Surgery Revision PDF

lOMoARcPSD|4776960
Surgery revision pdf
Medicine (Queen's University Belfast)
StuDocu is not sponsored or endorsed by any college or university

Downloaded by Vi Ma (vinibala11@gmail.com)
lOMoARcPSD|4776960
General Surgery
Michael Grant
Notes based on QUB online Med Portal lectures, QUB student manual, Oxford Clinical
handbook and various external online resources
lOMoARcPSD|4776960
Surgery: Page 2 of 85
1 Acute Abdomen
The emergencies of the GI tract are important to recognise and treat; patients need to
have adequate resus followed by specific management. Surgical emergencies can be
divided classified by their location:
l Oesophagus
- Acute dysphagia
l Presentation - cannot swallow
l May have benign stricture or malignant neoplasm (especially
exophitic)
l Triggered by food bolus or tablet
l Treatment
§ Remove bolus by endoscopy then deal with underlying
oesophageal disease
- Perforation
l High mortality
l Causes – Iatrogenic 55% (i.e. Post-OGD esp. if there is benign/malignant stricture), Boerhaave syndrome 10%
(excessive vomiting), pill esophagitis, Barrett's oesophagus, infectious ulcers (e.g. Herpes in AIDs), corrosives
l Presentation – acute chest/abdominal pain, odynophagia,
l CXR - Air in mediastinum and subcutaneous emphysema (crackling sensation over skin) and, if Boerhaave, +
exudative pleural effusion
l Treatment
§ Benign causes are treated with surgery (followed by PPI, ABx)
§ If due to malignant ulcer, then intubation
- Bleeding
l Causes - Oesophagitis, Mallory Weiss, Varices
l Variceal bleeding – tends to be most severe & can be catastrophic – use Rockall Score and/or AIMS65
l Treatment of Varices
§ Firstly, stabilise: Fluids, Blood transfusion, IV Omeprazol (80mg – 40mg BID) somatostatin/octreotide
(25mcg bolus then 25mcg/hr IVI) GH–inhibiting hormone & synthetic; are vasoconstrictors), Erythromycin
(Promotility, enhances visualization on OGD, 3 mg/kg IV over 20mins prior to OGD), Sengstaken-
blakemore tube,
§ Move on to definitive treatment, e.g. band ligation/stent insertion (later especially if longterm alco)
l Stomach/duodenum
- Perforation
l Presentation - abdominal pain, rigidity/prostration, peritonism, shock, pneumoperitoneum X-ray
l Treatment - ABx, resuscitate, followed by surgical repair
- Bleeding
l Presentation: Haematemesis +/- Melaena, if severe; Increased HR>90, Fall BP<100
l Causes: Erosions (NSAIDs, alcohol) PUD - either DU or GU
l Treatment: Transfusion, identify cause, inject DU during OGD
§ Non-variceal bleeding: Injection with 1:10,000 adrenaline, thermal coag. w/ adrenaline, mechanical clips,
Fibrin or Throbin (w/ adrenaline); followed by PPI treatment post-op
§ Resistant/recurrant: surgery to oversew ulcer, consider more extreme surgeries – selective vagotomy
(vagus supply to lower oesophagus and stomach interrupted by nerve of Latarget left intact for pylorus
function), gastrectomy (Billroth, Billroth 2, Roux-en-Y)
l Gallbladder/Biliary Tract
- Cholecystitis
l Presentation: Acute RUQ pain, +/- Pyrexia, +/- Rigors, Murphey’s sign or sonographic Murphy sign (max
pain when visualising GB)
l Diagnosis – FBC, WBCC, USS (shows gallstones and gallbladder wall thickening >3mm)
l Treatment: Antibiotics, analgesics, early surgery
- Cholangitis
l Presentation: Acute RUQ pain, +/- Pyrexia, +/- Rigors (also seen in Charcot's triad for ascending
cholangitis; if low BP and altered mental status, then it is Reynolds' pentad),
- Obstructive jaundice
l Yellow skin, sclerae, pruritus, pale stools, dark urine, +/- Pain, Murphey’s sign, +/- Courvoisier’s
sign (palpably enlarged, non-tender gallbladder, accompanied with painless jaundice means the
cause is unlikely to be gallstones)
l CT – dilated bile ducts, mass in pancreas, gallstones
l Establish diagnosis – Gallstones, Ca Head of Pancreas (esp. if pain free)
l Appropriate treatment, e.g. ERCP, cholecystectomy, Whipples’
l Pancreas
- Acute pancreatitis
- Presentation: Constant pain, vomiting, shock
- Causes: Gallstones, or alcohol
- Diagnosis: Serum amylase elevation (+/- LFTs), USS
- Complications: pseudocyst (collection in lesser sac), phlegmon (spreading diffuse inflammatory process with
formation of purulent exudate – usually without bacterial infection), abscess
Michael Grant
lOMoARcPSD|4776960
l Small intestine
- Intestinal obstruction
l May arise due to adhesions, hernia, tumour (usually a large bowel
tumour that the small has become adherent to rather than
primary)
l Presentation: Colicky abdominal pain, vomiting, absolute
constipation (no feaces or flatus)
l XR: Valvulae conniventes, rigler’s sign
l Treatment:
l General principles: Cause, site, speed of onset, and
completeness of obstruction determine definitive therapy:
strangulation and large bowel obstruction require surgery;
ileus and incomplete small bowel obstruction can be
managed conservatively, at least initially
l Immediate action: ‘Drip and suck’—NGT and IV fluids to
rehydrate and correct electrolyte imbalance
l Surgery: Strangulation needs emergency surgery, as does ‘closed loop obstruction’; Stents may be used for obstructing
large bowel malignancies either in palliation
- Mesenteric Infarct
l Sudden occlusion of small bowel arterial supply by thrombus or other embolus
l Presentation: Classical clinical triad of acute severe abdominal pain; no abdominal signs; rapid
hypovolaemia leading to shock +/- peritonitis, rigidity, silent bowel sounds
l Treatment: resuscitate, operate ASAP
l Treat in order 1 septic peritonitis and 2 prevent SIRS becoming multi-organ dysfunction syndrome
(MODS), mediated by bacterial escape from dying bowel; Resuscitation with fluid, antibiotics
(gentamicin + metronidazole) and, usually, heparin are required
l If arteriography is done, thrombolytics may be infused locally via the catheter
l At surgery dead bowel must be removed. Revascularization may be attempted on potentially
viable bowel but it is a difficult process and often needs a 2nd laparotomy
- Infectious diarrhoea
- Crohn’s Disease
- Meckel’s Diverticulum
l Rare, diverticulum of terminal ileum from embryonic remnants of vitelline duct
containing gastric and/or pancreatic epithelium. There may be gastric acid secretion,
causing GI pain & occult bleeding - can present like appendicitis
l "2 inches long, within 2 feet of ileocecal valve, 2 times as common in males than
females, 2% of population, 2x2=4% symptomatic, 2 types of ectopic tissue: gastric and
pancreatic"
l Meckel’s Scan - Technetium-99m radionucleotide scan looks for ectopic gastric mucosa;
more sensitive and specific in children
l Complications: Perforation, Ulceration, Littre’s hernias (hernial sacs containing
strangulated Meckel’s)
l Large Bowel (+ App)
- Acute Appendicitis
- Acute Diverticulitis
l Outpouching of the gut wall, usually at sites of entry of perforating arteries
l Diverticulosis means that diverticula are present, and diverticular disease
implies they are symptomatic
l Maximal in (L) colon, usually in the Middle aged or elderly
l Presentation: LIF pain, fever, tenderness, leukocytosis
l CT abdomen is best to confirm acute diverticulitis and can identify extent/
complications
l Enema or colonoscopy risk perforation in the acute setting.
l Treatment: analgesia, NBM, IV fluids, antibiotics, CT-guided percutaneous
drainage (if abscess)
l Complications: Haemorrhage, perforation, fistula, abscesses, post-infective stricture
- Lower GI bleeding
l Causes: Diverticulum, colitis, Crohn’s, tumour
l Present with Fresh Red Blood P/R
l Tendency to be more conservative than with upper GI
l Treatment: Resuscitate, consider transfusion
- Perforation
l Causes: Diverticulum, colitis,
l Presentation: sudden severe abdominal pain, rigidity from faecal peritonitis, Pyrexia, shock
l AXR: Free gas on X-ray
l Treatment: Resuscitate, ABx, prepare to operate
- Intestinal obstruction
Michael Grant
lOMoARcPSD|4776960
- Uncontrolled ulcerative colitis
l Presents: bloody diarrhoea, pyrexia, leukocytosis and may develop toxic megacolon (acute form of
colonic distension characterised by a very dilated colon – can progress to perforation)
l Treatment: IV fluids, IV Steroids to management acute inflamm., surgery on failure
l Perintoneal cavity
- Peritonitis
l Causes: Any perforation, pancreatitis, inflamm. In adjacent organ
l Presentation: Abdominal pain, tenderness, guarding, silent abdomen, shock
l Treatment: Rx of underlying condition
- Intra-abdominal abscess
2 Acute Appendicitis
The appendix is a blind-ended tube connected to the cecum, from which it develops
embryologically. It is a vermiform (worm-like) organ found at the origin of the teniae coli (the 3
longitudinal ribbons of smooth muscle on the outside of large colon).
Incidence:
l Most common surgical emergency (lifetime incidence = 6%) and accounts for 2% of all hospital
admissions
l Can occur at any age, though highest incidence is between 10–20yrs - but is rare before age 2
because the appendix is cone shaped with a larger lumen
l Affects men more than woman but women have more operations for it
Pathogenesis:
l Gut organisms invade the appendix wall after lumen obstruction by:
o Lymphoid hyperplasia
o Faecolith (very impacted, potentially calcifed, faeces)
o Filarial worms
o Tumour
o Foreign body
o Secondary bacterial infection
l This leads to oedema, ischaemic necrosis and perforation
Symptoms/Signs:
l Crampy colicky abdominal periumbilical pain
o Usually becomes sharper and more localised pain to the RIF
l Maximal tenderness of McBurneys point (two thirds of the way from umbilicus
to ASIS) as inflammation moves to parietal peritoneum
l Anorexia is an important feature; vomiting is rarely prominent — pain normally
precedes vomiting in the surgical abdomen; likely to smell fetor
l Constipation is usual but diarrhoea may also occur (esp. if pelvic appendix)
l Urinary symptoms can occur with retrocecal appendix, direct inflammation
spread to right ureter
l Abdominal mass may be felt – important to establish if this is cancer or appendix
mass
l Specific signs:
o Rovsing’s – pain in RIF increases on palpation of LIF
o Psoas sign – pain on flexion of right hip, as retrocecal appendix contacts
psoas
o Obturator/Cope’s sign – pain on internal rotation and flexion of right hip, as
appendix contacts obturator internus
o Tender right sided PR examination – may be only sign on low-lying pelvic
appendix
Investigations:
l Predominantly a clinical Diagnosis
l WCC – left shift of white cells, neutrophil leucocytosis
l URINE – rule out stone or UTI
l PREGNANCY TEST
l Scoring Systems - ALVARADO
l USS Appendix – and consider ordering USS Pelvis/Renal tracts (rule out stones)
l CT has high accuracy and useful in situations where the differential is unclear – but do not delay surgery
for this if patient unstable
Treatment:
l If diagnosis unclear: Observation, analgesia, IV fluids and reassessment
o Appendix mass can result from inflamed appendix wrapped by omentum; Some advocate early
surgery but a trial of conservative management —NBM and antibiotics
§ If mass resolves, an interval appendicectomy (i.e. delayed) can be considered
§ If deterioration, then there is the possibility that an appendix abscess has form: surgical
drainage by laparotomy or CT/US guided percutaneous is required
Michael Grant
lOMoARcPSD|4776960
l If diagnosis clear:
o Prompt appendicectomy:
§ Lanz laparotomy (muscle sparing)
§ Grid iron laparotomy (muscle cutting, risk of hernia)
§ Laparoscopy - Has diagnostic and therapeutic advantages especially in
women and the obese but not recommended in cases of suspected
gangrenous perforation as the rate of abscess formation
o ABx: Metronidazole 500mg/8h + cefuroxime 1.5g/8h, IV starting 1h pre-op,
reduces wound infections
§ Give a longer course depending on severity, assessed visually:
• Inflammed/injected – single dose
• Purulent Exudate – 48hrs
• Perforated – 5 day treatment
§ Any pus is sent for culture
o If appendix normal (10-20% cases) - still removed and other causes excluded, e.g.
Meckel’s
Complications:
l Short term
o Post-op Ileus
o Infection
o Wound
o Pelvic Abscess
§ Failure of Appendix stump ligation
o Urinary retention, Pneumonia, DVT, PE
l Longer term
o Hernia (esp. if Grid Iron used)
o Adhesions
l Hospital stay
o Uncomplicated 24-48hrs
o Complicated - variable
o Return to normal activities in 2-8 weeks depending on severity and post op complications
3 Fluids and Electrolytes
Michael Grant
lOMoARcPSD|4776960
4 Hernia
The definition of a hernia is “The abnormal protrusion of all or part of an organ through an opening in
the cavity in which it is usually contained”.
However, the main focus of our course in general surgery is the inguinal hernia. This is the protrusion of
the contents of the abdominal cavity or pre-peritoneal fat through a defect in the inguinal area. These
types of hernia can be best thought of as consisting of a neck, sac and contents.
It is very common and 15% of males over the age of 75 will have had inguinal hernia repair, with a total
lifetime incidence of up to 20%. They can be described as reducible (or irreducible if their contents
cannot be pushed back into place), incarcerated (contents of sac are stuck inside by adhesions),
obstructed (bowel contents are unable to pass through herniated segment) or strangulated (if ischaemia
occurs). Reduction should be performed as a part of assessment, however it is important to avoid
reduction en masse, in which a strangulated bowel and sac back into the abdominal cavity – still in a
strangulated configuration.
The inguinal canal is a 4cm passage than transverse the 4 muscle layers of the abdomen (made up of
external oblique, internal oblique, transverus abdominus and rectus abdominus). It’s design allows for it to
withstand changes in intra-abdominal pressure by using an oblque passage. It’s anterior wall protected by
external oblique, poster wall by conjoint tendon that allow the canal to be flattened when these muscles are contracted.
Superior wall (roof):

Medial crus of
aponeurosis of external
oblique
Musculoaponeurotic
arches of internal oblique
and transverse abdominal
Transversalis fascia
Anterior wall: Posterior wall (floor):
aponeurosis of transversalis fascia
external oblique conjoint tendon (inguinal
Fleshy part of falx,reflected part of inguinal
internal oblique ligament, medial third of canal
(inguinal canal)
(lateral third of only)[4]
canal only)[3] Deep inguinal ring (lateral third of
superficial inguinal canal only – lies just medial to
ring (medial third of position of femoral pulse, 40% of
canal only)[4] way from ASIS to pubic tubercle
Inferior wall:
Inguinal ligament
Lacunar ligament (medial
third of canal only)[4]
Iliopubic tract (lateral third
of canal only)[3]
The classic description of the contents of spermatic cord in the male are:
• 3 arteries: artery to vas deferens (or ductus deferens), testicular artery, cremasteric artery;
• 3 fascial layers: external spermatic, cremasteric, and internal spermatic fascia;
• 3 nerves: genital branch of the genitofemoral nerve (L1/2), sympathetic and visceral afferent fibres, ilioinguinal nerve (N.B. outside
spermatic cord but travels next to it and only passes through the superficial ring before descending into the scrotum)
Michael Grant
lOMoARcPSD|4776960
• 3 other structures: pampiniform plexus, vas deferens (ductus deferens), testicular lymphatics
Aetiology:
• Patent processus vaginalis – embryonic failure of processus to fuse (most common cause, in 4% of all male infants; if found in female, rule
out testicular feminisation)
• Collagen disorder – in older adults, weaker collagen is produced
• AAA – similar to above, if collagen is week in the aorta it may also be weak in the canal
• Cigarette smoking and COPD – both from coughing and changes to collagen make-up
• Ascites/Continuous Ambulatory Peritoneal Dialysis/
• Long term heavy work
• Constipation/chronic urinary retention
• African heritage (narrow, taller hip)
Examination:
1. Ask patient to lay supine and inspect area for scars
2. Ask patient to cough and look to see if impulse is visible and increases size of lump
3. Ask if lump is visible and for patient to point out
4. Palpate and ask patient if they can reduce it (if not, rule out the possibility of a scrotal lump)
5. To determine if inguinal or femoral (more common in women):
a. Inguinal – point of exit from abdomen will be above and medial to pubic tubercle
b. Femoral – point of exit from abdomen will be below and lateral to pubic tubercle
6. If inguinal, to determine if direct or indirect (although not clinical relevant as management is
the same):
a. Reduce the hernia and occlude the deep inguinal ring (1.5cm above femoral
pulse at the mid-inguinal point)
b. Ask patient to stand or cough – if hernia remains reduced then it is indirect (i.e. comes through the deep inguinal ring lateral
to inf. Epigastric vessels) but if not then it is direct (i.e. bowel comes directly through hesselbach’s triangle – medial to inf.
Epigastrics and lateral to rectus abdominus)
Pre-operative:
• Is operation necessary? Older patients with no symptoms; does risk outweigh benefit?
• Suitable for day surgery? Halves the cost of operation.
• Explain procedure and alternatives; e.g. attempt at conservative management (weight loss and smoking cessation)
• Counsel regarding risks: chronic pain, infection, bleeding, recurrence
• Old advice was 4 weeks rest and 10 weeks convalescence but now, with modern mesh and
laparoscopic techniques, can return to work and driving in 2 weeks or less if feeling up to it:
o Walk from hour one
o Encourage activity
o Return to work 5 to 7 days
o Avoid heavy lifting for one month
Operative management
• Herniotomy – only really suitable for paeds with patent processus vaginalus, and simply
involves ligation of the proximal sac
• Lichtenstein Tension-Free Hernia Repair
o An open technique that involves dissecting into the inguinal canal, cutting open the
peritoneum that forms the sac of the hernia, pushing the bowel contents back into the
abdomen followed by ligating and/or removing the sac.
o A polypropylene mesh is the stitched in to reinforce the deep inguinal ring to prevent
recurrence
• Laparoscopic (preferable in recurrent and bilateral hernias) both can similar steps but TAPP
requires access into the peritoneum and thus has an additional incision that increases risk of
visceral damage.
o TAPP (transabdominal preperitoneal) repair
o TEP (totally extraperitoneal) repair
§ Blunt dissection and insertion of ports into pre-peritoneal space
§ Complete dissection of pre-peritoneal space
§ Dissection of retro-pubic space
§ Dissection of hernia
§ Placement of mesh
Complications:
These are significant issue, however 95% have no early/immediate complications
• Pain – especially chronic pain (44% of patients have long-term mild-moderate pain)
• Recurrence
• Haematoma
• Infection
• Urinary retention
Michael Grant
lOMoARcPSD|4776960
5 Pre-operative assessments
Goals of pre-assessment:
l Improve efficiency and enhance patient care
l Identify potential problems
l Plan appropriate investigations and referrals
l Risk assessment
l Enable liaison with surgical team
l Patient education / counselling
The toll of major surgery on the energy reserves of patients is considerable, i.e. equivalent to
running a half-marathon or marathon for a fit personMajor surgery produces an inflammatory
response that increases metabolic demands – increased heart rate is needed to accommodate
oxygenation this so patients should be assessed for cardiac redundancy. Return to pre-op levels of
fitness can take 3 to 6 months.
A thorough assessment will include:

• History:
o PC – Presentation, effect on general health, treatment
o PMH - Cardiorespiratory conditions (surgery itself), reflux (airway), renal or hepatic (drug excretion), endocrine problems (stress
response)
§ Previous Anaesthetic Hx - Anaesthetic Difficulties, Airway problems, PON&V, Adverse Reactions
o Family Hx – unexplained ICU deaths, specific conditions
o Exercise tolerance - Physical Activity Levels & Limiting Factors
o Drug Hx
§ OCP/HRT – stop 4 weeks before (DVT/PE risk)
§ Aspirin – can probably be continued unless v. v. high risk
§ Beta-blockers – continue until day of surgery
§ Tricyclics – increase the action of adrenaline
• Examination:
o Full examination of systems
o Airway assessment:
§ Predictors of difficulty with ventilation:
• The Obese (body mass index > 26 kg/m2)
• The Bearded
• The Elderly (older than 55 y) – muscle wasting of
face
• The Snorers
• The Edentulous – no teeth
§ Assessment of airway:
• Look for Facial trauma/ Large incisors/ Beard/ Large tongue
• Evaluate 3-3-2: Inter-incisor distance (3 fingers), Hyoidmental distance (3
fingers), thyroid to floor of mouth (2fingers)
• Mallampati Grade
• Obstruction – swelling, foreign body
• Neck movement – chin to chest, and absence of severe RhA/Ank
Spond./Down’s/Acromegaly (others see box)
• Investigations:
o Bloods:
§ FBC - Should be performed if clinical signs of anaemia, bleeding disorders,
History of chemotherapy or large blood loss expected
§ U&E - Should be performed in over 70s, and with a potential abnormality- ie
diuretics, renal disease, diarrhoea or vomiting
§ Coag Screen - Only required if a history of bleeding disorder, anticoagulatant use,
liver disease or major surgery
§ Crossmatch - Either a group and save or a crossmatch should be performed
depending on the pre-operative Hb and the risk of blood loss
§ Finger prick glucose
o ECG – if older than 50 or if older than 45 and major surgery; cardiovascular disease
and/or severe renal disease.
o CXR - Indicated if an acute condition suspected ie chest infection, congestive cardiac
failure
o Echo - Maybe indicated for evaluation of undiagnosed murmur, dyspnoea or worsening
symptoms in CCF or valve disease
o Lateral cervical spine x-ray (flexed and extended) – if Hx of RhA/Ank Spond./Down’s
Michael Grant
lOMoARcPSD|4776960
Risk assessment:
• Patient factors – medical conditions, PMHx (esp. Cardiac, diabetes or renal) Urgency of
Surgery
• Surgical factors:
o Low risk <1% - endoscopic procedures, superficial, cataract, breast surgery
o Intermediate <1-5% - intraperitoneal, intrathoracic, head and neck, orthopaedic, prostate
o High >5% - aortic and major vessel surgery, peripheral vascular surgery
Functional Risk Cardiovascular
Functional capacity can be assessed by using The Duke Activity Status Index. It is a self-administered Status
Assessment Status
questionnaire that measures a patient's functional capacity by asking questions about patients ability to
complete certain activities (2 flights of stairs without stopping, cycling, swimming) and using this to estimate
the maximum number of METs (1 kcal/kg/hour – energy used sitting) they can generate.
Surgery Factors
Risk Prediction:
• American Society of Anaesthesiologists Status Classification:
Pre operative Management:

• Hold on day of surgery:
o Diuretics - unless severe heart failure
o ACE inhibitors & ARBs - depends on procedure & risk of hypotension
o Insulin & Oral Hypoglycaemics- most hospitals have protocol; switch
to insulin sliding scale
o Vitamins & Iron
• Preparation
o Bowel prep?
§ Meta-analysis shows no benefit and may increase anastomotic
leakage following GI
§ Indicated in colonoscopy for better visualisation
o Prophylactic ABx?
§ 20% of wound infection post-GI surgery so is indicated as a single dose pre-op (30 minutes for most, 2h for metronidazole)
§ Base drug choice on local policy
o DVT prophylaxis?
§ TED stockings, Flowtron, etc.
§ Enoxaparin can be given as 20mg (or 40mg if major-risk surgery) SC, started 2 hours pre-op
o Tubes?
§ Catheterise and/or insert NG tube
before induction if necessary
6 Gallstones

Biliary Tree anatomy:
• Portal confluence: joining of left and right
hepatic
• Ampulla of Vader enters 2nd part of duodenum
• Gallblader is musclular sac - Cholecystokinin is synthesized and secreted by enteroendocrine cells
in the duodenum, causes the release of digestive enzymes and bile from the pancreas and
gallbladder
Gallstone formation:
Stones form when there is a set of pro-lithogenic factors:
Michael Grant
lOMoARcPSD|4776960
1. Lithogenic bile – bile saturated with fats becomes known as sludge (increased cholesterol,
decreased phospholipids/lecithin, deacresed bile salts), which eventually promotes the
crystalisation of sludge contents to form macroscopic stones; this can be interpreted using
Admirand’s Triangle (to right)
2. Stasis – obstruction to flow, or reduce flow
3. Nidus – a place to accumulate; e.g. the gallbladder
Gallstone composition:
Stones are formed from different compounds that can be found in the lithogenic bile and only 10% are
radiopaque (however, may show radiopaque “porcelain”, calcified GB – 15% associated with cancer)
1. Mixed composition (80%)
• Cholesterol and calcium salts of bile pigments (calcium bilirubinate)
2. Pure cholesterol stones (8%)
• Large, egg shaped, solitary
3. Pure pigment stones (12%)
• High bilirubin disorders – e.g. haemolysis – small, friable and irregular
Epidemiology of stones:
• 12% men and 24% woman
• 10 – 30% become symptomatic
• Increasing prevalence with age
• Risk factors for mixed / cholesterol calculi
o Family history
o Obesity
o Diabetes
o Ileal resection
o Sudden weight loss (changes composition of bile)
Pathogenesis:
• Biliary Colic is symptomatic of cystic duct or CBD obstruction – with pain caused by smooth muscle
trying to force stone alone and increased pressure from backlog of bile
o Colicky epigastric pain that is poorly localised and may be associate with V&D for < 24 hours
§ May radiate to back
§ May RARELY present with jaundice also
o Fatty meals may precipitate the pain
o Mucocoele can follow – in which GB fills with mucous/pus secreted by GB wall
o Rx: Analgesia, rehydration, NBM
• Cholecystitis is caused by the impaction of sludge of stones in the neck of
gallbladder and is differentiated from biliary colic by it’s inflammatory
component (SIRS/Sepsis, local peritonism, fever, raised WBC, ect.); will be
Murphey’s sign +ve (two fingers palpating the RUQ will cause pain and arrest of
inspiration, w/o same in LUQ)
o Acute presents w/ epigastric or RUQ pain (radiated to R. shoulder), vomiting, fever, local peritonism or phelgmon (palpable GB mass
as omentum wraps around inflamed GB)
§ Empyema can form if infected and may lead to perforation (requiring emergency OPEN cholecystectomy)
§ Ix: WCC, USS may show: thick-walled shrunken GB, pericholecystic fluid, stones (with acoustic shadow), CBD dilation (>6mm)
• If USS unclear use HIDA cholescintigraphy - Tc-labled hepatobiliary iminodiacetic acid is injected through any accessible
vein and then allowed to circulate to the liver, where it is excreted into the bile ducts
§ Rx: Analgesia, fluids, NBM, ABx (usually cefuroxime), early or delayed cholecystectomy
o Chronic cholecystitis can be more difficult to diagnose due to vague symptoms: bloating, nausea, flatulence, fat intolerance
(cholecystokinin release)
§ Use USS to look for stones or CBD dilation before cholecystectomy
• If CBD dilation – use ERCP w/ sphincterotomy
• If symptoms remain after surgery consider: hiatus hernia, IBS, peptic ulcer, relapsing
pancreatitis
• Choledocholithiasis is the presence of dile duct stones
o Usually arise in gallbladder, multiple & enlarge in-situ to obstruct and dilated proximal tree
o Calculus impaction leads to obstructive jaundice
o Can be asymptomatic or lead to ascending cholangitis
• Pancreatitis can be caused by the passage of calculus through the pancreatic head
o Serum amylase greater than 3x upper of normal
o Gallstones commonest aetiological factor (35%-65%)
o Calculi versus sludge - sludge may not show up on scan but can cause pancreatitis
• Gallstone Ileus is small bowel obstruction due to a gallstone escaping into the GI tract via a cholecyst-duodenal fistula
o Presents w/ signs of obstruction (vomiting, nausea, pain, constipation)
o Usually in elderly with persistent inflam
o Typically lodges in terminal ileum (due to diameter) but can occasionally obstruct in the duodenum (Bouveret’s syndrome)
o AXR – gas in biliary tree (pneumobilia), radiopaque mass in RIF
Michael Grant
lOMoARcPSD|4776960
• Other:
o Perforation – can follow empyema but is typically rare due to dual blood supply of GB (cystic branch and branches of hepatic)
o Mirizzi’s syndrome – inflammation of stone in GB or cystic duct causes compression of CBD leading to obstructive jaundice
o Cholangitis – bile duct infection showing charcot’s triad (RUQ pain, jaundice, rigours [may be ascending cholangitis if + altered GCS
& shock – i.e. Reynolds’ pentad])
Investigations:
• Ultrasound scans – look for gallstones (and accompanying acoustic shadow), wall thickness, pericholecystic fluid, duct dilation (>6mm)
• MRCP – non-invasive, sensitive specific and accurate
o Contraindications: Claustrophobia, implanted devices, penetrating eye injuries (shrapnel, builders’ equipment, etc.)
Treatments:
• Medical:
o Ursodeoxycholic acid
§ Effective on multiple small stones made of exclusively cholesterol
calculi
§ Recurrence of gallstones on stopping treatment
§ Troublesome side effects: V&D, nausea, skin rash
• Surgical:
o Laproscopic cholecystectomy:
§ Minimally invasive with shorter hospital stay
§ Rapid return to full activity
§ Cosmetic advantages (4 small port scars: 2 larger (10-12mm), 2
smaller (6mm))
§ Equivalent safety profile to open procedure
o Open cholecystectomy:
§ Kocher’s subcostal incision
§ My be a conversion from laparoscopic approach, if previous unsuccessful
§ Usually reserved for emergency procedures especially perforation, when there has previous surgery, or when cancer suspected
§ Complications of both:
• Injury to bile duct (0.6%)
• Injury to bowel / blood vessels
• Bleeding
• Infection
o Percutaneous Cholecystostomy can be used to treat critically ill patients with empyaema / sepsis that
aren’t suitable for surgery
§ Drainage tube inserted into gallbladder (arrow)
§ Percutaneous under radiological guidance
§ Later cholecystectomy can be performed
o Bile duct calculi procedures:
§ Endoscopic Retrograde Cholangiopancreatography (ERCP)
• Invasive – side viewing endoscope catharsises ampulla
• Therapeutic endoscopic sphincterotomy and CBD calculi extraction – trawled with balloon
• Complications – pancreatitis, bleeding, perforation
• Cholecystectomy still necessary
§ Exploration Common Bile Duct:
• Laparoscopic versus Open
• Indications
• One procedure
• Equivalent outcome compared to ERCP and cholecystectomy
7 Shock
SEE POEM NOTES Hypo-perfusion
Definition: Acute circulatory failure with

inadequate tissue perfusion leading to cellular
hypoxia, dysfunction and failure of major organ
Cellular hypoxia
systems.
Hypoperfusion can arise from: Inadequate energy Anaerobic Lactic acid

• Heart - Inadequate preload, Inadequate production metabolism production
myocardial contractility, Excessive afterload
• Blood volume – hypovolaemia
Blood vessel - Excessive vasodilatation,
Cell dysfunction and
• Metabolic failure Metabolic acidosis
excessive systemic vascular resistance
cell death
Michael Grant
lOMoARcPSD|4776960
Classifications:
• Myocardial infarction/contusion
Cardiogenic • Cardiac failure
• Arrhythmia
Compensated Uncompensated Irreversible

• Haemorrhage
Hypovolaemic • Vomiting and diarrhoea
• Burns, pancreatitis
• Tachycardia • Hypotension • Multi-organ failure
• Tachypnoea • Rapid thready pulse • Death imminent
• Sepsis
• Cold peripheries • Peripheral cyanosis
Distributive • Neurogenic
• Anaphylaxis • Oliguria • Agitation/confusion
• Altered mental
• Pulmonary embolus status
Obstructive • Cardiac tamponade
• Tension pneumothorax

Pathophysiological response:
• Biochemical
o Increased Catecholamine release
o Activation of Renin-Angiotensin system
• Hormonal
o Increase glucocorticoid and mineralcorticoid release
• Neural
o Activation of Sympathetic nervous system
8 Colorectal carcinoma
Aetiology of Colorectal carcinoma:
l Pre-existing polyps via multistep process (adenoma-carcinoma march) of
malignant change:
l Should be biopsied and removed if signs of malignant changes;
most can be reached by flexible sigmoidoscopy and diathermy
l Inflammatory – UC, Crohn’s, Lymphoid hyperplasia
l Hamartinatous – juvenile polyps, Peutz-Jeghers (benign
hamartomatous polyps in the gastrointestinal tract and
hyperpigmented macules on the lips and oral mucosa)
l Neoplastic – tubular or villous adenomas, malignant potential
esp. if > 2cm
l Genetics
l FAP (APC gene - 5q)
l HNPCC (MMR – mismatch repair gene)
l Diet (Low fibre, high red meat)
l Alcohol
l Bile Acids
l Predisposing conditions - Ulcerative colitis, Crohns, PSC, Gastric
surgery
l Smoking
l Prevention: Aspirin (reduces incident and mortality – inhibition of
COX-2 overexpression in multistep process)
Spread:
l Direct – kidney, duodenum, uterus, bladder
l Lymphatic – look for virchow’s node
l Blood – via portal to LIVER, lungs
l Transcoelomic – omental, peritoneal, krukenburg ovarian tumours
History:
• Change in bowel habit? Frequency relative to normal, consistency,
calibre, completion
• Rectal bleeding? Colour, mixed
• Pain? Abdo. cramps, painful defecation (more common in benign
conditions)
• Red flag criteria:
o 40-60 yrs old, rectal bleeding and change bowel for >6 weeks.
o >60 yrs old, rectal bleeding OR change in BO only for > 6 weeks.
o Palpable abdominal OR rectal mass
o Unexplained microcytic anaemia (Men <11g/dL, Women <10g/dL)
Michael Grant
lOMoARcPSD|4776960
Screening:
l FOB home test kit every 2 years for 60-75 yr old
l Positive FOB -> Colonoscopy
l Reduce cancer deaths 16%
Imaging modalities:
• Endoscopy/Sigmoidoscopy – with histopathology
o 5% concurrent CA, 40% concurrent adenoma
o Can only visual up until the splenic flexure – so need to CT colon
• CT Virtual Cologram shows 3D view of colon and is very sensitive
o Scan in supine and prone positions after IV buscopan (blocks the muscarinic receptors
found on the smooth muscle walls reducing gut movement) and inflation with air
o Avoid uncomfortable colonoscopies and the small risk of perforation that comes with
them
• Barium Enema – less commonly used by can show pathonomic “apple core” lesions where
masses are
• Staging scans:
o CT Abdomen
o CT Chest / Pelvis
• FOLFOX regimen – 5-FU, folinic acid, oxaliplatin
o 20% mets at presentation Adjuvant Node positive disease – reduce Dukes’ C mortality by 25%
o MRI pelvis – rectal cancer Chemotherapy • Improves disease free survival
Management and treatment: Palliative • Metastatic disease

Chemotherapy • Survival benefit
• Non-operative:
o Iron supplements – treat associated anaemia
o Colonic stenting – treat bowel obstruction by mass instead of (in Short Course • Rectal cancer
Radiotherapy • Reduces local recurrence
unfit) or as a bridge to definitive surgery
o Chemo- and radiotherapy has roles in specific types:
§ Radiotherapy is typically palliative in colon cancer but can be Long Course • Rectal cancer
Chemoradiotherapy • Downstages tumour
used pre- and post-op in rectal tumours
§ Chemo can be used through Duke stages to improve
outcomes; see diagram to right Biologics Cetuximab for KRAS wild-type
§ Biologics can be used in specific mutants of cancer
• Surgical:
o Hartmann’s procedure can be used in emergency settings of malignant obstruction, perforation or palliation
o Other resections depend on the location of the tumours:
Principles Management
• Blood supply • Right hemi-colectomy

• Oncological resection • Left hemi-colectomy
• Site tumour • Sigmoid colectomy
• Anastomosis • Anterior resection (upper 2/3 or rectum)

• Stoma • APER (Abdomino-perineal excision of
rectum – permanent colostomy for
• Metastatic disease tumours <8cm from anus
• Liver / lung resection – typically if limited
to single lobes
9 Abdominal Aortic Aneurysm

