

Assessment:

 Most diagnoses are made clinically based on the history and examination.
 The history will tell you how acute the presentation is and other key features
that are important to note are whether there is itching or discharge.
 In the history also look for the presence of other systemic conditions
affecting the skin such as
o eczema,
o psoriasis
o connective tissue diseases.
o

The table below shows the clinical features associated with the most common causes
of balanitis, whether they occur in children or adults and how common they are:
 Acute or Children
Diagnosis Frequency Chronic? Features or Adults?
Candidiasis Very Acute Usually occurs after intercourse Both
common and associated with itching and
white non-urethral discharge
Dermatitis Very Acute Itchy, sometimes painful and Both
(contact or common occasionally associated with a
allergic) clear non-urethral discharge.
*Often there is no other body area
affected
Dermatitis Very Both Very itchy but not associated with Both
(eczema or common any discharge and there will be a
psoriasis) medical history of an
inflammatory skin condition with
active areas elsewhere on the
body
Bacterial Common Acute Painful and can be itchy with Both
yellow non-urethral discharge
and most often due
to Staphylococcus spp.
Anaerobic Common Acute May be itchy but is most Both
associated with a very offensive
yellow non-urethral discharge
Lichen planus Uncommon Both May be itchy, the main diagnostic More
feature is the presence of commonly
Wickham's striae and violaceous adults
papules
Lichen Rare Chronic May be itchy, associated with Both
sclerosus white plaques and can cause
(balanitis significant scarring
xerotica
obliterans)
Plasma cell Rare Chronic Not itchy with clearly Both
balanitis of circumscribed areas of
Zoon inflammation
Circinate Uncommon Both Not itchy and not associated with Adults
balanitis any discharge. The key feature is
painless erosions and it can be
associated with Reiter's syndrome

Investigations:

 The majority of conditions are diagnosed clinically based on the history and
physical appearance of the glans penis.
 In the cases of suspected infective causes a swab can be taken for
microscopy and culture which may demonstrate bacteria or Candida
albicans.
  When there is a doubt about the cause and there is extensive skin change,
then a biopsy can be helpful in confirming the diagnosis.

General treatment:

 There are three things which form the basis of management of all causes of
balanitis;
o gentle saline washes
o ensuring to wash properly under the foreskin
o more severe irritation and discomfort: Short-term 1% hydrocortisone

 When the cause is not clear, these measures can often resolve the condition
alone.

Specific treatment:

 In the case of candidiasis the treatment is with topical clotrimazole which

has to be applied for two weeks to fully treat the infection.
 Bacterial balanitis is most often due to Staphylococcus spp. or Group
B Streptococcus spp. and can be treated with oral flucloxacillin or
clarithromycin if penicillin allergic.
 Anaerobic balanitis is managed with saline washing and can also be managed
with topical or oral metronidazole if not settling.
 Dermatitis and circinate balanitis are managed with mild potency topical
corticosteroids (e.g. hydrocortisone)
 Lichen sclerosus and plasma cell balanitis of Zoon are managed with high
potency topical steroids (e.g. clobetasol).
 Circumcision can help in the case of lichen sclerosus.

Epididymo-orchitis
Epididymo-orchitis describes an infection of the epididymis +/- testes resulting in
pain and swelling. It is most commonly caused by local spread of infections from the
genital tract (such as Chlamydia trachomatis and Neisseria gonorrhoeae) or the
bladder.

**The most important differential diagnosis is testicular torsion. This needs to

be excluded urgently to prevent ischaemia of the testicle.

Features
  unilateral testicular pain and swelling
 urethral discharge may be present, but urethritis is often asymptomatic
 factors suggesting testicular torsion include patients < 20 years, severe pain
and an acute onset

Management

 the British Association for Sexual Health and HIV (BASHH) produced
guidelines in 2010
 if the organism is unknown BASHH recommend: ceftriaxone 500mg
intramuscularly single dose, plus doxycycline 100mg by mouth twice daily
for 10-14 days
 further investigations following treatment are recommended to exclude any
underlying structural abnormalities

Circumcision
Circumcision has been performed in a variety of cultures for thousands of years.