Definition:
l An aneurysm is an abnormal dilation of a blood vessel with increase of >50% the expected diameter
l Aorta > 3cm considered Aneurysm (begin monitoring every 12 months):
l < 5.5 cm Small Aneurysm
l > 5.5 cm Large Aneurysm - consider treatment if this size or increasing at >1cm/year or symptomatic
l Weakening of the Arterial Wall, leads to:
l Dilation of wall
l Thrombus in Sac
l Perivascular Inflammation in 10% (can lead to conditions such as retroperitoneal fibrosis in AAA)
l Fistula/pressure on nearby structures
Sub-classifications of Aneurysms:
l Anatomy: Aortic, Iliac, Popliteal, etc.
l Aetiology: Atherosclerotic, Mycotic (due to infection in vessel wall – endocarditis, tertiary syphilis)
Michael Grant
lOMoARcPSD|4776960
l Morphology: Fusiform, Saccular
l Pathology: True (all-layers), False (collection of blood in the adventitia that communicates
with the lumen following trauma)
Aetiology:
• Inflammatory Cell Infiltrate
• Extracellular Matrix Degradation by Matrix Metallo-proteinases (MMPs)
• Elastolysis leading to dilation by degeneration of elastic laminae and smooth muscle
Risk factors:
• Genetic Factors:
o Hereditary Risk: 10-fold (20x if a female has one)
o Gender Male: 6-fold
o Polymorphisms
o Collagen Vascular Diseases (Marfan’s Syndrome)
• Environmental Factors:
o Age
o Smoking (very relevant – directly alters collagen)
o Hypertension
o Cardiovascular Disease esp. atheroma
Presentation:
• Asymptomatic
o Symptoms: none
o Signs: Epigastric mass – pulsatile and expansile, non-tender
• Symptomatic
o Symptoms: abo pain, radiation to back/groin, intermittent claudication
o Signs: Epigastric mass, pulsatile & expansile, tender to palpation, abdo bruit
§ Systemic: chronic/acute limb ischaemia, retroperitoneal
fibrosis
• Rupture
o Symptoms: abdo pain, radiation to back/groin, collapse
o Signs: abdominal pulsatile mass, acute abdo, lumbar haematoma
§ Systemic: acute limb ischaemia, shock, LOC
Imaging:
• Ultrasound scan
• CT Angiogram
Management:
• Surveillance
o Asymptomatic Aortic Aneurysm*
§ <3 cm (normal): Discharge Problems Management
§ 3 – 4.4 cm: Surveillance USS every 12 months
§ 4.5 - 5.4 cm: Surveillance USS every 3 months
§ > 5.5 cm: Consider for Active Treatment • Anatomy • MDT Planning
• Medical: strict BP control • Contrast Nephropathy • Fenestrated Grafts
• Endovascular (EVAR): • Branch Vessel Occlusion • Branched Grafts
o Anatomical suitability 60 – 80% • Limb Occlusion • Surveillance
o Preferred older high-risk patients • Endoleak • Secondary Endovascular
• Late Rupture Intervention
o Mortality 1 – 2%
• Secondary Open Conversion
o Reintervention 10% (higher than in open repair due to
failures of stent graft to fully exclude blood flood to defect, Figure 1 - EVAR
i.e. “endoleak”)
o Lifetime CT follow-up Problems Management
• Open surgical repair:
o Versatile: suitable ALL Anatomy • Anatomy • MDT Planning
o Durable: low re-intervention rate (can be discharged
• Fitness for Surgery • Anaesthetic Assessment
after 3 months)
o Preferred young low-risk patients • Hostile Abdomen • Surgical Approach
o Mortality 2 - 8% • Blood Loss / Clamp Time • Good Exposure / Control
o Additional complications such as wound infection • Branch Vessel Ischaemia • ICU / HDU
• Complications
Michael Grant
lOMoARcPSD|4776960
10 Pain control
Effects of poorly managed pain:
l Increased sympathetic activity
- Increased HR and BP
- Increased myocardial O2 demand, risk of ischaemia
l Detrimental effects on respiratory function
- Poor cough, atelectasis, infection, hypoxia
l Other effects
- Anxiety, insomnia
- Immobility, increased DVT risk
- Increased risk of developing chronic pain
Methods:
l Peripherally:
- NSAIDs: reduce inflammatory mediator production
- Local anaesthetics: topical, infiltration, nerve block
l At spinal cord level:
- Opioids, local anaesthetics: modify or block
nociceptive input
l At cortical level:
- Opioids, NSAIDs and other analgesics reduce the
perception of pain
WHO Analgesia ladder:

l Incremental analgesia
- Level of analgesia tailored to the severity of the pain
- Clinical assessment may move treatment up or down the ladder
l Multimodal analgesia
- Combination of analgesic therapies with synergistic effects give better analgesia
- Reduced individual doses decrease adverse effects
l NSAIDs caution in:
- Bleeding disorders: Anti-platelet activity (esp with non-selective NSAIDs)
- Active peptic ulcer disease:Loss of protective prostaglandin activity
- Asthma: 10% asthmatics suffer exacerbation with NSAIDs, most likey in those with nasal polyps / seasonal rhinitis
- Severe renal impairment: Eliminated by the kidneys and renal blood flow helped by prostaglandins
- Hepatic impairment: Inactivated in the liver, can get elevated levels and links with hepatocellular toxicity
l Opioids:
- Tramadol increases activity of noradrenaline and serotonin, well absorbed orally and
less sedative than other strong opioids
- Caution with:
l Sedation: occurs before respiratory depression, major aspect of monitoring after
opioid administration
l Respiratory depression: potential to lead to respiratory arrest - Naloxone must be
prescribed and available if patients are on PCA
l Nausea, vomiting: Common, especially with PCA morphine
l Anti-emetic should be prescribed on kardex
l Other adverse effects: Pruritis, Reduced bowel motility, Urinary retention
- Standard PCA regimen:
l Morphine sulphate 250mg in 250ml
l Bolus dose = 1mg morphine (1 ml)
l Lockout time = 5 minutes
l 4 hourly limit = 40mg
l Rescue – if pump fails:
l Contact APS / anaesthetist on call if possible
l ANY RESCUE OPIOID MUST BE INTRAVENOUS
l Titrate cautiously to effect (1-2mg boluses)
l Stay with the patient
l Monitor frequently during administration and after
l SpO2, BP, HR, Resp rate
l Epidurals:
- Catheter inserted into the epidural space by an anaesthetist as a sterile procedure (theatre)
- Local anaesthestic with added opioid administered down the catheter; e.g. L-bupivacaine 0.1% + fentanyl 2mcg/ml
- Pain controlled by continuous infusion from a pump can be boosted by bolus request “patient controlled epidural analgesia”
(PCEA)
- Benefits: less sedations, improved: mobility, bowel motility and respiratory function (less atelectasis, fewer infections)
- Problems: Hypotension, leg weakness, haematoma (trauma at insertion) and infection (epidural abscess)
l Test sensory level with ice (caution if above C4), markedly reduced leg power (exclude hamatoma/abscess)
Michael Grant
lOMoARcPSD|4776960
11 Jaundice
l 7g of haemoglobin is removed from the blood everyday – broken down into
bilirubin (lipid soluable) transported bound to albumin, thus cannot pass
through lipid membranes or be excreted in urine
l Conjugated to glucronic acid – bilirubin glucuroniride (conjugated bilirubin)
l Lost by feaces and via urine by enterohepatic recirculation
What is jaundice?
l Clinical: Yellow discoloration of the skin, mucus membranes and sclera due to
excess plasma bilirubin
l Biochemistry: Bilirubin higher than 30mmol/l (normal = 5-17)
l Physiology: Too much bilirubin in the circulation and impaired liver conjugation
Causes of jaundice:
l Pre-hepatic (unconjugated - pale lemon tinge to skin, no changes to urine):
- Overproduction: Haemoylsis – Haematoma, Malaria, DIC, Spherocytosis,
Sickle cell
- Impaired uptake: Drugs (contrast agents, rifampicin), right sided heart failure
- Impaired conjugation: Gilbert’s syndrome (reduced activity of the enzyme
glucuronyltransferase, 3-12% of population)
l (Conjugated - deeper yellow or almost orange skin with dark urine and pale stools)
- Hepatic
l Hepatitis – viral (Hep A, B, C; CMV, EBV), drugs (see table), autoimmune
l Cirrhosis – alcohol, NAFLD
l Metastases/abscesses
l Haemochromatosis/Wilson’s disease/alpha 1 anti-trypsin deficiency
l Failure to excrete: Dubin-Johnson syn (mutation in MRP2 limits
hepatocyte ability to secrete conjugated bilirubin, also results in black
pigmented liver), Rotor syn (similar to DJ but no pigment)
- Post-Hepatic (obstructive):
l Primary biliary cirrhosis & primary scleroising cholangitis
l Gallstones (CBD or Mirrizi’s syndrome)
l Tumour of the head of pancreas (Courvoisier's law – stones cause
tender, fibrosed gallbladder than cannot expand to become palapable)
l Caroli’s disease (saccular dilations of intrahepatic ducts with congenital
hepatic fibrosis)
History:
Examination:
HxPC Duration, onset, progression, associated symptoms: pain,
l General exam
itch, change in urine and stools, weight loss
- Skin and sclera – best seen in natural light PMHx Previous episodes (Chronic?), gallstones, liver disease,
- Scratch marks – from pruiritis blood disorders, blood transfusion
- Lymphadenopathy
- Evidence of liver disease – spider naevi, finger Family Hx Gallstones/liver disease/blood disorders
clubbing
l Abdominal exam Social Hx Alcohol, drug use, recent travel + abroad, contacts with
- Tenderness, known hepatitis carriers
- Distension (ascites, palpable mass)
- Hepato/Splenomegaly (portal hypertension) Drug Hx medications/allergies
Investigations:
l Urinary bilirubin and urobilinogen – tested fresh as pH changes
and light degradation can change results
l Liver function tests – ask for levels of conjugated/unconjugated,
protect samples from light (lowers levels) and do not shake (raises
levels)
o GGT is sensitive by not specific for alcohol hepatitis – ALT
should be raised too; GGT plus ALP raised suggests cholestasis
l Full blood picture – include reticulocyte count, blood smear,
consider ESR in PBC
l Coagulation studies – liver produces clotting factors
Michael Grant
lOMoARcPSD|4776960
Imaging:
l ABX – only 10% of stones visible so not that useful
l USS – can detect masses, hepatomegaly and gall stones (including biliary tree dilation >6mm,
suggesting CBD stone)
l Contrast CT – lesions within liver and abdomen
l MRCP – useful if USS isn’t definite
l ERCP
o Inject dyes into the ducts through sphincter of oddi in the billiary tree and pancreas so
they can be seen on x-rays
o Diagnose and treat:
§ Gallstones (sphincterotomty and trawl)
§ Inflammatory strictures (insert stents)
§ Leaks (trauma or surgery)
§ Cancer (biopsies can be taken)
Causes:
l Gallstones
l Malignant biliary tree tumours (cholangiocarcinoma)
l Head of pancreas tumours
l Benign biliary tree lesions (Strictures)
l Failed palliative procedures or therapeutic endoscopy procedures
l Liver transplant/resection
Management:
1. Fluids
2. Assess for sepsis – look for Charot’s triad (or Reynolds’ pentad; plus shock and reduced GCS)
3. Monitor Prothrombin time – administer vit K if needed
4. Avoid or stop hepatotoxic drugs
12 Post-operative complications
Post operative complications can be classified in two ways:
• General or specific to the type of surgery
• Timing: immediate, early, late
When asked to give your thoughts on the complications of an operation—maybe with an examiner or a patient—a good starting point is to divide
them up accord- ingly (and for each of the following stratify as immediate, early and late):
• From the anaesthetic: (p574) eg respiratory depression from induction agents.
• From surgery in general: (see p578 and BOX 1) eg wound infection, haemorrhage, neurovascular damage, DVT/PE
• From the specific procedure: eg saphenous nerve damage
Post-operative haemorrhage can be caused by coagulation effects, surgical technique and local factors.
• Coagulation factors:
o Anticoagulation, eg. Warfarin, or antiplatelet therapy, eg. Aspirin or Clopidrogel
o Thrombocytopenia, eg. ITP
o Severe blood loss / transfusion
o Obstructive jaundice
o Long-term steroid therapy
o Severe sepsis with DIC
• Timing:
o Primary haemorrhage: Continuous bleeding, starting during surgery. Replace blood loss. If severe, return to theatre for adequate
haemostasis. Treat shock vigorously.
o Reactive haemorrhage: Haemostasis appears secure until BP rises and bleeding starts. Replace blood and re-explore wound.
o Secondary haemorrhage (caused by infection) occurs 1–2 weeks post-op.
Michael Grant
lOMoARcPSD|4776960
• Management:
o Check coagulation screen and Hb
o Discontinue any antithrombotic therapy
o Reverse coagulation defects (Vitamin K, Protamine Sulphate, FFP,
platelets)
o Surgical exploration (Evacuate the blood and clot, Identify bleeding
point, Control bleeding)
Deep vein thrombosis occur in 25–50% of surgical patients, however 65% of

below-knee DVTs are asymptomatic; these rarely embolize to the lung.
• Risk factors:
o Surgical procedures lasting >90 minutes, or >60 minutes if involves
pelvis or lower limb
o Acute surgical admission with inflammatory or intra-abdominal
condition
o Expected significant reduction in mobility
o One or more risk factors from the right:
• Diagnosis:
o History: Pain, Calf swelling
o Examination: Swollen leg, Calf tenderness, Calf red and hot, Positive
Homan’s sign, Fever
o Investigation:
§ D-dimer
§ Venography
§ Doppler ultrasound
o Prevention: Stop the Pill 4wks pre-op, Mobilize early; Low molecular weight
heparin (LMWH, eg enoxaparin 20mg/24h SC, 40mg for high-risk patients, starting
12h pre-op), physical measures:
§ Venous support stockings
§ Intermittent pneumatic compression stockings (flowtron)
or electrical calf stimulators
o Treatment: LMWH (eg enoxaparin 1.5mg/kg/24h SC) is superior to unfractionated
heparin
§ In others, start warfarin simultaneously with LMWH (warfarin is
prothrombotic for the first 48h)
• Stop heparin when INR is 2–3; treat for 3 months if post-op (6 months if
no cause is found; lifelong in recurrent DVT or thrombophilia).
§ Inferior vena caval filters may be used in active bleeding, or when
anticoagulants fail
o Complications:
§ Pleuritic chest pain § Low oxygen saturation
§ Dyspnoea § Sinus tachycardia
§ Cough/haemoptysis § S1Q3T3 on ECG
§ Pleural rub § Check blood gas
§ Raised JVP § Confirm with CTPA
• Respiratory complications of surgery:
o Atelectesis
o Chest infection
o PE
o Aspiration
o Pleural effusion
o Pneumothorax - CVP line, intercostal block or mechanical ventilation
o ARDS
o General preventative measures:
§ Sit patient up and give O2
§ Adequate analgesia
§ Regular physiotherapy
§ Encourage mobilisation
§ Ventilatory support if required
• Confusion may manifest as agitation, disorientation, and attempts to leave hospital, especially at night. Gently reassure the patient in well-
lit surroundings – causes include:
o Pain, Infection, Nutrition (especially alcohol withdrawal), Constipation, Hydration/Hypoxia (pneumonia, atelectasis, LVF, PE, MI or
stroke), Medications, Enviroment
o Occasionally, sedation is necessary; consider lorazepam 1mg PO/IM (antidote: flumazenil) or haloperidol 0.5–2mg IM.
• Blood pressure:
o Hypotension - tilt bed head-down and give O2; Check pulse and BP yourself; compare it with pre-op values.
§ Often from hypovolaemia resulting from inadequate fluid input, so check fluid chart and replace losses.
§ Monitor urine output (may need catheterization).
§ A CVP line can help monitor fluid resuscitation (normal is 0–5cm H2O relative to sternal angle)
Michael Grant
lOMoARcPSD|4776960
o Hypertension - may be from pain, urinary retention, idiopathic hypertension (eg missed medication) or inotropic drugs. Oral cardiac
medications (including antihypertensives) should be continued throughout the perioperative period even if NBM:
§ Treat the cause, consider increasing the regular medication, or if not absorbing orally try 50mg labetalol IV over 1min
• Infection is common after surgery and it is important to check likely sites of origin:
o Wound
o Body cavity
o Pelvis
o Subphrenic area
o Chest
o Urine
o Cannula site
o Risk factors: Diabetes, Immunosuppression, Malnutrition, Jaundice,
Corticosteroid therapy, Obesity
o Complications: Antibiotics
§ Intra-abdominal infection/Abscess
• Culture and sensitivity
• Abdominal distension • Hospital antibiotic prescribing policy
• Prolonged ileus • Shortest duration necessary
• Increasing pain
Surgical drainage
• Ultrasound or CT scan to confirm
• Removal of sutures or skin clips
• Rx (box to right) • Percutaneous drainage under radiological guidance
• Wound breakdown: • Open surgical drainage
o 7-10 days post-op
o Serous-sanginous discharge
o Superficial dehiscence
o Deep -Abdominal contents protruding through wound
o Rx: Superficial – conservative management, deep - Theatre for resuturing
§ Consider vac dressing: Used in infected or dehiscence
wound – sponge with negative pressure draws out
inflam. fluid and increases angiogenesis
• Nausea/vomiting can be due to any mechanical obstruction,
ileus, or emetic drugs (opiates, digoxin, anaesthetics).
o Consider AXR, NGT, and an anti-emetic (not
metoclopramide because of its prokinetic property)
• Hyponatraemia over-administration of IV fluids may exacerbate
the situation. Correct slowly. SIADH can be precipitated by
perioperative pain, nausea, and opioids as well as chest infection.
• Urine output (oliguria) aim for >0.5mL/kg/h. Anuria often means
a blocked or malsited catheter while Oliguria (first 24 hours
post-op, this may be normal) is usually due to too little
replacement of lost fluid - Acute renal failure may follow shock,
drugs, transfusion, pancreatitis or trauma:
o Look for: r/v fluid balance chart, r/v drugs, palpable bladder,
establish normovolaemia (a CVP line may help here)
o U&E and urine osmolality (if latter high, then failure unlikely
– otherwise get senior help and fluid restrict)
13 Inflammatory bowel disease
Epidemiology:
l 1/250 in Western world
l UC:CD = 3:2
l Any age, commonest 15-40 years
l Slightly commoner in women
l CD commoner in smokers, UC less common (3x)
l Bimodal distribution of age:
Michael Grant
lOMoARcPSD|4776960
UC is a relapsing and remitting inflammatory disorder of the colonic mucosa. It may affect just the rectum (proctitis, as in ~50%) or may spread
proximal and extend to involve part of the colon (left-sided colitis, in ~30%) or the entire colon (pancolitis, in ~20%)
l Only present proximal to ileo-cecal valve with “backwash ileitis”
l Hyperaemic/haemorrhagic granular colonic mucosa ±
pseudopolyps
l Punctate ulcers may extend deep into the lamina propria
but the disease is seldom transmural
l Symptoms: Episodic or chronic diarrhoea (± blood &
mucus); crampy abdominal discomfort
l Signs: May be none or, in acute, severe UC: fever,
tachycardia, and a tender abdomen
l Tests:
o Cultures to rule out bacterial causes of bloody diarrhoea
o CRP & ESR for inflam
o FBC for anaemia
o AXR: No faecal shadows; mucosal thickening/ islands, colonic dilatation (>6cm)
o Erect CXR: air if perforation
o Ba enema: can show loss of haustra - Never do during severe attacks or for diagnosis
o Colonoscopy shows disease extent and allows biopsy:
§ Look for inflammatory infiltrate; goblet cell depletion; glandular distortion; mucosal
ulcers; crypt abscesses.
o Radio-labelled white cell scan
l Complications:
o Bleeding +/- perforation
o Toxic mega colon (mucosal islands, colonic diameter >6cm) +/- perforation
§ Stool microbiology / C difficile toxin to exclude this
o Venous thrombosis
o Colonic cancer: risk≈15% with pancolitis for 20yrs
§ Neoplasms may occur in flat, normal-looking mucosaso surveillance colonoscopy, eg 2–4yrs, with 4 random biopsies/10cm
o PSC entails progressive cholestasis with bile duct inflammation and strictures
§ Symptoms/signs Pruritus ± fatigue; if advanced: ascending cholangitis, cirrhosis and end-stage hepatic failure
§ Cancers: Bile duct, gallbladder, liver and colon cancers are more common, so do
yearly colonoscopy + ultrasound; consider cholecystectomy for gallbladder
polyps.
§ Tests: Alk phos, then increase in bilirubin; hypergammaglobulinaemia; AMA –ve,
but ANA, SMA, and ANCA may be +ve
• ERCP distinguishes large duct from small duct disease
• Liver biopsy shows a fibrous, obliterative cholangitis.
§ Treatment: Liver transplant is the mainstay for end-stage disease; recurrence
occurs in up to 30%; 5yr graft survival is >60%.
§ Prognosis is worse for those with IBD, as 5–10% develop colorectal cancer
post-transplant
• Ursodeoxycholic acid may protect against colon cancer and improve LFT
(histological benefit is less clear)
l Treatment:
o Inducing remission:
§ Mild: 5-ASA (eg sulfasalazine or mesalazine) plus steroids (20mg prednisolone PO +/- hydrocortisone foam PR); if improvement
within 2 weeks, wean steroids – otherwise treat as moderate…
§ Moderate: 4x 5-ASA dose plus 40mg prednisolone PO + twice daily budesonide enema PR; if improvement within 2 weeks,
wean steroids – otherwise treat as severe…
§ Severe: admit for nil by mouth & IV hydration, hydrocortisone IV and PR
• Consider TPN if very malnourished and transfuse if <90g/L
• If on day 3 CRP >45 or >6 stools/d, action is probably needed: colectomy or rescue therapy (ciclosporin or infliximab)
o Maintaining remission: 5-ASAs (relapse rate 80% to 20% at 1yr) e.g. lifelong sulfasalazine, mesalazine (newer, less S/E as no
sulapyridine group as mesalazine is 5-ASA dimer)
§ S/E of sulfalazline relate to sulfapyridine (carries 5-ASA to the colon, where it is cleaved) intolerance (headache, nausea,
anorexia), also: rash, haemolysis, hepatitis, pancreatitis, paradoxical worsening of colitis, and reversible oligospemia
o Immunomodulation can be used if no remission comes with steroids, or if prolonged use is required
§ Agents: azathioprine, methotrexate, infliximab, adalimumab or calcineurin inhibitors (ciclosporin; tacrolimus – inhibits
calcineurin which activates Nuclear Factor of Activated T-cells Cytoplasmic (NFATc) transcription factor that upregulates IL-2)
o Surgery (needed at some stage in ~20%):
§ Indications: Perforation, massive haemorrhage, toxic megacolon, failed medical therapy
§ Proctocolectomy + terminal ileostomy: It may be possible to retain the ileocecal valve, and hence reduce liquid loss with
§ Colectomy with ileo–anal pouch later
§ Ileorectal anastomosis is very rarely possible in UC due typical distal ascending disease from anus; anal involvement is
contraindicates anastomosis
Michael Grant
lOMoARcPSD|4776960
CD is an inflammatory GI disease characterized by transmural granulomatous inflammation
affecting any part of the gut from mouth to anus (esp terminal ileum (in ~70%) and proximal
colon). Unlike UC, there is unaffected bowel between areas of active disease (skip lesions).
l Cause: Unknown but associated with mutations of the NOD2/CARD15 gene; increased risk
in smokers; NSAIDs may exacerbate
o Environmental agents are implicated
o Genetics: colon involvement goes up with CARD15 gene expression in macrophages &
intestinal epithelial cells
o Dysregulated immune responses might be primary or from infecting gut commensals,
eg Mycobacterium avium para-TB; E. coli adhesins
l Symptoms: Diarrhoea/urgency (+/- blood/mucous), abdominal pain (more likely than in UC
and worse after food), weight loss/failure to thrive, fever, malaise, anorexia, + Mass in RIF
l Signs: Aphthous ulcerations; abdominal tenderness/mass; perianal abscess/fistulae/ skin
tags; anal strictures, clubbing, skin, joint & eye problems
l Tests:
o Cultures (blood, stool, etc.) to rule out bacterial causes of bloody diarrhoea
o CRP & ESR for inflam
o FBC for anaemia
o Ba enema: (used less now) cobblestoning, ‘rose thorn’ ulcers ± colon strictures.
o Colonoscopy shows disease extent and allows biopsy:
§ even if mucosa looks normal (20% have microscopic granulomas)
o MRI can assess pelvic disease and fistulae, disease activity and shows site of strictures
o Capsule enoscopy
o Radio-labelled white cell scan
l Complications: Small bowel obstruction; toxic dilatation (rarer than in UC – but still look for C Diff stool toxin); abscess formation
(abdominal, pelvic, or ischio-rectal); fistulae (present in ~10%; eg colovesical, colovaginal, perianal, enterocutaneous); perforation; rectal
haemorrhage; colon cancer; fatty liver, PSC (see above in UC complications), cholangiocarcinoma,
renal stones, osteomalacia, malnutrition, amyloidosis (may have effects on liver & kidney, as they
filter amyloid)
l Treatment:
o Optimise nutrition: enteral is preferred (eg polymeric diet); consider TPN as a last resort
§ Fe / B12 / Folate
§ Micronutrients – vitamins, trace elements
§ Osteoporosis prophylaxis – vit d and calcium
§ Elemental diets (E028®) contain amino acids and can give remission
o Assess severity: T°, pulse, ESR, WCC, CRP + albumin increase may merit admission (liver often
switches to making CRP-type proteins rather than albumin)
§ Mild attacks: (Symptomatic but systemically well) - Prednisolone 30mg/d PO for 1wk, then
20mg/d for 4wks; wean when well
§ Severe: Looks ill. Admit for IV steroids, nil by mouth, and IVI
• Treat rectal disease: steroids and metronidazole (good in rectal disease or
superadded infection)
o Crohn’s Perianal disease occurs in about 50%. MRI and examination under
anaesthetic (EUA) are an important part of assessment. Treatment includes oral antibiotics, immuno-suppressant
therapy ± infliximab, and local surgery ± seton insertion
• Consider need for blood transfusion (if Hb <100g/L) and parenteral nutrition.
• If improving after 5d, transfer on to oral prednisolone (40mg/d).
o If not, infliximab and adalimumab have a role (esp. in fistulizing Crohn’s). CI: CCF; infection. NICE 2010
• Consider abdominal sepsis complicating Crohn’s disease especially if abdominal pain (ultrasound, CT & MRI)
o Additional therapy:
§ Azathioprine (Prodrug of mercaptopurine; metabolites are incorporated into replicating DNA,
halting replication, as well as blocking the pathway for purine synthesis) can be a used as a steroid-
sparing agent, eg if steroid SEs, and if there are multiple/rapid relapses. It takes 6–10 weeks to work.
§ Methotrexate – 25mg IM weekly for remission induction, can enabe complete withdrawal from
steroids in patients with refractory Crohn’s
o Surgery: 50–80% need ≥1 operation in their life. It never cures andcan become a devastating cycle of
deterioration.
§ Indications: drug failure (most common); GI obstruction from stricture (strictureplasty);
perforation; fistulae; abscess.
§ Surgical aims are:
• 1. Defunction (rest) distal disease, eg with a temporary ileostomy
• 2. Resection of the worst areas — but avoid short bowel syndrome
o If limited to colon, treatment options are as per UC
§ Bypass and pouch surgery is not done in Crohn’s because of risk of recurrence
o Psychosocial support: National Association for Colitis & Crohn’s Disease (NACC)
Michael Grant
lOMoARcPSD|4776960
Extraintestinal manifestations of IBD:
l Joints - Arthropathy, sacroiliitis, ankylosing spondylitis
l Finger clubbing
l Eyes - Episcleritis / uveitis
l Skin - Erythema nodosum / pyoderma gangrenosum (Note
purple-ish colour at edges)
l Aphthous oral ulceration
l Primary Sclerosing Cholangitis
l Nutritional deficits
l Amyloidosis
14 Haematemesis and melaena

Upper GI bleeding canpresent as:
l Haematemesis
o Vomiting blood
o Fresh
o ‘Coffee-grounds’ (acid conversion of haemoglobin to
methaemoglobin)
l Melaena
o Passage of black tarry malodorous stools
o Oxidisation of haem by intestinal and bacterial enzymes
Peptic ulcer/erosive disease:

l Strong association with Helicobacter pylori
- Eradication (‘triple therapy’) reduces the risk of recurrent ulcers (and
bleeding)
l NSAIDs
- Inhibit the action of cyclooxygenase
- Leads to impaired mucosal defense against acid
l Oesophagitis
- Associated with reflux of acid or alkali (can lead to Barrett’s)
- Also infection in immunocompromised (HIV/Diabetes – can
get candida or herpes infection)
l Mallory-Weiss tear
- Tear in lower oesophagus secondary to forceful vomiting
- If full thickness > rupture (Boerhaave Syndrome – chest
pain, SOB, subcut emphysema)
l Oesophageal Varices
- Chronic liver disease
- Portal hypertension > portal-systemic shunting; esophageal,
rectal, umbilical
l Malignancy
- Uncommon cause of bleeding; exophitic, ulcerative and
diffuse subtypes – ulcerative more likely to bleed
- Worldwide leading cause of GI malignancy
History:
l Confirm the presence of bleeding
l Estimate the amount of blood loss
l Identify the source / potential cause
o Vomiting fresh or clotted blood suggests ongoing bleeding
l Associated symptoms
o Sudden onset pain with vomiting
o Dyspepsia / heartburn
o Weight loss / dysphagia
l Previous history
o Previous peptic ulcer disease
o Cirrhosis
o Clotting disorder
l Medications
o NSAIDs
o Anticoagulants
o Steroids
Michael Grant
lOMoARcPSD|4776960
Initial treatment for upper GI bleeds:
l Stabilise the patient
o ABC
o IV access and fluids (incl, FBP, U&E, LFTs, coag, X-match)
o Urinary catheter and hourly urometry
o Transfuse as necessary (Hb 8-10g/dl)
o Correct coagulopathy
l Proton-pump inhibitors
o Initially given intravenously (80mg Omeprazole)
o Maintain gastric pH > 6.0
o Protects ulcer clot from fibrinolysis
l Early endoscopic intervention
o Optimum resuscitation is essential first to reduce cardiorespiratory complications
o Should be undertaken within 24h (<4 if haemodynamically unstable)
o Shown to reduce transfusion requirement and hospital stay – risk of mortality Rockell Score
o Endoscopic strategies:
§ Injection > adrenaline (vasoconstriction and tamponade)
or sclerosant/alcohol (risk of necrosis & potentially perf.)
§ Thermal > coagulation using heater probe
§ Mechanical > endoscopic clips
o Rebleeding:
§ Repeat endoscopy
§ Radiology – selective embolisation
§ Surgery (laparotomy and haemorrhage control)
• Underrunning vessel
• Gastrectomy (Billroth I, II or Roux-en-Y)
l Specific management of variceal bleeding:
o Endoscopy
§ Variceal band ligation
§ Injection sclerotherapy
o Pharmacology
§ Vasoactive drugs (reduction in portal blood flow – octreotide (somatostatin analogue) or terlipressin (vasopressin analogue)
§ Antibiotics (Eyrthromycin 3mg/kg – prokinetic, improves visualisation)
o Balloon tamponade by Sengstaken – Blakemore tube
15 Varicose veins
The anatomy of the
venous drainage is vital
to know before being
able to understand the
pathology at play in
varicose veins. There
are the deep veins
(namely the femoral
view and the popliteal
vein; seen in the image
on the right in black)
and the superficial
veins (the great and
small saphenous veins).
The great saphenous

vein runs along the
medial side of the leg
from the anterior of the
medial malleolus to the groin, where it joins with the femoral vein at the sapheno-femoral
junction. The small saphenous vein runs up the posterior aspect of the lower leg joins the
popliteal vein at the sapheno-popliteal junction.
Michael Grant
lOMoARcPSD|4776960
There are communications between the deep and superficial veins, at the junctions and through the perforator veins. These valves in these
structures only allow flow form superficial to deep and in one
direction from feet to heart. Varicose veins can be classified as:
If valves in these become incompetent, venous blood pools in the • Primary trunk: commonly seen and are derived from
superficial veins causing venous hypertension and dilation. the greater or small saphenous
• This can be: • Secondary trunk: deep venous disease causes
o Primary as is the cause with degenerative changes superficial veins to act as collaterals
o Extensive varicose veins, signs of chronic
(unknown case) or in congenital valve absence (very
venous insufficiency (e.g. haemosiderin) or
rare) hx of DVT can alert you to this type
o Secondary as is the case in: • Reticular veins: are not true varicose veins, they lie
§ Obstruction (DVT, fetus, ovarian tumour) close to the surface of the skin and - even when non-
§ Valve destruction (e.g. during DVT pathological – form highly visible, dark blue reticular
healing) veins.
§ Arteriovenous malformations (increased o They are unsightly and may trigger patients,
especially those with fair skin, to present but
pressure in venous system)
they require no treatment
§ Overactive muscle pumps (e.g. in cyclists, • Spider veins/venous flares: occur mostly in woman
muscle tone forces blood from deep to (may be associated with hormonal changes) but can
superficial through sheer force – past the also be seen in conjunction with varicose or reticular
valves) veins. They require no treatment.
• Risks included advancing age, pregnancy, family hx, female • Venous malformations
gender (2:1) and the OCP.
• Prolonged standing and obesity have been linked with exacerbation but not causation of varicous veins.
Distention
• Prevalence estimates vary widely, but large studies suggest 80% of people show some kind of venous disease (35%
with trunk varices, the remainder with spider veins)
• A saphena varix is a dilation of the SFJ that transmits a cough impluse and, thus, may be confused with an inguinal
hernia. However, on closer examination, it may reveal a bluish hue.
Presentation can be either: Oedema

• Uncomplicated – issues with comesis, minor symptoms (heaviness, aching, restlessness, cramps, swelling),
reassurance
• Complicated patients present with:
o Superficial thrombophlebitis – a sterile inflammation due to superficial thrombosis causes a hard, painfull, Haemosiderin
swelling • Occurs as phagocytes engulf
haemoglobin in RBCs from
§ Rx – NSAIDs and anticoag. There is NO ROLE for abx ruptured vessels
§ If phlebitis involves great saphenous, a duplex venous scan (combined US and Doppler) should
be performed to ensure that thrombus does not communicated with the femoral vein; if so, patient
should be warfarin-ised as per DVT treatment (3 months) Lipodermatosclerosis
o Lipodermatosclerosis and pigmentation – superficial inflammation leads to sclerosis, calcification and • skin hardness from
subcutaneous fibrosis caused by
necrosis of dermis components down the deep fascia. chronic inflam. and fat necrosis
§ Can lead to “champagne bottle leg” or can present acutely as a pseudo-cellulitis

§ High risk of ulceration
o Varicose eczema – occurs over the varicose veins and can be treated with steroids or by treating underlying Ulceration
cause • Plus atrophie blanche - white
scarring at sites of previous,
o Venous Ulceration - 80% of all leg ulcers are venous ulcers and a large shallow relatively painless ulcer with an now-healed ulcers
irregular granulating base in the 'gaiter' region of the leg (between the knee and ankle) is likely to be
venous in origin. There may be surrounding stasis dermatitis.
§ This region is affected primarily due to a perfect storm of greatest force of blood (due to the effects of gravity) acting
on the smallest surface area (finest calibre) of saphenous vein
o Haemorrhage – can occur spontaneously and is relieved by pressure and elevation
Assessment should include:

• History: asking in regard previous vascular pathology (e.g. DVT – risk of deep vein occlusion or insufficiency
that may rule out ablation, Intermittent claudication – arterial disease may also be present), vascular surgery,
other health problems, exact symptoms (complicated vs. uncomplicated).
• General examination: patient should be in a standing position and exposed so both abdomen and the entire
length of leg can be examined. Look at:
o Location – e.g. medial aspect likely to be great saphenous, post. Lower leg likely to be small
saphenous
o Signs of chronic changes – oedema, haemosiderin deposition, lipodermatosclerosis,
ulceration/atrophic blanche?
o Scars – previous treatment?
• Special tests:
o Trendelenberg’s test: patient lays flat with leg elevated so that blood can be “milked” out. A tourniquet (or
hand) is then placed just inferior to the sapheno-femoral junction to occlude it and the patient asked to
stand. Filling should be gradual and slow, coming from the most inferior point of the superficial veins – so
rapid filling at this time indicates incompetence in the perforating veins. When the occlusion on the SFJ is
release, slow filing should continue – however if there is rapid changes then there is likely to be
incompetence in the great saphenous vein valves also.
Michael Grant
lOMoARcPSD|4776960
o Perthes’ test: a tourniquet is applied to just inferior to the SFJ. Patient is asked to stand and elevate themselves repeatedly onto
their toes. If deep veins are occluded, the already dilated viens will become more prominent and pain
occurs – thus a secondary trunk varicose vein.
• Doppler hand held scanner has mostly replaced the above tests and can be performed in outpatients by clinician. A
scanner can be placed onto the palapated femoral artery then moved medially to find SFJ (or placed onto popliteal
and moved laterally to find SPJ). With patient standing and scanner placed onto junction of interest, the calf is
squeezed to cause a prograde signal from the scanner. If incompetence or reflux is present, the release of the calf will
cause a change in the established signal that is great than 1 second in length (some allowance for blood shifting back
to next distal functional valve in the case where there is no pathology) – producing a retrograde signal as the blood
flows back toward gravity.
• Duplex ultrasonography should ideally be performed in all patients. It can be used to diagnose the extent and
location of superficial incompetence, as well as deep insufficiency (including the presence of DVT), and can identify
the outcome of previous endovascular varicose treaments.
Treatment can include:

• Reassurance
• Compression tights work by having a higher level of external pressure at the ankle than then calf and thigh
o It is classed by the level of compression (Class I – 14 to 17mmHg, II – 18 to 24mmHg, III – 25 to 35mmHg)
and can be below knee (most common) or above knee
o Prevents recurrence and progression to ulceration – but must be replaced every 6 months as washing
decreases elasticity
o Useful in patients when origin of symptoms may not be varicose veins and in those unfit for other
treatments
• Foam sclerotherapy (Liquid can be used in below knee varicosities with no gross SFJ incompetence)
o A mix of sodium tetradecyl sulphate and air (1:4) are mixed and injected into veins to causes a phlebitis that
leads to vein occlusion
o Can be injected into GSV, SSV or other varicosity when cannulated under ultrasound guidance
o Compression tights worn for week following treatment
o Late term side effects are unknown but about 80% efficacy after 1 year
• Endovascular ablation can be performed in the outpatient setting as a catheter is threaded superiorly after the GSV/SSV
is cannulated under ultrasound and tip threaded to 1cm distal of SVJ/SPJ (important to not cause a thrombus in the
parent vessel)
o Radiofrequency uses infrared energy to achieve temperatures of 120 degrees to destroy
endothelium is as good as surgery at 3 months
o Laser uses light energy to achieve the same, but results only match surgery at the 2 year
mark
o Compression tights are required for 6 weeks with NSAIDs for pain (due to bruising and/or
phlebitis)
o Review is at the 6 week period, at which point 20% will have residual varicosities that can
be treated with foam
• Conventional surgery can consist of:
o SFJ ligation and stripping of the GSV to the level of the knee, achieved by stripping
catheter inserted beyond ligation
o SPJ ligation with no stripping distal
§ Stripping of the SSV is no longer performed due to high risk of damage to the
sural nerve
o Phlebectomies
o Complications: bruising (common), bleeding, infection, nerve injury, DVT (uncommon)
Decreased
16 Blood transfusion red cell
production
marrow
Deciding when to Transfuse: failure
l If patient is under 65, stable and has no cardiovascular or
cerebrovascular problems consider transfusion below 7 g/dl
l If patient is over 65, stable and has no cardiovascular or cerebrovascular
problems consider transfusion below 8 g/dl Red cell
l If patient has known cardiovascular / cerebrovascular history count
consider transfusion below 9 g/dl decreased
l Consider transfusion below 10 g/dl if: Increased
red cell Increased
l the patient is appropriately symptomatic such as dyspnoea, destruction red cell loss
angina, tachycardia, orthostatic hypotension or syncope haemolytic bleeding
l or if the patient has known marrow failure or is receiving problems
chemotherapy / radiotherapy
Michael Grant
lOMoARcPSD|4776960
l or has obvious evidence of ongoing significant bleeding ( >
500ml hour)
Overtransfusion is considered as: “Transfusing to a haemoglobin level more

than 2g/dl above the transfusion threshold for that patient”
Maximum Surgical Blood Ordering Schedule ( MSBOS)
General Surgery Operation Tariff
Open Cholecystectomy/Laproscopic Cholec ystectomy G+S