Today it is mainly people of the Jewish and Islamic faith who undergo circumcision
for religious/cultural reasons.

Circumcision for religious or cultural reasons is not available on the NHS.

The medical benefits of routine circumcision remain controversial although some

evidence has emerged that it:

 reduces the risk of penile cancer

 reduces the risk of UTI
 reduces the risk of acquiring sexually transmitted infections including HIV

Medical indications for circumcision

 phimosis
 recurrent balanitis
 balanitis xerotica obliterans
 paraphimosis

It is important to exclude hypospadias prior to circumcision as the foreskin may be

used in surgical repair. Circumcision may be performed under a local or general
anaesthetic.
Cryptorchidism
A congenital undescended testis is one that has failed to reach the bottom of the
scrotum by 3 months of age. At birth up to 5% of boys will have an undescended
testis, post natal descent occurs in most and by 3 months the incidence of
cryptorchidism falls to 1-2%. In the vast majority of cases the cause of the
maldescent is unknown. A proportion may be associated with other congenital
defects including:

Patent processus vaginalis

Abnormal epididymis
Cerebral palsy
Mental retardation
Wilms tumour
Abdominal wall defects (e.g. gastroschisis, prune belly syndrome)

Differential diagnosis
These include retractile testes and, in the case of absent bilateral testes the possibility
of intersex conditions. A retractile testis can be brought into the scrotum by the
clinician and when released remains in the scrotum. If the examining clinician notes
the testis to return rapidly into the inguinal canal when released then surgery is
probably indicated.

Reasons for correction of cryptorchidism

 Reduce risk of infertility

 Allows the testes to be examined for testicular cancer
 Avoid testicular torsion
 Cosmetic appearance
Males with undescended testis are 40 times as likely to develop testicular cancer
(seminoma) as males without undescended testis
The location of the undescended testis affects the relative risk of testicular cancer
(50% intra-abdominal testes)

Treatment

 Orchidopexy at 6- 18 months of age. The operation usually consists of

inguinal exploration, mobilisation of the testis and implantation into a dartos
pouch.
 Intra-abdominal testis should be evaluated laparoscopically and mobilised.
Whether this is a single stage or two stage procedure depends upon the exact
location.
  After the age of 2 years in untreated individuals the Sertoli cells will degrade
and those presenting late in teenage years may be better served by
orchidectomy than to try and salvage a non functioning testis with an
increased risk of malignancy.

Erectile dysfunction
Erectile dysfunction (ED) is the persistent inability to attain and maintain an erection
sufficient to permit satisfactory sexual performance.

It is a symptom and not a disease and the causes can broadly be split into organic,
psychogenic and mixed.

It is important to try and differentiate between organic and psychogenic causes of

erectile dysfunction.

Factors favouring a psychogenic

Factors favouring an organic cause causes
Gradual onset of symptoms Sudden onset of symptoms
Lack of tumescence Decreased libido
Normal libido Good quality spontaneous or self-
stimulated erections
Major life events
Problems or changes in a relationship
Previous psychological problems
History of premature ejaculation

Other than increasing age, risk factors include:

 cardiovascular disease risk factors: obesity, diabetes mellitus, dyslipidaemia,

metabolic syndrome, hypertension, smoking
 alcohol use
 drugs: SSRIs, beta-blockers

Investigations

As part of the assessment for erectile dysfunction Clinical Knowledge Summaries

(CKS) recommend that all men have their 10-year cardiovascular risk calculated by
measuring lipid and fasting glucose serum levels.

Free testosterone should also be measured in the morning between 9 and 11am.
If free testosterone is low or borderline, it should be repeated along with:
- follicle-stimulating hormone
- luteinizing hormone
- prolactin levels.

If any of these are abnormal refer to endocrinology for further assessment.

Management

PDE-5 inhibitors (such as sildenafil, 'Viagra') have revolutionised the management of

ED

 they should be prescribed (in the absence of contraindications) to all patients

regardless of aetiology
 sildenafil can be purchased over-the-counter without a prescription.

Vacuum erection devices are recommended as first-line treatment in those who

can't/won't take a PDE-5 inhibitor.