Laparoscopy G+S
Laparotomy-with Low Risk of Blood Loss G+S
Consent: Laparotomy-for Intestinal Obstruction 2
L iver Biopsy G+S
l Give written information in advance Percutaneous Gastrostomy T ube G+S
l Explain benefit of giving transfusion Colostomy 2
I leostomy 2
l Discuss possible complications I leostomy +Pan Proctocolectomy 4
l Inform patient they can no longer be a blood donor Oesophageal Dilation G+S
Partial Gastrectomy G+S
l Give opportunity for questions E RCP G+S
l Document consent in notes T otal/Partial M astectomy G+S
Oesophagastrectomy 4
Partial Cole ctomy 2
Reactions during blood transfusion may be Hepa tectomy 4
Pancreatectomy- Partial/Whipple 4
l Minor or severe
l Minor – fever, urticaria, rash, pruiritis
l Major – pyrexia, hypotension, lion/back pain, pain at infusion site, respiratory distress/TRALI, dark urine (haemolysis), unexpected
bleeding (DIC)
l Early or delayed
l Important to monitor patient during transfusion
Management of minor reaction:

Management of severe reaction:
1. Stop the transfusion
1. Stop the transfusion
(check patient and component compatibility) Replace the administration set and IV access should be
2. Appropriate treatment (antipyretic / antihistamine) maintained with normal saline(check patient and component
compatibility)
3. Reassess patient
2. Resuscitation drugs / trolley may be needed
4. If signs & symptoms worsen within 15 minutes à 3. Monitor and reassess patient frequently
treat as a severe reaction 4. Inform the Laboratory and return the component
5. Mild reactions should be documented in the patient case notes 5. Document event in patient case notes
6. Legal requirement to report event to monitoring body.
17 Infection control
General Infection Control Measures:
l Maintain good standard infection control
l Hand hygiene (soap/water or alcohol sanitizer)
o REMEMBER soap and water if patient has diarrhoea (C.Diff resistant to alcohol)
l Bare below the elbows (watches/jewellery)
l Environmental hygiene
l Use of peri-operative supplemental oxygen is a practical method of reducing the incidence of surgical wound infections.
Prophylactic Antibiotics:
Used if significant risk of infection due to unavoidable contamination of
surgical wounds in areas difficult to sterilse and/or in operations where
infection would have serious consequences (e.g. dacron graft)
l *Always use single dose* unless:
o Duration of surgery > 4 hours
o Blood loss exceeds 1.5 litres
o Emergency surgery for dirty or contaminated wounds
o Infection already present
l Timing of ABx:
o Bactericidal levels in tissue and serum at time of incision
o Greater than 2 hours pre-op ineffective
o Optimal time 30-60 mins (except metronidazole PR, which is 2 hours before)
l Example of general surgery prophylaxis:
o Co-amoxiclav 1.2gm IV, or if penicillin allergic, Gentamicin 2mg/kg IV plus Metranidazole 500mg
§ If MRSA Above plus Teicoplanin 400mg IV
Michael Grant
lOMoARcPSD|4776960
18 Malnutrition and Nutrition Support

Over 25% of hospital inpatients may be malnourished. Hospitals can become so
focused on curing disease that they ignore the foundations of good health—malnourished
patients recover more slowly and experience more complications
Why are so many hospital patients malnourished?

• Increased nutritional requirements (eg sepsis, burns, surgery, CF)
• Increased nutritional losses (eg malabsorption [Crohn’s, UC, short bowel syndrome],
output from stoma)
• Decreased intake (eg dysphagia, nausea, sedation, coma)
• Effect of treatment (eg nausea, diarrhoea)
• Enforced starvation (eg prolonged periods nil by mouth)
• Missing meals during off-ward procedures/investigations
• Difficulty with feeding (eg lost dentures; no one available to assist; handicap [RA,
MS])
• Unappetizing food
Overnutrition and its’ consequences:

• Hypertension/ Hyperlipidaemia/Coronary Artery Disease
• Type 2 Diabetes
• Osteoarthritis
• Gallbladder disease
• Obstructive Sleep Apnoea
• Cancer
Identifying the malnourished patient

• History: Recent weight loss (>20%, accounting for fluid balance); recent reduced in-
take; diet change (eg recent change in consistency of food); nausea, vomiting, pain,
diarrhoea which might have led to reduced intake.
• Examination: State of hydration, dehydration can go hand-in-hand with malnutrition,
and overhydration can mask malnutrition.
o Evidence of malnutrition: skin hanging off muscles (eg over biceps); no fat
between fold of skin; pressure sores; sores at corner of mouth.
o Calculate body mass index; BMI <20kg/m2 suggests malnourishment
o Anthropomorphic indices, eg mid arm circumference, skin fold measures and
grip strength are also used.
• Investigations: Generally unhelpful but low albumin suggestive
Indications for Artificial NS:

• Severe anorexia
• Moderate or severe malnutrition but unable to eat sufficient orally
• Pre-op patient with wt loss ≥ 10% BW
• Oral diet not anticipated for ≥ 10 days
• Intestinal failure
• Enteral nutrition:
o Advice from dietician is essential
o If at all possible, give nutrition by mouth; even an all-fluid diet can meet
requirements (but get advice from dietician)
§ If danger of choking or aspiration (eg after stroke), consider semi- solid diet
before abandoning food by mouth.
§ Enteral is superior to Parenteral for cost, maintenance of intestinal structure
and function, and outcome (infectious complications)
o Tube feeding: Liquid nutrition via a tube, eg placed endoscopically,
radiologically, or surgically (directly into stomach, ie gastrostomy) with most
brands meeting the majority of patients’ requirements with 2L/24h:
§ Polymeric feeds consist of undigested proteins, starches and long chain
fatty acids (eg Nutrison standard®, Osmolite®)
§ Elemental feeds consist of individual amino acids, oligo- and
monosaccharides needing minimal digestion.
§ Use fine-bore (9 Fr) nasogastric feeding tube when possible and check position of
Dextrose 50-70%
nasogastric tube (pH testing) or nasoduodenal tube (X-ray) before starting feeding. Calories
Fat 30-50%
§ Build up feeds gradually to avoid diarrhoea and distension
• Parenteral nutrition can be given supplementary or as a only source of nutrition (TPN) but should be Nitrogen L-amino acids
avoided if possible
Fluid
o Indications: malnourished (likely to become) with gastrointestinal tract is not functioning (eg
bowel obstruction), and is unlikely to function for at least 7d Additrace (zinc, copper,
Trace elements
manganese, selenium)
§ Contraindicated in those with terminal disease; higher risk of complications in those with CCF
and diabetes Vitamins MV 1-12
Michael Grant
lOMoARcPSD|4776960
o Can be peripheral (short term) or central lined (or PICC) – CHECK POSITION WITH X-RAY
o Complications: Sepsis (Blood & tip of line cultures), thrombosis (+/- PE, SVCO), Metabolic imbalance (Electrolyte abnormalities,
acid-base disturbance from increased CO2 production, elevated blood glucose), mechanical (pneumothorax during central line
insertion, embolism of line tip)
o Liaise closely with line insertion team, nutrition team and pharmacist.
o Meticulous sterility on insertion and do not use central venous lines for uses other than nutrition.
o Remove the line if you suspect infection. Culture its tip.
o Review fluid balance at least twice daily Weight (kg) Male Female
How many calories? 15-18 17.6 x W + 656 13.3 x W + 690

1. Determine Basal Metabolic Rate (table - Schofield Equation)
2. Adjust for stress factor (nomogram to right) 18-30 15.0 x W + 690 14.8 x W + 485
3. Adjust for activity
• Bedbound immobile + 10%
30-60 11.4 x W + 870 8.1 x W + 842
• Bedbound mobile or sitting + 15-20%
• Mobile on ward + 25%
>60 11.7 x W + 585 9.0 x W + 656
4. Adjust for energy stores
Bluffer’s guide to PN prescription: 60

50 Burns 25-90%
• Fluids 30 ml/kg/day
40 Severe sepsis
• Calories 30 kcals/kg/day
Multiple trauma
• Fat 30% Total Burns 30 persistent fever >2C
•
•
•
Protein
Na
K
1 g/kg/day
1 mmol/kg/day (1-1.5)
1 mmol/kg/day (0.75-1)
10-25%
{
Multiple #’s
20
10
0 }
persistent fever >1C
Burns 10% single #
IBD, postop
• Cl 1 mmol/kg/day -10
-20 } Partial starvation
19 Benign and Malignant Thyroid disease

SEE GEN MED NOTES
20 Peripheral Arterial Disease

Pathogenesis is most often in the form of atherosclerosis, which can be
thought of as occurring in 4 major steps:
1. Endothelial injury
2. Lipid deposition
3. Inflammatory cell infiltrate
4. Smooth muscle cell migration
This disrupts blood flow by:
• Narrowing of lumen (stenosis)
• Complete occlusion
• Plaque rupture (thrombosis in-situ)
• Emobolisation (distal occlusion arising from arterial origin, e.g. AF)
Clinical manifestation depends on:

• Site of disease
o E.g. buttock pain likely to be iliac origin, common
femoral can give thigh symptoms, superficial femoral
artery disease will present as calf pain.
o Leriche syndrome, is a form of peripheral artery disease involving the blockage of the abdominal aorta causing buttock
pain and impotence
o Thromboangiitis obliterans (also known as Buerger's disease) is a
recurring progressive inflammation and thrombosis
(clotting) of small and medium arteries and veins of the
hands and feet. It is strongly associated with heavy use of tobacco
products, esp. in the young.
• End artery or well collateralized (supporting secondary arteries will
compensate for occlusion of a larger one)
• Speed of disease progression (Chronic more likely to progress from
claudications > pain on rest > ulceration [Fontaine classification],
while acute limb ischaemia seen with the 6 P’s – pain, pulseless, pale,
perishingly cold, paralysed, paraesthetic
Michael Grant
lOMoARcPSD|4776960
Prevalence:
• 16% of adult population over 55 years have signs of PAD
• 2/3 asymptomatic
• 1/3 intermittent claudication
• 1-3% present with critical limb ischaemia
• 5 year mortality: 30% PAD die from MI/ Strokes, 50% critical limb
ischaemia
Risk factors:
Modifiable* factors should be targeted aggressively, as soon as PAD is
discovered
• Age
• Gender
• Cigarette smoking*
• Hypertension*
• Hyperlipidaemia*
• Diabetes mellitus*
Presentation:
Based on the Fountaine Classification:
• Stage I asymptomatic
• Stage II intermittent claudication
• Stage III ischaemic rest pain
• Stage IV ulceration or tissue necrosis (gangrene)
The cardinal feature of PAD is intermittent claudication:

• No pain at rest or first few steps
• Relatively consistent walking distance
• Relief on standing for 1-3 minutes
• No need to sit or lie
• Recurrence on walking a similar distance (i.e. claudication distance)
• Worse walking quickly or uphill (150-1000 mls/min)
As the disease progresses, PAD can go critical ischaemia that possess the cardinal features of:
• Pain at rest (starting most distally, i.e. the foot)
o Pain at rest for greater than 2 weeks
o Pain at night: “does the pain wake you from your sleep?”
o Not relieved by simple analgesia
o Relief by hanging foot out of bed – also known as the “vascular position” as gravity helps flow
• Ulceration – atrophic, “punched out” looking ulcers
• Gangrene (Can be “dry” [black discolouration as iron reacts with hydrogen sulphide from
anaerobic bacteria to form iron sulphate] or “wet” [superimposed infection/cellulitis as necrotic
tissue becomes infected]
Acute limb ischaemia presents with different symptoms as the onset is much more sudden
• A surgical emergency (6 hr window)
• Often embolism, thrombosis and trauma
• Ask “is the patient in AF?”, “previous hx claudication?”
• Look for the 6 p’s – pulseless, pale, pain, perishingly cold, paralysed and paraesthesia
Examination
• Should assess the circulatory system “as a whole”:
• “supra-aortic”- rate/rhythm/character/volume/symetry
• BP both arms
• Carotid/renal bruits (absence does not exclude)
• Cardiac murmurs
• Presence of AAA
• Absent/ weak pulses – recording if volume is absent, diminished, normal or bounding
Michael Grant
lOMoARcPSD|4776960
• Pallor with increased cap refill
• Buerger’s angle (serve if <20-30 degrees) leg is lifted to 45 degrees for 1-2
minutes causing pallor followed by compensatory vasodilation that turns the foot
red upon return to gravity – reactive hyperaemia due to build up of anaerobic
metabolites
• Muscle atrophy
• Loss of hair growth
• Venous guttering
• Brittle crumbly nails
• Neuropathy
Investigations
• Ankle-Brachial Pressure Index
o Using a Doppler and sphygmomanometer to measure BP the best ankle and
brachial pressure and divide ankle systolic by brachial systolic
o >1.3 is a sign of indispensable vessels, especially those that have become
calcified in those with diabetes
o 1 to 1.2 is considered normal
o 0.5 to 0.9 confirms PAD, and <0.5 or ankle pressure of <50mmHg confirms
critical limb ischaemia
• Duplex Ultrasonography (Grayscale structural US plus Doppler flow measurement)
• MR Angiography
o Good images with no radiation has led to increasing use
o Contraindicated in those with ferrous-containing implants – e.g. pacemakers
o Gadolinium contrast has been linked to pulmonary fibrosis in those with renal
impairment
• CT Angiography
o High resolution anatomical detail but comes with a radiation dose
o Iodine contrast nephrotoxicity
o Iodine allergy
o eGFR <30mls/min - avoid or rehydrate before and after
o Metformin held for 48 hours post-exposure as there is a risk of lactic acidosis
• Digital Subtraction Angiography (DSA) is a type of fluoroscopy technique used in interventional radiology to clearly visualize blood
vessels in a bony or dense soft tissue environment. Images are produced using contrast medium by subtracting a 'pre-contrast image' or
the mask from later images, once the contrast medium has been introduced into a structure; it remains the gold standard
o Invasive and involves x-ray radiation
o Contrast allergy/nephrotoxicity
o Puncture site problems
o More commonly second line (when intervention is anticipated)
• ESR/CRP to rule out arteritis
• Coag screen plus homocysteine
Treatment
• Risk factor modification
• Lifestyle
• Smoking cessation
st
• Clopidogrel is recommend as 1 line
• Weight reduction
• Lipid control in the form of a statin to achieve:
• Total Chol<4mmol/l
• LDL-Chol<1.8mmol/l
• glycaemic control
• HbA1c <7%
• BP control
• PAD (no DM or renal insufficiency) <140/90
• PAD(with DM or renal insufficiency) <130/80
• “Claudicant”
• Exercise therapy esp. supervised-poor compliance usually at 2h per week for 3 months
• Pharmacotherapy e.g. Naftidrofuryl oxalate (offers only a modest help)
• Endovascular intervention
• Percutaneous transluminal angioplasty (balloon dilation)/stents
• Better for proximal “aorto-iliac disease”
• Infra-inguinal disease has poor long term patency (5 year patency is 79% in Iliac and 55% in femoral)
• Surgical option
• Bypass/endarterectomy
• Vein/dacron/ PTFE/ bovine pericardium
• Invasive
• Better long term results
• Critical limb ischaemia has the same treatment options as claudication plus:
• Amputation is needed in <3% and should be reserved until other interventions have failed (gabapentin may be used for
phantom pain)
Michael Grant
lOMoARcPSD|4776960
21 Pancreatitis
Definitions:
• Acute pancreatitis – acute inflammatory process of the pancreas (mild 80% or severe 20%)
o Self-perpetuating inflammation from auto-digestion
o 50% of cases that progress to necrosis will develop a superadded infection
• Pancreatic necrosis – focal or diffuse development of non-viable parenchyma which may become infected (infected necrosis)
• Pancreatic abscess – collection of pus
• Pseudocyst – collection of pancreatic juice, inflammatory exudate, and sometimes necrotic pancreas & fat, in the lesser sac without a
compete epithelial lining
Aetiology:
• Alcohol (approx 20-30%)
• Idiopathic (approx 15-20%)
• Rarer causes (approx 5-10%)
o Trauma (ERCP, blunt abdominal trauma)
o Drugs (steroids, thiazide diuretics)
o Metabolic (hyperlipidaemia, hypercalcaemic)
o Infection (mumps, coxsackie virus)
o Hereditary pancreatitis
o Nutritional (anorexia, bulimia, malnutrition)
o Hypothermia
o Scorpion venom
Clinical features:
• Symptoms
o Severe epigastric pain (may radiate to back and relieved by leaning forward)
o Nausea
o Vomiting
• Signs
o Epigastric tenderness
o Shallow breathing (deep breathing will move pancreas)
o Flank bruising – blood and fluid due to vessel autodigestion retroperitoneal space (Grey-Turner’s sign)
o Peri-umbilical bruising – blood and fluid in falciform ligament (Cullen’s sign)
Tests:
• History & clinical examination
• Serum amylase (>1000u/ml or x3 normal)
o However also may be raised – other typically not as much – in cholecystitis,
mesenteric infarction, GI perforation, renal failure (excreted via kidneys)
• Serum lipase
• AXR: may show loss of psoas shadow (due to reteroperitoneal fluid), “sentinel loop” of
proximal jejunum due to ileus (solitary air-filled dilation)
• CT scan – scanning modalitiy of choice; look for swelling, inflam., necrosis
o Indicated in all severe cases
o Contrast – enhanced
§ Viable pancreas – intact blood supply, enhances (white)
§ Necrotic pancreas – no enhancement (black)
o Balthazar score – ratio of viable to necrotic on CT (Most accurate after day 4 or 5) Figure 2 - necrotic pancreas w/ infection (note gas bubbles)
• MRI can also be used and is very sensitive
Grading severity:
• Glasgow (Imrie) and Ranson systems (at 48 hrs)
• C-reactive protein (CRP)
o severe attack (> 210 mg/l first 4 days or > 120 at end of first week)
o Handbook says >150mg/l after 36h is severe pancreatitis
• APACHE II score
Managament:
• Mild – see flow chart to right
• Gallstone:
o Ultrasound scan
Michael Grant
lOMoARcPSD|4776960
o Gallstones should be removed within 2-4 weeks of acute attack – otherwise high risk of recurrance
o Laparoscopic cholecystectomy or ERCP +
Diagnosis of acute pancreatitis
sphincterotomy (serum amylase) • Pain relief
• IV fluid resuscitation
o MRCP or intra-op cholangiogram to exclude + electrolytes
Initial management • Anti-emetic
CBD stones • Nil by mouth (NBM)
• Severe acute pancreatitis: • NG suction (severe vomiting)
Grading of severity
o Management in HDU or ICU (Glasgow (Imrie) or CRP)
o Hourly urinary output monitoring Mild Severe
o Central venous access (CVP monitoring)
Supportive management +
o Arterial line if significant CVS compromise Aetiological assessment
monitoring for complications
o Nutritional support (TPN or fine bore NG/NJ
tube)
Treatment/removal of
Treatment of complications
aetiological factor
Complications:
• Pseudocyst
o Collection of fluid in lesser sac that may be palpable per abdomen w/ abdo pain and
delayed gastric emptying (due to pressure)
o May resolve spontaneously – esp. if <6cm w/o pain
o Drainage into stomach
§ Cystgastrostomy; ant. wall of pseudocyst stitched to opening in post. wall of
stomach
• endoscopic
• open surgery
• Necrosis – 50% progress to this (can become infected)
o Initially conservative – ICU support for organ failure
o Minimally invasive resection of pancreas (MIRP) – laparoscopic
o Open surgical debridement (necrosectomy)
• Abscess
• Erosion of major vessel by elastase – selective embolisation may be life saving
• Exocrine insufficiency – steatorrhoea
• Endocrine insufficiency - diabetes
• Chronic pancreatitis
o Fibrosis of pancreas – tissue replaced by scar
§ Stricturing & dilatation of pancreatic duct
o Pseudocyst fomation
o Increased risk of pancreatic cancer
o Calcification in gland on x-ray or CT scan
o Chronic abdominal pain
o Exocrine insufficiency
§ Steatorrhoea
§ Managed by oral enzyme supplementation (Creon)
o Endocrine insufficiency – diabetes
22 Breast Cancer
Anatomy:
• Upper outer contains greatest bulk of tissue and is most frequent location of tumours
(benign and malignant)
nd th
• Borders of base of tissue: 2 to 6 rib, midline to axillary line
• Medial breast isn’t well imaged in mammogram, some aggressive cancers form here and
are missed
Risk factors:
• Increasing age
Michael Grant
lOMoARcPSD|4776960
• Environmental factors greater than genetic (< 5% related to a genetic risk history)
• Menstrual onset and end, age at first pregnancy is important
• BMI (peripheral estrogen), alcohol (estrogen), diet, the pill may be important
• Previous breast disease - CIS, atypical hyperplasia
• Exogenous Estrogen
o Hormonal replacement therapy (HRT) - 30% increased risk with long term use (5
years or more)
o Oral Contraceptives (OC) - Risk slight – 7 years or more of use
o Progesterone is not protective for Breast CA as it is with endometrial
• Genetics: BRCA-1, BRCA-2
Presentation:
• Lump
• Nipple discharge, nipple retraction/inversion
• Skin changes- rash, scaling, puckering (paget’s?)
• Pain
• Through screening (2 view – cranio-caudal and obligue - mammography - every 3 years
age 50-70)
o Reduction of death by 30% in women >50
• Family History - genetic risk identified
Types of breast cancer:

• Carcinoma in situ in which malignant cells are confined to the normal structures (ducts and
lobules) with no access to lymphatics meaning no current risk of metastasis. There are 2
types:
o Ductal CIS (more common type) is seen as dilated ducts with large populations of
cells forming thick peripheries of the duct – reducing the diameter of the lumen –
calcification due to necrosis may also be seen
§ Rarely presents as lump or calcification on mammo
§ Unilateral
§ Any age
§ Significant risk of invasion
o Lobular CIS tend to be smaller, more uniform and do not undergo either necrosis or calcification
§ Usually an incentaloma in the premenopausal
§ Bilateral and multifocal
• Invasive carcinoma:
o Ductal carcinoma
§ Many subtypes: Non-specific, mucinous, tubular, medullary, papillary
§ Histologically, I t is a collagenous mass of a malignant gland (central lumen with a rim of malignant cells) that forms a discreet
mass
o Lobular carcinoma does not form a discreet mass and is difficult to diagnose other than from biopsy
§ Histologically, cells grow linearly and around other tissue (indian filling) amd cells ten to be quite uniform
Triple assessment:
1. History/Examination
• 3 S’s, 3 T’s, 3 C’s
• Worrying signs: Paget’s disease of the nipple? Peau D’Orange
(implies lymphatic spread)?
• Discharge – clear (usually physiological), green opaque
(mutliduct – usually ectasia; single duct – papilloma/DCIS), blood
(investigate)
2. Mammography/Ultrasound (occasionally MRI in younger)
• USS – look to see if cystic/solid (cysts almost always benign) and
for outline (smooth more likely to be benign)
• Mammography – better in older patients due to background fatty
tissue
3. FNA/Core Biopsy
• Fine needle aspiration
o Performed with a 22-24 gauge needle.
o If fluid clear is aspirated and swelling cyst resolves, diagnosis is a simple cyst
Michael Grant
lOMoARcPSD|4776960
o If fluid bloody, send for cytology and consider further assessment
o If no fluid, further assessment necessary
• Core needle biopsy
o Performed with a 14-18 gauge needle, generally using U/S or
stereotactic mammography
o Histological specimen obtained
Surgery:
• Primary Tumour Surgery
o Remove Tumour:
§ Modified radical mastectomy
• skin, areola, nipple, and most axillary lymph nodes
§ Simple mastectomy
§ Partial mastectomy/Wide local excision (followed by radiotherapy)
• Localised cancer: screen detected that can be excised with a
tumour free margin (WLE – wide local excision)
• No contraindications to irradiation (needed post)
• Patient wishes conservation
§ Axillary clearance vs sentinel node
biopsy
o Restore Anatomy
§ Deep inferior epigastric perforator flap
(DIEP – muscle sparing)
§ Transverse rectus abdominus
myocutaneous (TRAM – muscle
destroying)
§ Lat. Dorsi. Flap
§ Less used due to risks, Implant
• Staging of disease (Node assessment)
• Treatment - Cure, Risk Reduction, Palliation
• Complications:
o General Complications:
§ Anaesthesia complications
§ Immobility related - LRTI, DVT/PE
§ Wound infection
o Specific complications:
§ Nerve damage (long thoracic)
§ Chronic wound pain
§ Cosmetic/psychological
§ Lymphoedema (esp. with axillary node clearance)
Radiotherapy:
• Recommended for all patients with invasive cancer after WLE (recurrence decreases from 30% to <10% at 10yrs)
• Axillary radiotherapy used if lymph node +ve on sampling and surgical clearance not performed (risk of lymphoedema and brachial
plexopathy)
• S/E: pneumonitis, pericarditis and rib fractures
Chemotherapy:
• Improves survival & reduces recurrence in most groups of women (consider in all except excellent prognosis patients), eg epirubicin +
‘CMF’ (cyclophosphamide + methotrexate + 5-FU)
Endocrine agents:
• Aim to reduce estrogen activity and are used in oestrogen receptor (ER) or progesterone receptor (PR) +ve disease
• The ER blocker tamoxifen is widely used, eg 20mg/d PO for 5yrs post-op (may rarely cause uterine cancer so warn to report vaginal
bleeding)
• Aromatase inhibitors (eg anastrozole) targeting peripheral oestrogen synthesis are also used (may be better tolerated) - They are only
used if post-menopausal
The Lumen Bleeding

Tumour - 1° or 2 °
Inflammation – IBD
The Wall diseaseObstruction
Diverticular
Stricture
Vasculitis
Bloating
Intussusception Collapse
Colicky Pain
TB granuloma
Dehydration
Vomiting
Distension
Adhesions
Outside the Wall Perforation
Pressure (may even lead to perforation) Constipation
Herniae - 1° or 2° (External or internal)
Increased
Volvulus Peristalsis
Fluid loss (up to 9L/d to 3rd space and K+ loss)
Michael Grant
lOMoARcPSD|4776960
23 Intestinal obstruction
Types of obstruction:
• Mechanical
o Partial / Complete
o Simple / Strangulation
• Functional
o Paralytic Ileus
o Pseudo-obstruction
§ Symptoms of mechanical but no cause found – may respond to Neostigmine
§ Ogilvie syndrome is the acute dilation >10cm of the colon in the absence of any
mechanical obstruction in severely ill patients
Aetiology of mechanical:
• Adhesions
• Neoplastic
• Hernia Foreign Body
• Intussusception Bezoar
• Volvulus
o Sigmoid (coffee Adhesions Foreign Body bean)
o Ceacal
o Rarely: Gastric Herniae
Crohn’s Disease
§ Triad of Diverticular
gastro-oesophageal obstruction may occur: vomiting (then
retching), Gallstone
Tumour
Disease
pain, and failed attempts to pass an NG tube
§ Risk factors: Congenital (Paraoesophageal hernia; congenital bands; bowel
malformations; pyloric stenosis), Acquired (Gastric/oesophageal surgery)
§ Tests: Look for gastric dilatation and a double fluid level on erect films.
• Foreign Body
• IBD
• Stricture
• CF/ haematomas
• TB (Granuloma - developing world)
Cardinal signs of obstruction:

• Vomiting
• Colicky pain
• Constipation (usually absolute but may not be if obstruction is
high)
• Distension
Examination:
• Tachycardia
• Hypotension
• Fever
• Distension – greater with distal obstruction
• Scars
• Hernias
• Auscultation – tinkling, absent (if latter may be pseudo-
obstruction; no structural cause found)
• PR examination – essential
Bloods:
• Likely to be normal but check for dehydration: FBC and U&E
• Amylase
Imaging:
• AXR: Small bowel (valvulae conniventes), large bowel
(Haustra, gas proximal to obstruction but not in rectum – unless PR already performed, if ileo-cecal valve is functional then pain may be felt
over a distended cecum)
o Gastrografin is hyperosmolar and may stimulate peristaltic activity of the small bowel, can help to identify small bowel obstruction
and can guide treatment (if contrast within the colon in 24hr, it predicts conservative resolution)
• Erect CXR looking for pneumoperitoneum
• Barium swallow/Barium enema
• CT many occasionally be helpful if XR inconclusive; may show fluid filled bowel with transition zone
Important questions:
• Small or large bowel?
• Ileus or mechanical?
o Ileus will have no pain or bowel sounds
Michael Grant
lOMoARcPSD|4776960
o Ileus can be caused be recent surgery, electrolyte disturbance, systemic infection, ischaemia, etc.
• Is obstruction simple/closed loop/strangulated?
o Simple – one obstruction point with intact vascular supply
o Closed loop – obstruction at 2 points (e.g. volvulus, functional ileo-cecal) with gross distention usually over cecum due thinnest wall
and widest section (>12cm needs urgent surgery due to pending perforation)
§ Sigmoid volvulus (coffee bean) can sometimes be treated with sigmoidoscopy and flatus tube
o Strangulated – blood supply is compromised (e.g. in strangulated hernia) with sharper, constant and localised pain; peritonism, fever
and raised WCC demonstrate the mesenteric ischaemia
Management:
• Immediate
o Analgesia
o “Drip and suck” – IV fluid resus, NG tube aspiration and urinary catheter to
track fluid status
§ NBM is insufficient due to bowel outputting up to 9L/day
o Order imaging – AXR, erect CXR, ?CT, ?Gastrografin, ?Barium swallow/enema
o DVT prophylaxis
o Depending on type may be managed conservatively:
§ Paralytic Ileus
§ Known adhesions
§ Metastatic disease
§ Inflammatory
§ Partial small bowel
• Although, occasionally, SBO due to adhesion may require surgical intervention
• Surgery
o Strangulation and closed loop obstruction require emergency surgery; depends on viability of tissue but typically resection with
primary anastomosis
o Malignant obstructions can have stents placed to relieve
• Resolution
o Less pain
o Less distension
o Decreased NG losses
o Return of bowel function
24 Sepsis
Infection:
“A microbial phenomenon characterized by an inflammatory response to the presence of micro-organisms or the invasion of normally
sterile host tissue by those organisms.”
Bacteraemia:
“The presence of viable bacteria in the blood.”
Systemic Inflammatory response syndrome (SIRS):

“The SYSTEMIC inflammatory response to a VARIETY of severe clinical insults”
l SIRS
• Temperature >38 degrees Celsius or <36 degrees Celsius.
• Heart rate >90 beats per minute.
• Respiratory rate>20 breaths per minute or PaCO2<32mmHg.
-1 -1
• White blood cell count > 12,000 cells μL , <4,000 cells μL , or >10%
band forms.
Sepsis:
l “Systemic Inflammatory response syndrome caused by INFECTION”
l “Systemic illness caused by MICROBIAL INVASION of normally sterile parts of the body”
l “Sepsis is a term that specifically serves to differentiate an illness of MICROBIAL ORIGIN from an IDENTICAL CLINICAL SYNDROME that
can arise in conditions of NON-MICROBIAL ORIGIN.”
l Severe sepsis:
Michael Grant
lOMoARcPSD|4776960
l SEPSIS plus >1 organ dysfunction - Requires escalation to Level 2 care
l Septic shock:
l “SEPSIS induced with HYPOTENSION despite adequate resuscitation along with the presence of perfusion abnormalities which may
include, but are not limited to lactic acidosis, oliguria or an acute alteration in
mental status.”
l Multiple organ dysfunction syndrome (MODS):
l “The presence of ALTERED ORGAN FUNCTION in more than 2 organs, in an
acutely ill patient such that HOMEOSTASIS cannot be maintained without
intervention.”
Pathophysiology:
• Stimuli
• Host response
• Immune response via upregulation of NF-kB
• Pro and anti-inflammatory cytokines (mostly macrophage and lymphocytes)
• Further Macrophage stimulation (release of prostaglandins, proteases, free radicals)
• Stimulation of the coagulation cascade (Endothelial cells upregulate adhesion
molecules and decrease in protein c receptors)
• Microvascular plugging
• Decreased tissue perfusion - Hypoxia
• Progressive
• Death
General supportive measures:

l Circulatory support Infection
- Fluid resuscitation; usually hartmann’s
- Adequacy of fluid resuscitation
Vasodilation Inflammatory Mediators
- Catecholamines Endothelial Dysfunction
l Noradrenaline or Dopamine
l Adrenaline Hypotension Microvascular Plugging Vasoconstriction Oedema
l Non catecholamine drugs

l Mechanical ventilation Maldistribution of Microvascular Blood Flow
l Renal dialysis
l Nutritional support Ischaemia
l Immune modulation
l Surgery /Interventional radiology/ Endoscopy Cell Death
l Antimicrobials
- Activated Protein C [Drotrecogin alfa - recombinant Organ Dysfunction
form of human activated protein C (serine protease)

that has anti-thrombotic, anti-inflammatory, and profibrinolytic properties]
l Corticosteroids
l Immunoglobulins and statins
l Inflammatory response mediators
- HMGB-1 neutralizing antibodies and small molecule inhibitors
- Alpha 7 nicotinic acetylcholine receptor agonists
25 Diverticular disease
Diverticulosis – presence of diverticula in bowel wall
Diverticulitis – inflammation of diverticula
Diverticular disease – entire spectrum of clinical consequences
Pathogenesis:
• Mucosal herniations that may be congenital or acquired
o 30% of westerner’s have diverticuli by age 60
• Points of weakness – where vasa recta vessels pass through wall to supply mucosa
• Beside taeniae – occur parallel through circular muscle
• Majority in sigmoid – 95% of complicatinos arise in this location
• False diverticula – do not involve muscle layer
• Most in sigmoid colon where intraluminal pressure is highest (although can occur in rest
of large bowel)
Michael Grant
lOMoARcPSD|4776960
• None in rectum – tinea coli spread out to form continuous muscle layer,
reinforcing wall
• Areas of high pressure - segmentation
• Lack of dietary fibre
o Large volume; wide diameter – less segmentation of bowel
o Fluid absorpted creating more liquid stool – less pressure required
o Swift passage - less strain on sigmoid
Presentation:
• Asymptomatic
• Altered bowel habit ± left-sided colic relieved by defecation
• LIF discomfort
• “Rabbit –like” stools; links well with “warren-like” appearance of diverticuli on
colonoscopy
• Exclude sinister pathology
Investigations:
• Barium enema (double contrast) can clarify the diagnosis in patients with
abdominal pain and altered bowel habit
• Colonoscopy
o Enema or colonoscopy risk perforation in the acute setting
• CT abdomen is best to confirm acute diverticulitis and can identify extent of
disease and any complications
Treatment:
• High fibre diet
• 20-30 gm bran to reduce symptoms
• Reduces pain not complications
• Fibre supplements Diverticulitis
• Anti-spasmodics (mebeverine)
Phlegmon
Diverticulitis presents with features of diverticulosis + pyrexia, raised WCC, raised Perforation
(Surrounded by Fistula Bleeding
omentum)
CRP/ESR, a tender colon ± localized or generalized peritonism.