Other points

 for a young man who has always had difficulty achieving an erection, referral
to urology is appropriate
 people with erectile dysfunction who cycle for more than three hours per
week should be advised to stop

Vasectomy
Male sterilisation - vasectomy

 failure rate: 1 per 2,000 - male sterilisation is a more effective method of

contraception than female sterilisation
 simple operation, can be done under LA (some GA), go home after a couple of
hours
 doesn't work immediately
 semen analysis needs to be performed twice following a vasectomy before a
man can have unprotected sex (usually at 16 and 20 weeks)
 complications: bruising, haematoma, infection, sperm granuloma, chronic
testicular pain (affects between 5-30% men)
 the success rate of vasectomy reversal is up to 55%, if done within 10 years,
and approximately 25% after more than 10 years
Testicular disorders

Testicular cancer
Testicular cancer is the most common malignancy in men aged 20-30 years. Around
95% of cases of testicular cancer are germ-cell tumours. Germ cell tumours may
essentially be divided into:

Tumour
Tumour type Key features markers Pathology
Seminoma  Commonest  AFP usually Sheet like
subtype normal lobular patterns
(50%)  HCG elevated of cells with
 Average age in 10% substantial
at diagnosis = seminomas fibrous
40  Lactate component.
 Even dehydrogenase; Fibrous septa
advanced elevated in 10- contain
disease 20% seminomas lymphocytic
associated (but also in many inclusions and
with 5 year other conditions) granulomas may
survival of be seen.
73%
Non seminomatous germ  Younger age at  AFP elevated Heterogenous
cell tumours (42%) presentation =20-30 in up to 70% of texture with
years cases occasional
 Teratoma  Advanced disease  HCG elevated ectopic tissue
 Yolk sac tumour carries worse in up to 40% of such as hair
 Choriocarcinoma prognosis (48% at 5 cases
 Mixed germ cell years)  Other markers
tumours (10%)  Retroperitoneal rarely helpful
lymph node
dissection may be
needed for residual
disease after
chemotherapy

Image demonstrating a classical seminoma, these tumours are typically more uniform
than teratomas
 Image sourced from Wikipedia

Risk factors for testicular cancer

 Cryptorchidism
  Infertility
 Family history
 Klinefelter's syndrome
 Mumps orchitis

Features

 A painless lump is the most common presenting symptom

 Pain may also be present in a minority of men
 Other possible features include hydrocele, gynaecomastia

Diagnosis

 Ultrasound is first-line
 CT scanning of the chest/ abdomen and pelvis is used for staging
 Tumour markers (see above) should be measured

Management

 Orchidectomy (Inguinal approach)

 Chemotherapy and radiotherapy may be given depending on staging
 Abdominal lesions >1cm following chemotherapy may require retroperitoneal
lymph node dissection.

Prognosis is generally excellent

 5 year survival for seminomas is around 95% if Stage I

 5 year survival for teratomas is around 85% if Stage I

Benign disease

Epididymo-orchitis
Acute epididymitis is an acute inflammation of the epididymis, often involving the
testis and usually caused by bacterial infection.

 Infection spreads from the urethra or bladder. In men <35 years, gonorrhoea
or chlamydia are the usual infections.
 Amiodarone is a recognised non infective cause of epididymitis, which
resolves on stopping the drug.
 Tenderness is usually confined to the epididymis, which may facilitate
differentiating it from torsion where pain usually affects the entire testis.
Testicular torsion

 Twist of the spermatic cord resulting in testicular ischaemia and necrosis.

 Most common in males aged between 10 and 30 (peak incidence 13-15 years)
 Pain is usually severe and of sudden onset.
 Cremasteric reflex is lost and elevation of the testis does not ease the pain.
 Treatment is with surgical exploration. If a torted testis is identified then both
testis should be fixed as the condition of bell clapper testis is often bilateral.

Hydrocele

 Presents as a mass that transilluminates, usually possible to 'get above' it on

examination.
 In younger men it should be investigated with USS to exclude tumour.
 In children it may occur as a result of a patent processus vaginalis.
 Treatment in adults is with a Lords or Jabouley procedure.
 Treatment in children is with trans inguinal ligation of PPV.

Testicular cancer
Testicular cancer is the most common malignancy in men aged 20-30 years. Around
95% of cases of testicular cancer are germ-cell tumours. Germ cell tumours may
essentially be divided into:

 seminomas
 non-seminomas: including embryonal, yolk sac, teratoma and
choriocarcinoma

Non-germ cell tumours include Leydig cell tumours and sarcomas.

The peak incidence for teratomas is 25 years and seminomas is 35 years. Risk factors
include:

 infertility (increases risk by a factor of 3)

 cryptorchidism
 family history
 Klinefelter's syndrome
 mumps orchitis

Features
  a painless lump is the most common presenting symptom
 pain may also be present in a minority of men
 other possible features include hydrocele, gynaecomastia
 AFP is elevated in around 60% of germ cell tumours
 LDH is elevated in around 40% of germ cell tumours
 seminomas: hCG may be elevated in around 20%

Diagnosis

 ultrasound is first-line

Management

 treatment depends on whether the tumour is a seminoma or a non-seminoma

 orchidectomy
 chemotherapy and radiotherapy may be given depending on staging and
tumour type

Prognosis is generally excellent

 5 year survival for seminomas is around 95% if Stage I

 5 year survival for teratomas is around 85% if Stage I

Testicular torsion
Basics

 twist of the spermatic cord resulting in testicular ischaemia and necrosis.

 most common in males aged between 10 and 30 (peak incidence 13-15 years)

Features

 pain is usually severe and of sudden onset

 the pain may be referred to the lower abdomen
 nausea and vomiting may be present
 on examination there is usually a swollen, tender testis retracted upwards. The
skin may be reddended
 cremasteric reflex is lost and elevation of the testis does not ease the pain
Management

 treatment is with surgical exploration. If a torted testis is identified then both

testis should be fixed as the condition of bell clapper testis is often bilateral.

Acute bacterial prostatitis

Acute bacterial prostatitis is typically caused by gram-negative bacteria entering the
prostate gland via the urethra.

Escherichia coli is the most commonly isolated pathogen.

Risk factors for acute bacterial prostatitis include

- recent urinary tract infection,
- urogenital instrumentation,
- intermittent bladder catheterisation
- recent prostate biopsy.

Features
 the pain of prostatitis may be referred to a variety of areas including the
perineum, penis, rectum or back
 obstructive voiding symptoms may be present
 fever and rigors may be present
 digital rectal examination: tender, boggy prostate gland

Management
 Clinical Knowledge Summaries currently recommend a 14-day course of a
quinolone
 consider screening for sexually transmitted infections

Prostate cancer: PSA testing

Prostate specific antigen (PSA) is a serine protease enzyme produced by normal and
malignant prostate epithelial cells.

Age-adjusted upper limits for PSA were recommended by the PCRMP:

Age PSA level (ng/ml)

50-59 years 3.0
60-69 years 4.0
> 70 years 5.0

However, NICE Clinical Knowledge Summaries currently suggest a different cut-off:

 men aged 50-69 years should be referred if the PSA is >= 3.0 ng/ml OR
there is an abnormal DRE
 note this is a lower threshold than the PCRMP 60-69 years limits
recommended above

PSA levels may also be raised by*:

 benign prostatic hyperplasia (BPH)

 prostatitis and urinary tract infection (NICE recommend to postpone the PSA
test for at least 1 month after treatment)
 ejaculation (ideally not in the previous 48 hours)
 vigorous exercise (ideally not in the previous 48 hours)
 urinary retention
 instrumentation of the urinary tract

Poor specificity and sensitivity

 around 33% of men with a PSA of 4-10 ng/ml will be found to have prostate
cancer. With a PSA of 10-20 ng/ml this rises to 60% of men
 around 20% with prostate cancer have a normal PSA
 various methods are used to try and add greater meaning to a PSA level
including age-adjusted upper limits and monitoring change in PSA level with
time (PSA velocity or PSA doubling time)

*whether digital rectal examination actually causes a rise in PSA levels is a matter of
debate
Prostate cancer
Prostate cancer a common condition and up to 30,000 men are diagnosed with the
condition each year. Up to 9,000 will die in the UK from the condition per year.