• Treatment: Analgesia, NBM, IV fluids, IV antibiotics (Broad spectrum Localised Generalised Colovesical Coloenteric
Stricture
penicillin and metronidazole), CT-guided percutaneous drainage (if abscess) Abscess Peritonitis Colovaginal Colocutaneous
o F/U BE or Colonoscopy in 4-6 weeks
• Complications:
o Perforation - There is ileus, peritonitis ± shock. Mortality: 40%. Manage as for an acute abdomen
§ Sudden onset, shock, tender, guarding, rebound
§ Erect CXR – look for pneumoperitoneum; large suggests perforation of colon, small suggest peptic ulcer perforation
§ At laparotomy a Hartmann’s procedure may be performed (temporary colostomy + partial colectomy) with extensive lavage at
the end of the prodecure; large bore drains
o Haemorrhage - is usually sudden and painless
§ Technetium red cell scan with angiography - Vasopression; embolisation
• Embolisation or colonic resection may be necessary after locating bleeding points by angiography or colonoscopy (here
diathermy ± local adrenaline may prevent need for surgery)
§ Surgery – emergency colectomy
o Fistulae Enterocolic, colovaginal, colovesical or colocutaneous (depends on site: pneumaturia/faecaluria ± intractable UTIS, PV
faeces, Cellulitis)
§ Colovesical - BE (80%), Bourne test (look for barium in urine), cystoscopy, CT (e.g. to the right – air fluid level in bladder and
loss of plane between colon and bladder)
§ Colovaginal - BE, vaginal examination
§ Rx for all is Sigmoid colectomy; Omental pedicle (placed between organs of fistulation to prevent recurrence), urinary catheter
o Abscesses - swinging fever, leucocytosis, and localizing signs, eg boggy rectal mass (pelvic abscess—drain rectally)
§ If no localizing signs, remember the aphorism: pus somewhere, pus nowhere = pus under the diaphragm; urgent USS
§ Mangagment:
• Broader spectrum antibiotics – e.g. Pipericillin with tazobactam
• CT scan
•Percutaneous drainage under radiological guidance – drain left in situ until pus yield diminishes
•If no resolution – Surgery: Hartmann’s (Safe; but 50% not reversed) or sigmoid colectomy + loop ileostomy (higher risk
due to anastomosis; but easier reversal)
o Phlegmon followed by post-infective strictures may form in the sigmoid colon
§ >10% of complications – caused by recurring inflammation and healing with fibrosis
§ Crampy abdominal pain, constipation/diarrhoea, thin stools, abdominal distension
• Management:
o Barium enema
Michael Grant
lOMoARcPSD|4776960
o Colonoscopy – may be difficult to pass through stricture
o Sigmoid colectomy
26 Perianal conditions
Anorectal anatomy:
• The anal canal is completely extraperitoneal. The length of the anal canal
is about 4 cm (range, 3-5 cm), with two thirds of this being above the
pectinate line (also known as the dentate line) and one third below the
pectinate line.
• Dentate line marks the beginning of the transition zone (1cm long
segment where stratified squamous transitions to columnar)
• Ducts of mucous glands empty to area just proximal to dentate line
• Dentate line mark watershed boundary of lymph drainage – below; inguinal,
above; mesorectal
Examination:
• Inspection
• Digital Rectal Examination
• Rigid Sigmoidoscopy
• Proctoscopy
• Flexible Sigmoidoscopy
• Colonoscopy
Investigations:
• Endo-anal ultrasound
• Barium studies
• Ano-rectal manometry (pressure measurement - useful in the investigation of
patients with faecal incontinence and obstructed defecation)
• Defaecating proctogram
• Fistulogram
• Magnetic resonance imaging
• Rectal mucosal biopsy
Haemorrhoids:
• Hypertrophy of physiologic haemorrhoids
• Can be internal, external or mixed
• Classifications:
o 1st Degree: Bleeding – fresh red, although make sure to investigate for
more malicious causes
o 2nd Degree: Prolapse and reduce spontaneously
o 3rd Degree: Remain prolapsed but can be reduced manually
th
o 4 degree: Cannot be reduced
• Management:
o CONSERVATIVE: Avoid constipation and straining, adjust diet
(fibre, fluids), use faecal soften ers (lactulose).
o MINOR PROCEDURES: Rubber band ligation, injection (almond
oil and phenol), infra-red photocoagulation
o OPERATION: Transfixion and excision, circular stapling
o Specimen should be sent for histological examination if cancer
is suspected
• Thrombosed External Haemorrhoid:
o Very painful – blood pools and forms thrombosis
o Rx: incision under local, squeeze out thrombus
Perianal abscess
• Aetiology: common condition that is usually due to a
blocked anal gland that subsequently becomes infected
(cryptoglandular origin)
o Diabetes, Crohn's disease or those who are
immunocompromised are susceptible
o The abscess may discharge spontaneously to the skin,
and if a communication to the skin is established then a
fistula may result - fistula-in-ano (a.k.a. Anal fisula) in
50% of patients.
• Types: of perianal abscess: (A) ischiorectal, (B) perianal, (C) intersphincteric, and (D) submucosal
Michael Grant
lOMoARcPSD|4776960
• Abscesses that involve the upper portion of the anal sphincters are complex and require specialist management
• Diagnosis: history of constant throbbing pain made worse by defecation and visual inspection, which demonstrates localised swelling,
tenderness and redness.
o A large or a deep-seated abscess, such as an ischiorectal abscess, often presents with systemic symptoms of sepsis and fever
o PR may be impossible due to spasm of sphincter
• Investigations:
o FBC and blood glucose level
o EUA
• Treatment: ABx alone are NOT ENOUGH - incise and drain the abscess under local anaesthesia
o Antibiotics are used if the sepsis is extensive or if the patient is immunocompromised
o If recurs, consider fistula
Anal fistula:
A fistula is an abnormal communication between two epithelial-lined surfaces. Afistula-in-ano implies a
communication between the anorectum and the perineal skin.
• Causes:
o Idiopathic - probably related to anal gland infection.
o Anal gland infection
o Crohn's disease
o Iatrogenic – perianal surgery, cyst drainage
o Carcinoma
o Trauma, especially obstetric.
o Foreign body (Occasionally a chicken or fish bone may get stuck in the anal canal
and cause a fistula)
o Radiation damage
o Tuberculosis, actinomycosis
• Types of perianal fistulas:
o Intersphincteric
o Trans-sphincteric
o Supra-sphincteric
o Extra-sphincteric
• Presentation: recurrent perianal abscesses or with a bloody and purulent discharge
w/ pain and discomfort
• Investigations: EUA, sigmoidoscopy, MRI
• Treatment:
o Seton silicon thread is treatment is used as incision would damage sphincters –
irritation from thread causes inflammation, fibrosis and seals the canal
Anal fissure:
• Small, linear ulcer of the anal verge; caused by mismatch in sphincter tightness and stool consistency
• Usually at the 6 or 12 o’clock position
• Rx: Conservative – diet advice and lactulose, Medical – GTN or diltiazem ointment, Surgery – botox injection
or internal anal sphincterotomy
Perianal Warts:
• HPV (most commonly genotype 6) – in situ carcinomatous changes within the perianal warts may occur
potentially lead to SCC
• Most often seen in adult homosexual males and less frequently in the heterosexual population
• About two-thirds of patients with perianal warts also have warts within the anal canal
• Rx:
o Diathermy fulguration and scissor excision
o Podophyllotoxin (PPT), also known as podofilox, is a medical cream (MOA: destabilizes microtubules) that is
used to treat genital warts and molluscum contagiosum
Anal cancer:
• The majority are squamous cell carcinomas (SCC)
• The reason for the higher prevalence in women is unclear but it may be due to human papilloma
virus (HPV) infection from secondary spread from cervical HPV (genotypes 16 and 18) or from the
practice of receptive anal intercourse
• Commonly seen in male homosexuals often in association with AIDS-related illnesses.
• Bowen's disease and extra-mammary Paget's disease are important premalignant skin conditions
that may give rise to an invasive cancer of the anal verge
• Treatment:
o Treatment depends on location, size and extent of local spread of the tumour.
Michael Grant
lOMoARcPSD|4776960
o Surgery (WLE or APER) and chemo +/- radiotherapy
Rectal prolapse:
• Full thickness prolapse is painless and can be reduced manually by
patient
o Can have partial thickness, mucosal prolapse
• Look for in elderly, females, spinal cord disease, psych patients
• Rx: Rectal shortening surgery
Pruritus Ani:
• Pruritus ani is an unpleasant yet common condition; however, it is poorly understood (?coffee may make
worse) and often poorly managed
• The patient complains of varying degrees of discomfort and itching around the anal area
• Rx related to cause
27 Patient safety
• Drug: omission; comission

• Dose; Frequency; Concentration; Rate
• Failure to note an allergy or drug interaction
Prescribing • Clerical: Writing illegibly / Incorrect patient details / Date &
Time
• Transcription errors
• Drug not available

Preparation • Wrong reconstitution
• Dose; Concentration
• Drug: omission; comission

• Dose; Frequency; Concentration; Rate
Administration • Wrong route
• Wrong technique
An incident is defined as:

l Any event which could have or did lead to patient harm.
l Includes
• Safety compromises you have been involved in or witnessed
• Near misses
• Minimal harm
• More serious harm
• Errors / accidents
Medicines reconciliation seeks to ensure that correct medication is provided at all transition points within the hospital, at risk times:
l Admission
l Discharge
l Movement between wards
Michael Grant
lOMoARcPSD|4776960
28 Level of care and monitoring

Critical Care Outreach Services (CCOS) is defined as:
l Introduced into the NHS 10 years ago
l Involves a team of nurses or doctors with ICU experience who visit patients outside the ICU environment
l They may be called to see patients at the request of general ward staff
l They may carry out routine visits to patients who for example have been recently discharged from ICU to the general ward
l Three main objectives:
l To provide expert advice to ward staff which may help avert admissions to ICU
l To ensure timely admission to ICU and thus avert poor outcomes due to delays in ICU admission,
l To enable more secure discharges from ICU through providing a safer
ward environment with diminished risk of ICU readmission
29 Hypercalcaemia and
hyperparathyroidism
Essential calcium functions in the body:
• Muscle contraction
• Conduction of nerve impulses
• Intracellular signaling
• Blood clotting
• Glandular secretions
Calcium cycle:
• Dietary intake - Intestinal absorption
• Skeletal remodeling – released to and from serum
• Urinary excretion
• 50-60% bound to proteins or complexed with anions (citrate, phosphate) with the
remaining ionized (free) calcium responsible for physiological processes – thus
corrected calcium is the test of interest:
o Correct total Ca2+ for albumin as follows: add 0.1mmol/L to Ca2+ level for every
4g/L that albumin is below 40g/L, and a similar subtraction for raised albumin.
• Regulation:
o Parathyroid hormone
§ Half-life 3 minutes
2+ 2+
§ Responds to changes in extracellular Ca via Ca sensing receptor on the
cell surface of parathyroid chief cells
§ PTH increases osteoclastic activity
o Vit D & Calcitriol (1,25-dihydroxyvitamin D) – activated vitamin D
§ Vit D is hydroxylated first in the liver to 25-hydroxy-vit D, and again in the
kidney to 1,25-dihydroxy-vit D (calcitriol), the biologically active form.
Calcitriol production is stimulated by reduced Ca2+, PO43–, and PTH
(controls 2nd hydroxylation in kidney)
2+ 3–
§ Actions are: increase Ca and PO4 absorption from the gut and the
kidney; inhibition of PTH; enhanced bone turnover
o Calcitonin: Made in C-cells of the thyroid, acts to oppose parathormone
(decreases Ca2+ and PO43–)
o Magnesium: Decreased Mg2+ prevents PTH release, and may cause
hypocalcaemia.
Hypercalcaemia:
• The level of calcium in the blood is normally between 2.1-2.6 mmol/L
• Hypercalcaemia can be classified as mild, moderate, or severe based on the
adjusted serum calcium concentration. However, the severity of symptoms also
depends on the rate of onset of hypercalcaemia:
o Mild hypercalcaemia is an adjusted serum calcium concentration of 2.65–3.00
mmol/L.
§ Polyuria and polydipsia, dyspepsia, vague depressive complaints and mild cognitive impairment
o Moderate hypercalcaemia is an adjusted serum calcium concentration of 3.01–3.40 mmol/L.
o Severe hypercalcaemia is an adjusted serum calcium concentration of greater than 3.40 mmol/L.
Michael Grant
lOMoARcPSD|4776960
§ Between 2.8 to 3.5 mmol/L - In addition to above, apathy, weakness,
nausea anorexia, constipation
• Greater than 3.5 mmol/L - severe symptoms: As above & dehydration, abdominal
pain, lethargy and coma
• Signs and symptoms:
o Bones
§ Bone pain
§ Joint pain
§ Increased risk of fracture
§ Gout
o Stones
§ Polyuria
§ Polydipsia
§ Nocturia
§ Nephrolithiasis
o Groans
§ Constipation
§ Anorexia
§ Heartburn
§ Peptic ulcer disease
§ Pancreatitis
o Psychic moans
§ Weakness
§ Depression
§ Memory loss
§ Psychosis
o Ectopic calcification
o Shortened QT interval
• Causes:
o Non-parathyroid mediated
§ Malignancy-associated hypercalcaemia
• Humoral hypercalcaemia of malignancy (PTHrP, Calcitriol)
• Local osteolytic hypercalcaemia
§ Granulomatous disease (e.g. sarcoid, TB)
§ Endocrinopathies (e.g. hyperthyroidism, adrenal insufficiency)
2+
§ Drugs (thiazides, Ca supplements, Vitamin D intoxication)
§ Immobilisation
§ Rare: Milk-alkali syndrome
o Parathyroid mediated
§ Primary hyperparathyroidism
• Presentation:
o Asymptomatic disease (50%)
o Skeletal involvement
o Renal manifestations
o Neuromuscular / Neuropsychiatric manifestations
o Gastrointestinal involvement
• Causes:
o Parathyroid adenoma (85%)
o Parathyroid hyperplasia (15%)
o Parathyroid carcinoma (<1%)
• Who needs surgery:
o Those with complications
o Serum Ca > 0.25mM/L above ref range
o 24-hr urinary Ca excretion >400mg/day
o 30% decrease in creatinine clearance
o T score < -2.5 - hip, distal radius, L-spine
o Age less than 50 yrs
• Parathyroid Imaging:
o Sestimibi scan – is a Technetium labelled lipophilic, cationic complex that bind to parathyroid and thyroid
mitochondria; it is washed out of thyroid cells more quickly so a delayed film shows parathyroid adenomas well
o Ultrasound scan of neck
• Surgical options:
o Bilateral neck exploration (if failure to localise prior to surgery)
o Unilateral neck exploration – if location identified before surgery on sestimibi
o Video or endoscopically assisted
o What to resect?
§ Adenoma (s) = the affected gland (s)
§ Hyperplasia Rx options:
Michael Grant
lOMoARcPSD|4776960
• Subtotal – 3.5 glands
• Total (all 4 removed) - resected glands divided into 1mm segments and autotransplant into SCM
(sternocleidomastoid muscle) or forearm
th
• Excise the thymus as this may be the location of a 5 parathyroid gland
§ Tertiary hyperparathyroidism – renal insufficiency
§ Familial hypocalciuric hypercalcaemia (rare; defect in calcium-sensing receptor)
§ Lithium therapy
• Presentation:
o Asymptomatic disease (50%)
o Skeletal involvement
o Renal manifestations
o Neuromuscular / Neuropsychiatric manifestations
o Gastrointestinal involvement
• Investigations:
o The main distinction is malignancy vs 1° hyperparathyroidism: Pointers to malignancy are reduced albumin, Cl–, alkalosis, K+ with
3–
raised PO4 & alk phos
o Corrected calcium levels
o Parathyroid hormone
o Phosphate
o 24-hour urine calcium excretion (for familial hypocalciuric hypercalcaemia).
o Bone densitometry DEXA scan +/- Isotope bone scan
o Also: FBC, protein electrophoresis, CXR
Hypocalcaemia:
• Apparent hypocalcaemia may be an artefact of hypoalbuminaemia
• Signs and symptoms: See BOX
o Mild: cramps, perioral numbness/paraesthesiae.
o Severe: carpopedal spasm (especially if brachial artery compressed,
Trousseau’s sign), laryngospasm, seizures
§ Neuromuscular excitability may also be demonstrated by tapping over
parotid (facial nerve) causing facial muscles to twitch (Chvostek’s sign)
§ Cataract if chronic hypocalcaemia
§ ECG: long QT interval
• Causes:
3–
o With raised PO4
§ Chronic kidney disease
§ Hypoparathyroidism (incl thyroid or parathyroid surgery)
§ Pseudohypoparathyroidism
§ Acute rhabdomyolysis
§ Vitamin d deficiency
§ Hypomagnesaemia
3–
o With normal or lowered PO4
§ Osteomalacia (alk phos)
§ Acute pancreatitis
§ Over-hydration
§ Respiratory alkalosis (total ca2+ is normal, but reduced ionized ca2+ due to
increased pH)
• Treatment:
o Mild symptoms: give calcium 5mmol/6h po, with daily plasma ca2+ levels
o Severe symptoms: give 10mL of 10% calcium gluconate (2.25mmol) IV over 30min, and repeat as necessary.
30 CCrISP Principles
SEE POEM NOTES ON ABC
31 Surface Anatomy
Head:
l Frankfort Line (inf. Orbital border to TMJ to occipital and palpable landmarks
l Vertex – peak of skull transition from cervical innervation posteriorly to cranial nerves
l Pterion – parietal/frontal/temporal/sphenoid; injury can lead to extra-dural haematoma
Neck:
• C3/4 level: CCA – ICA +ECA, upper thyroid cartilage
• C6 level: Pharynx-oesoph, larynx-trachea, inf. cricoid
• C7 Vertebra Prominens
Michael Grant
lOMoARcPSD|4776960
Abdomen:
Kidneys
l Left upper pole rib 11
l Right upper pole rib 12
l Hila L1
l Lower poles L3/4
Spleen
l Ribs 9-11
l Follows contour rib 10
l Upper pole left kidney to midaxillary line
Lower limb:
VASCULATURE
l Post Tibial a.
l Dorsalis Pedis a.
l Plantar a.s
l Dorsal v. arch
l Great SV
l Small SV
DERMATOMES
l L1 inguinal ligament
l L2 lat thigh
l L3 lower med thigh
l L4 med great toe
l L5 med side 2nd toe
l S1 little toe
l S2 back of thigh
l S3 gluteal fold
l (S4/5 perineum)
32 Neck swellings/Salivary glands

Neck Lumps:
• Benign:
o Lymph node enlargement most common cause (85%) and are typically:
• Reactive – especially in younger patients
• Infective (Consider TB, viruses such as HIV or EBV (infectious mononucleosis), any chronic infection)
• Malignant (Consider lymphoma (hepato- splenomegaly?) or metastases (eg from GI or bronchial
or head and neck neoplasia
§ History and examination
§ Investigation
o Sebaceous Cyst
§ Mobile, hx of infection
§ Presence of punctum
o Thyroglossal Cyst
§ Most common congenital lesion in the neck
§ In utero the thyroid develops in the tongue base and as the neck develops
the thyroid remains at the neck base, leaving a potential track from the
Foramen Caecum to the thyroid
§ A cyst can develop anywhere along this track, but usually midline at the
level of the hyoid
§ Examination
• Fluctuant
• Moves with tongue protrusion
§ Investigation
• U-S Scan (Also show Thyroid present)
• Aspiration may yield thick fluid
§ Surgical excision is the treatment of choice
• This must include excision of the body of the Hyoid - as the tract typically envelopes it
(Sistrunk procedure)
o Branchial Cyst
Michael Grant
lOMoARcPSD|4776960
§ Arises from 2nd Branchial cleft (ectoderm unlike its counterpart the pharyngeal pouch on the
endodermal side.).
§ Lateral neck, anterior triangle.
§ May be fluctuant, may transilluminate with fluid that contains cholesterol crystals
§ Usually young age but in those over 35 be suspicious of malignancy
§ Management
• Aspiration - may not recur but usually do; often infected
• U-S Scan - (CT/MRI over age 35)
• Surgical excision must be careful due to relation to carotid arteries
o May have tract to pharynx
o May have associated fistula
o Lipoma
§ Discrete tumour of fatty tissue that often become large
§ Indistinct capsule
§ Excise for cosmesis or pathology (can rarely progress to malignant liposarcoma)
o Submandibular and Parotid Gland conditions:
o Ranula
§ Name derives from Latin for frog - Rana
§ Usually arises from sublingual gland (occasionally submandibular)
§ Cystic swelling
§ May extend through Mylohyoid muscle (Plunging ranula)
§ Intraoral excision to include sublingual gland
o Cystic Hygroma
§ Lymphangioma - malformations of the lymphatic system
characterized by lesions that are thin-walled cysts that
transilluminate brightly
§ Most present by age 2 years
§ Watch if asymptomatic
§ Sclerosing agents (hypertonic saline) used/Surgery if problematic or
persistent recurrence
o Haemangiomas
§ Usually observation is fine, but Rx should be considered if near
eye/nose
§ Beta-blockers has caused regression in many of these lesions,
sclerosing agents (OK342), although observation may be enough
o Dermoid cyst
§ Contain dermal structures and are found at the junction of embryonic cutaneous boundaries, eg midline, lateral to the eye
§ If patient is <20yrs old, likely diagnosis is dermoid cyst
o Carotid Body Tumour
§ Paraganglioma of Chemoreceptor organ
§ Very rare, move from side to side but not up and down, are pulsatile and splay out the carotid bifurcation.
§ Suspect in any mass just anterior to the upper third of sternomastoid
§ Extirpation by vascular surgeon.
o Laryngocoele
§ C ongenital anomalous air sac communicating with the cavity of the larynx, which may bulge outward on the
neck
§ Uncommon cause of anterior triangle lumps. They are painless and may be made worse by blowing.
§ These cysts are classified as external, internal, or mixed, and may be associated with laryngeal cancer and
COPD
o Neurogenic Tumours (e.g. Schwannoma, Neurofibroma)
o Cervical ribs
§ Mass in post. triangle are enlarged costal elements from C7 vertebra
§ Majority are asymptomatic but can cause Raynaud’s syndrome by compressing subclavian artery and neurological symptoms (eg
wasting of 1st dorsal interosseous)
• Malignant:
o Primary malignancy
§ Lymphoma
§ Salivary
§ Laryngeal
§ Rare Sarcomas: Chondro-, Lipo-, Rhabdomyo-
o Secondary lymph nodes
§ Usually ENT - Nose, mouth, pharynx, larynx
§ Occasionally distant spread to lymph in neck – Stomach, Breast, Lung, Prostate
o Investigations:
§ Careful examination - including ENT examination.
§ Fine Needle Aspiration Cytology (FNAC)
• Rapid diagnosis
• Relatively painless
• Accurate
Michael Grant
lOMoARcPSD|4776960
§ MRI
§ PET/CT (for malignancy)
o Salivary pathology:
§ Anatomy:
• Parotid glands 2
• Submandibular glands 2
• Sublingual glands 2
• Minor salivary glands 600-1000
§ History: Lumps; swelling related to food; pain, acute swelling (?Mumps, ?HIV)
§ Examination: Note external swelling; look for secretions; bimanual palpation for stones; Examine VIIth nerve and regional
lymph nodes.
§ Cytology: This may be ascertained by FNA.
§ Salivary gland tumours:
• ‘80% are in the parotid, 80% of these are pleomorphic
adenomas, 80% of these are in the superficial lobe
• Benign salivary gland tumours:
o Pleomorphic adenomas: often present in middle age (mean age 40y) and grow slowly - remove
by superficial parotidectomy
§ 6% undergo malignant change
o Adenolymphomas (Warthin’s tumour): usually older men; soft; treat by enucleation (removal with
capsule)
o Carcinomas: rapid growth; hard fixed mass; pain; facial palsy. Treatment: surgery +
radiotherapy
o Oncocytoma
o Vascular tumours
o Myoepithelial adenoma
• Deflection of the ear outwards is a classic sign with VIIth nerve palsy meaning malignancy
• Malignant salivary masses:
o Mucoepidermoid
o Acinic cell
o Adenoid cystic – one of the most sinister
o Carcinoma ex-pleomorphic adenoma
o Adenocarcinoma
o Squamous cell
o Lymphomas
o Metastatic
• Treatment:
o Remove any salivary gland swelling for assessment if present for >1 month
Figure 3 - Facial nerve palsy due to
o Surgical: Excision - superficial/suprafacial/partial - parotidectomy division of facial nerve in parotid
§ May include frozen section during operation gland
o Radiotherapy +/- chemotherapy if malignant