Diagnosis

Early prostate cancers have few symptoms.

Metastatic disease may present as bone pain.
Locally advanced disease may present as pelvic pain or with urinary symptoms.
Prostate specific antigen measurement
Digital rectal examination
Trans rectal USS (+/- biopsy)
MRI/ CT and bone scan for staging.

PSA Test

The normal upper limit for PSA is 4ng/ml. However, in this group will lie patients with
benign disease and some with localised prostate cancer. False positives may be due
to prostatitis, UTI, BPH, vigorous DRE.
The percentage of free: total PSA may help to distinguish benign disease from
cancer. Values of <20% are suggestive of cancer and biopsy is advised.

Pathology

 95% adenocarcinoma
 In situ malignancy is sometimes found in areas adjacent to cancer. Multiple
biopsies needed to call true in situ disease.
 Often multifocal- 70% lie in the peripheral zone.
 Graded using the Gleason grading system, two grades awarded 1 for most
dominant grade (on scale of 1-5) and 2 for second most dominant grade
(scale 1-5). The two added together give the Gleason score. Where 2 is best
prognosis and 10 the worst.
  Lymphatic spread occurs first to the obturator nodes and local extra prostatic
spread to the seminal vesicles is associated with distant disease.

Treatment

 Watch and wait- Elderly, multiple co-morbidities, low Gleason score

 Radiotherapy (External)- Both potentially curative and palliative therapy
possible. Similar survival figures to surgery. However, radiation proctitis and
rectal malignancy are late problems. Brachytherapy is a modification allowing
internal radiotherapy.
 Surgery- Radical prostatectomy. Surgical removal of the prostate is the
standard treatment for localised disease. The robot is being used increasingly
for this procedure. As well as the prostate the obturator nodes are also
removed to complement the staging process. Erectile dysfunction is a
common side effect.
 Hormonal therapy- Testosterone stimulates prostate tissue and prostatic
cancers usually show some degree of testosterone dependence. 95% of
testosterone is derived from the testis and bilateral orchidectomy may be
used for this reason. Pharmacological alternatives include LHRH analogues
and anti androgens (which may be given in combination).
 In the UK the National Institute for Clinical Excellence (NICE) suggests that
active surveillance is the preferred option for low risk men. It is particularly
suitable for men with clinical stage T1c, Gleason score 3+3 and PSA density <
0.15 ng/ml/ml who have cancer in less than 50% of their biopsy cores, with <
10 mm of any core involved.
Candidates for active surveillance should:

 have had at least 10 biopsy cores taken

 have at least one re-biopsy.
If men on active surveillance show evidence of disease progression, offer radical
treatment. Treatment decisions should be made with the man, taking into account
co-morbidities and life expectancy.

Prostate cancer: features

Prostate cancer is now the most common cancer in adult males in the UK and is the second
most common cause of death due to cancer in men after lung cancer.

Risk factors

 increasing age
 obesity
 Afro-Caribbean ethnicity
 family history: around 5-10% of cases have a strong family history
Localised prostate cancer is often asymptomatic. This is partly because cancers tend to
develop in the periphery of the prostate and hence don't cause obstructive symptoms early on.
Possible features include:

 bladder outlet obstruction: hesitancy, urinary retention

 haematuria, haematospermia
 pain: back, perineal or testicular
 digital rectal examination: asymmetrical, hard, nodular enlargement with loss of
median sulcus

© Image used on license from Radiopaedia

Isotope bone scan (using technetium-99m labelled diphosphonates which accumulate in the bones) from a
patient with metastatic prostate cancer. The scan demonstrates multiple, irregular, randomly distributed foci of
high grade activity involving the spine, ribs, sternum, pelvic and femoral bones. The findings are in keeping
with multiple osteoblastic metastasis.

Prostate cancer: investigation

The traditional investigation for suspected prostate cancer was a transrectal
ultrasound-guided (TRUS) biopsy.

However, recent guidelines from NICE have now advocated the increasing use
of multiparametric MRI as a first-line investigation.

Complications of TRUS biopsy:

 sepsis: 1% of cases
 pain: lasting >= 2 weeks in 15% and severe in 7%
 fever: 5%
 haematuria and rectal bleeding

Multiparametric MRI is now the first-line investigation for people with suspected
clinically localised prostate cancer.

 the results are reported using a 5-point Likert scale

If the Likert scale is >=3 a multiparametric MRI-influenced prostate biopsy is offered

If the Likert scale is 1-2 then NICE recommend discussing with the patient the pros
and cons of having a biopsy.

Prostate cancer: management

Localised prostate cancer (T1/T2)

Treatment depends on life expectancy and patient choice. Options include:

 conservative: active monitoring & watchful waiting

 radical prostatectomy
 radiotherapy: external beam and brachytherapy

Localised advanced prostate cancer (T3/T4)

Options include:

 hormonal therapy: see below

 radical prostatectomy: erectile dysfunction is a common complication
 radiotherapy: external beam and brachytherapy. Patients are at increased risk
of bladder, colon, and rectal cancer following radiotherapy for prostate cancer
Metastatic prostate cancer disease - hormonal therapy

Synthetic GnRH agonist

 e.g. Goserelin (Zoladex)

 cover initially with anti-androgen (i.e. Flutamide) to prevent rise in
testosterone

Anti-androgen

 cyproterone acetate prevents DHT binding from intracytoplasmic protein

complexes

Orchidectomy

TURP syndrome
TURP syndrome is a rare and life-threatening complication of transurethral
resection of the prostate surgery.

The pathophysiology is venous destruction and absorption of the irrigation fluid.

There are risk factors for developing TURP syndrome are :

 surgical time > 1 hr

 height of bag > 70cm
 resected > 60g
 large blood loss
 perforation
 large amount of fluid used
 poorly controlled CHF

Post prostatectomy syndromes

Transurethral prostatectomy is a common and popular treatment for benign
prostatic hyperplasia. The procedure involves insertion of a resectoscope via the
penile urethra. The bladder and prostate are irrigated and strips of prostatic tissue
removed using diathermy.
Complications include haemorrhage, urosepsis, retrograde ejaculation and
electrolyte disturbances from the irrigation fluids used during surgery.

Complications of Transurethral Resection: TURP

T ur syndrome
U rethral stricture/UTI
R etrograde ejaculation
P erforation of the prostate

Benign prostatic hyperplasia

Benign prostatic hyperplasia (BPH) is a common condition seen in older men.

Risk factors

 age: around 50% of 50-year-old men will have evidence of BPH and 30% will
have symptoms. Around 80% of 80-year-old men have evidence of BPH
 ethnicity: black > white > Asian

BPH typically presents with lower urinary tract symptoms (LUTS), which may be
categorised into:

 voiding symptoms (obstructive): weak or intermittent urinary flow, straining,

hesitancy, terminal dribbling and incomplete emptying
 storage symptoms (irritative) urgency, frequency, urgency incontinence and
nocturia
 post-micturition: dribbling
 complications: urinary tract infection, retention, obstructive uropathy

Management options

 watchful waiting
 medication: alpha-1 antagonists, 5 alpha-reductase inhibitors. The use of
combination therapy was supported by the Medical Therapy Of Prostatic
Symptoms (MTOPS) trial
 surgery: transurethral resection of prostate (TURP)
Alpha-1 antagonists e.g. tamsulosin, alfuzosin

 decrease smooth muscle tone (prostate and bladder)

 considered first-line, improve symptoms in around 70% of men
 adverse effects: dizziness, postural hypotension, dry mouth, depression

5 alpha-reductase inhibitors e.g. finasteride

 block the conversion of testosterone to dihydrotestosterone (DHT), which is

known to induce BPH
 unlike alpha-1 antagonists causes a reduction in prostate volume and hence
may slow disease progression. This however takes time and symptoms may
not improve for 6 months. They may also decrease PSA concentrations by up
to 50%
 adverse effects: erectile dysfunction, reduced libido, ejaculation problems,
gynaecomastia