§ Inflammatory conditions:
• Acute viral
• Acute suppurative
• Chronic inflammatory disorders
• Granulomatous disease
• Sialolithiasis
o Re-current unilateral pain and swelling of gland when eating
o Affects Submandibular (80%) or Parotid
o Calculus may be palpable - especially submandibular duct in floor of mouth.
o Submandibular calculus removal is often curative
o Parotid sialogram is often curative – wash debris and calculi out
• Sjogrens (coexist with dry eyes and mouth and autoimmune disease, eg hypothyroidism,
Mikulicz’s or Sjögren’s syndrome, also bulimia)
§ Non-inflammatory condition:
§ Cysts: Congenital, acquired
§ Metabolic parotomegaly: Fatty infiltration in obesity, gout, Cushings, Myxoedema, Diabetes
33 Skin cancer & common 'lumps

& bumps'
Aetiology:
• UV radiation
• Skin type – fitzpatrick classification
• Marjolin's ulcer refers to an aggressive ulcerating squamous cell
carcinoma presenting in an area of previously traumatized, chronically
inflamed (e.g. overlying an area of osteomyelitis, or scarred skin.
Michael Grant
lOMoARcPSD|4776960
Malignant melanoma:
l Melanoma types:
- Superficial spreading
l Sub group arising within lentigo maligna- melanoma in situ that consists of malignant cells but
does not show invasive growth; transition to true melanoma is marked by the appearance of a
bumpy surface (itself a marker of vertical growth and invasion)
- Elderly patient
- Gradually increasing pigmentation
- Beware dark areas
- Nodular
l Rapid change
l Ulceration
l Urgent
- Acral lentiginous - most common subtype in people with darker skins
l Acral lentiginous melanoma is observed on the palms, soles, under the nails and in the oral
mucosa
- Subungal
l Beware unclear history of trauma
- Amelanotic
Non Melanoma Skin cancer:

• The majority of NMSCs are either basal cell carcinomas (BCCs), also known as rodent ulcers, or squamous
cell carcinomas (SCCs). Both forms are highly treatable and survival rates for NMSCs are over 95%
• Pre-malignant:
o Actinic keratosis
§ Sun-damaged skin
§ 25% progress to scc
o Bowens disease
§ If progress to SCC can be aggressive
§ Assoc with internal malignancy 7%
o Keratoacanthoma
§ Rapid
• Squamous cells:
o Two main types:
§ Verrucous
• Rare
• Typically on sole of foot
§ Nodular
• More common type
• Typically have
• Basal cell:
o Types:
§ Nodular
• Most common
• Surface ulceration/rodentulcer
§ Superficial
§ Sclerosing
§ Pigmented
o Rarely metastasizes
o Danger sites, due to local spread
§ Inner canthus (medial aspect of eye)
§ Alar base (of nose)
§ External auditory meatus
Treatment:
l All melanoma skin cancers should be referred to a specialist who works within a multidisciplinary team set up to deal with the full
spectrum of this condition
l History and examination vital
l Examination
- Tenderness
- Site
- Size
- Shape
- Colour
- Temperature
- Consistency
- Surface
l Ulceration
- Margin
Michael Grant
lOMoARcPSD|4776960
Traumatic lumps:
• Implantation
o Iatrogenic
o Self inflicted
o Accidental
• Implantation can result in inclusion cyst
Acquired lumps:
• Benign
o Sebaceous cyst
o Lipoma
o Other
• Malignant
o Sarcoma
o Metastatic
o Lymph node
o Cutaneous deposit
34 Dysphagia
Oesophageal anatomy:
Inner circular muscle Thickening of

circular smooth
muscle
Outer longitudinal muscle
Non keratinised
stratified squamous Crciopharyngeus forms upper spnchitner
epithelium
Submucosa –
fatty tissue,
vessels, nerves
Swallowing reflex
• Afferent signals from trigeminal,
glossopharyngeal and vagus nerves are
colated in the tractus solitarius
• Efferent signals travel to muscle via Outer longitudinal muscle
trigeminal, facial and hypoglossal nerves Auerbachs plexus
Inner circular muscle

Dysphagia is difficulty in swallowing and always
needs investigating urgently to exclude Meissners plexus
malignancy.
General causes – Oral, pharyngeal, or
oesophageal? Mechanical or motility related:
• Teeth
• Saliva production
• Medication
• Oral infection
• Neurological/neuromuscular disorders
o E.g. Bulbar palsy, MN disease, MS, MG
5 key questions to ask

1. Was there difficulty swallowing solids and liquids from the start?
a. Yes: motility disorder (esp if non-progressive, eg achalasia, CNS, or
pharyngeal causes)
b. No: Solids then liquids - suspect a stricture (benign or malignant).
2. Diffcult to make the swallowing movement?
a. Yes: Suspect bulbar palsy, especially if patient coughs on
swallowing.
3. Is swallowing painful (odynophagia)?
Michael Grant
lOMoARcPSD|4776960
a. Yes: Suspect cancer, oesophageal ulcer (benign or malignant), Candida (eg immunocompromised or poor steroid inhaler
technique) or spasm.
4. Is the dysphagia intermittent or is it constant and getting worse?
a. Intermittent: Suspect oesophageal spasm (Diffuse oesophageal spasm: causes intermittent dysphagia ± chest pain, Barium swallow:
abnormal contractions, eg corkscrew oesophagus)
b. Constant and worsening: Suspect malignant stricture.
5. Does the neck bulge or gurgle on drinking?
a. Yes: Suspect a pharyngeal pouch
Oesophageal obstruction:
• Extra oesophageal
o E.g. Tracheal neoplasm, dilation of L. Atrium, cerivcal osteopyte, large mediastinal lymph nodes
• Intramural
• Luminal
o Bolus (typically of meat) can occur in normal but usually those with narrow oesophagus
o Infection – esp. candida
o Eosinophilic oesophagitis an allergic inflammatory condition of the esophagus that involves eosinophils, not well understood, but
food allergy may play a significant role.
Mechanical causes of obstruction:

• Benign:
o Erosive oesophagitis +/- stricture
§ Benign stricture: Oesophageal reflux corrosives, surgery, or radiotherapy’ Treatment: endoscopic
balloon dilatation
• Malignant:
o Carcinoma (squamous or adenocarcinoma)
Functional obstruction:
• Achalasia: The lower oesophageal sphincter fails to relax (due to degeneration of the myenteric plexus),
causing dysphagia (for fluids and solids), regurgitation, substernal cramps, and weight loss
o Most common functional condition - absence of peristalsis, rasied pressure and failure of lower sphincter to
relax
o CXR: fluid level in dilated oesophagus (eg above heart)
o Barium swallow: dilated tapering oesophagus Underlying mucosa
preserved intact
o Treatment:
§ Endoscopic balloon dilatation, or Heller’s (lapropscopic)
cardiomyotomy —then proton pump inhibitors.
§ Botulinum toxin injection if a non-invasive procedure is needed Both muscle layers
(repeat every few months) are divided along
lower oesophageal
§ Calcium channel blockers and nitrates also relax the sphincter sphincter
o Longstanding achalasia may cause oesophageal cancer
• Oesophageal spasm
o Diffuse esophageal spasm (DES), where there are uncoordinated esophageal contractions
where several sections of the esophagus can contract at once (corkscrew oesophagus)
o Nutcracker esophagus (NE) also known as hypertensive peristalsis, where the contractions
are coordinated but with an excessive amplitude.
Assessment:
• Characterise dysphagia – swallowing or regurg.? Worse with solids or liquids (latter implies
achalasia)
• Associated symptoms – heartburn, PPI use, rule out carcinoma in Barrett’s oesphagus (heartburn
tends to resolve as metaplasia to more acid resistant coloumnar epithelium occurs )
• Weight change – not necessarily indicative of cancer, may reflect severity and length of dysphasia
• Lifestyle – older, thin, drinking, smoker (squamous cells); distal cancers more common in chronic GORD
• Family history
• Clinical examination: Oral cavity, neck and abdomen
• Investigations:
o CXR (mediastinal fluid level, no gastric bubble, aspiration)
o Barium swallow (esp. is ?pharyngeal pouch) – however this is being replaced by
OGD
o OGD +/- biopsy (shows oesophagitis, oesophageal cancer – mass or stricture)
Video fluoroscopy to identify dysmotility, eg achalasia
o Oesophageal manometry if barium swallow is normal
§ Similar to NG tube that measures pressure at different points using 8
overlapping tubes
o CT for cancer staging
Michael Grant
lOMoARcPSD|4776960
35 Benign Urological Conditions

Benign urological disease:
l Lower urinary tract obstruction
l Upper urinary tract obstruction
l Urinary tract infection
l Male external genitalia
Benign Prostatic Hyperplasia:

• 60% of 60 y/o
• 50% of those symptoms
• Glandular overgrowth - Static Obstruction
• Smooth muscle hyperplasia - Dynamic Obstruction
• Lower Urinary Tract Symptoms:
o Voiding
§ Poor flow
§ Hesitancy (due to time require for detrusor to build up enough pressure)
§ Intermittency
§ Straining
§ Terminal dribbling
o Storage
§ Incomplete emptying
§ Frequency
§ Nocturia
§ Urgency
o Complications:
§ Urinary retention
§ Urinary tract infection
§ Bladder calculus (seen on XR)
§ Haematuria – can clot cause clot retention)
§ Renal impairment
• Treatment:
o MEDICAL:
§ Static Obstruction: 5αReductase Inhibition – effectively blocking testosterone and
epithelial growth; usually decreases size by about 25%
§ Dynamic Obstruction: αlpha blockade – reduction of smooth muscle tone
o SURGICAL
§ Transurethral Resection (TURP) – via rigid cystoscopy and electro-cuttage
Stone disease:
• Aetiology
o Crystalluria
§ Calcium, Oxalate, Phosphate, Urate
§ Look at 24hr urine collection
o Hypercalcuria
o Socioeconomic
o Diet – increased sodium, increased urinary sodium > increases urinary ca and lowers ph, increase
risk of stones
o Dehydration – increased saturation increases risk of crystalisation
o Infection – esp. those with neurogenic bladder
st
o Family history – 1 degree relative 2x risk
• Stone Composition
o Mineralisation
§ Crystal component
§ Organic matrix component
o Calcium (80-90%) – visable on XR
o Struvite – Magnesium, Ammonium, Phosphate (associated with infection)
o Matrix only (soft)
o Uric Acid (don’t show on xray)
o Cystine (difficult Rx due to hardness)
o Xanthine
• Ureteric Calculi are likely to lodge in 3 places:
o Pelvi-Ureteric Junction
o Lower 1/3 Ureter – where iliac vessels cross
o Vesico-ureteric Junction
Michael Grant
lOMoARcPSD|4776960
• Presentation:
o Pain – severe colicky going from T9 to L1 before localising to the external genitalia as stone
moves
o Nausea
o Haematuria
o Obstruction
o Infection
• Investigations :
o Plain X-Ray
o Ultrasound – doesn’t show stones themselves but shows hydronephrosis from backlog
o CT – non-contrast (stones are radiopaque)
• Treatment:
o Conservative
§ Analgesia
§ 4-5mm - 40-50% passage
§ >6mm - <5% passage
§ Alpha-blockade to decrease smooth muscle tone in ureters to ease passage of
stone; Tamsulosin
o Emergency
§ Obtructed, infected GU tract
§ USS guided Nephrostomy to relieve initial blockage
§ This can later be converted to double - urine drains through stent and around
the obstruction
o Extracorporeal Shock Wave Lithotripsy

o Ureteroscopy
§ Flexible or rigid
§ Once stone reached – broken up using laser energy
o Percutaneous Nephrolithotomy
§ Stone broken up and extracted through skin
§ Useful for a large, so-called staghorn (because of its many
projections that resemble a deer's antlers) stones - fill almost
the entire renal pelvis (the central collecting chamber of the
kidney) and the tubes that drain into it (calyces)
Urinary Tract Infections:

• UNCOMPLICATED
o Normal urinary tracts
o No systemic disease
o Does not lead to renal impairment
o Usual suspects: E Coli, Staph Saprophyticus, Enterococci
o Presentation:
§ Acute Cystitis
§ Acute Pyelonephritis
§ Recurrent UTIs
o Symptoms:
§ Frequency
§ Urgency
§ Dysuria
§ Fever
§ Suprapubic/Loin pain
Michael Grant
lOMoARcPSD|4776960
o Treatment
Acute Cystitis Trimethoprim
§ Dipstick Urinalysis
Fluoroquinolones
§ Culture and Sensitivity - 100,000 organisms/ml, >10
leucocytes/ml Acute Pyelonephritis Fluoroquinolones
Cephalosporins
• Complicated UTI
o Bacteria Pseudomonas Aeruginosa Recurrent UTIs (esp. post menopausal)
Gm +ve Cocci Low dose
prophylaxis (e.g. nitrofurantoin)
o Stones Urease-producing organisms
Cranberry juice
Calculus Proteus (reduces bacterial adhereance)
Obstruction Klebsiella Oestrogen
Pseudomonas Pregnancy b-lactam
Stones themselves can allow start of infection also Nitrofurantoin
o Diabetes Abscesses Cephalosporins
Emphysematous pyelonephritis
Papillary necrosis
Xanthogranulomatous pyelonephritis - exuberant clustering of foamy macrophages among other inflammatory
cells (E Coli, Proteus) usually seen in those also with obstruction – can result in nephrectomy due to necrosis
• Male UTI
o Prostatitis
§ Acute: E Coli, Pseudomonas, Strep faecalis
§ Chronic: E Coli, Pseudomonas, Mycoplasma, Ureaplasma, Chlamydia
o Epididymo-Orchitis
§ Chlamydia, N Gonorrhoeae, Enterobacteriaceae, Pseudomonas
o Scrotal cellulitis
§ Gp A Streptococci, Staph Aureus
o Fournier’s gangrene - horrendous infection of the genitalia that causes severe pain in the genital area
(in the penis and scrotum or perineum) and progresses from erythema (redness) to necrosis (death) of
tissue
§ Usually in diabetes
§ Polymicrobial, synergistic (anaerobes and aerobes)
§ Rx: High dose IV Abx and aggressive resection
§ High mortality
o Periurethral abscess
§ May occur after instrumentation
§ Can be seen with spreading cellulitis
§ Gm -ve anaerobes
• Testicular Torsion
o Can occur during sleep. Internal twisting around spermatic cord, spotting
blood flow leading to infarction within 4-6 hours
o Attempt external detortion; often needs to go to threatre for bilateral
orchiopexy
• Scrotal Swellings
o Epididymal Cyst
§ Can be painful, palpable separate from test, thought
to be due to lymph obstruction and can be operated
on if large or infected
o Hydrocoele
§ May be due to patent tunica vaginalis, aspiration is
not used due to recurrence an d infection, surgical
removal if painful
o Varicocoele
§ Dilatation of pampiniform venous plexus, associated with
reduced fertility, treated by emoblisaiton or surgical ligation
(improves fertility)
• Peyronie’s disease
o Poorly understood connective tissue disorder most commonly
attributed to repetitive microvascular trauma during sexual
intercourse, resulting in penile curvature and painful erectile
dysfunction
o Middle age and older
o Connective tissue disorder, seen with:
§ Duputyren’s Contracture
§ Retroperitoneal Fibrosis
o High dose PO Vitamin E slows progress
o Manage associated depression
o Surgery - tunica plication ± penile prostheses (may help penetration)
Michael Grant
lOMoARcPSD|4776960
• Priapism
o Causes:
§ Erectile dysfunction treatment
• Intracavernous injection
• Oral agents
• Vacuum devices
§ Idiopathic
§ Recreational drugs
§ Sickle cell disease (low-flow priapism; also seen in CML, may respond to hydration, alpha-agonists,
eg phenylephrine, or aspiration of blood + irrigation with saline; if for >12h prompt cavernosus–
spongiosum shunting can prevent later impotence)
o TREATMENT: Figure 4 - Proximal cavernosal-
§ Conservative spongiosum shunt (Quackel shunt)
§ Aspiration surgically connects the proximal
corpora cavernosa to the corpora
§ Surgery spongiosum
o Risk of infection or thrombosis leading to permanent erectile dysfunction
36 Benign Breast Disease

Breast pain:
• Most common cause for referral to specialist breast clinics
• Cyclical and non-cyclical
• Rarely associated with breast carcinoma
• Often resolves after malignancy is excluded
• If bloody discharge (be careful – especially in unilobular; may be pappiloma or CA)
• Common causes:
o Hormonal stimulation of normal breast before menses (cyclical mastalgia)
o Fat necrosis, periductal mastitis
o Hidradenitis suppurativa (also known as acne inversa, is a chronic skin disease characterized by clusters of abscesses or
subcutaneous boil-like "infections" (often free of actual bacteria) that most commonly affects the underarms, under the breasts, inner
thighs, groin, and buttocks)
o Mondor’s disease (non-cyclical; thrombophlebitis of the superficial veins of the breast and anterior chest wall.)
o Chest wall (Tietze’s syndrome [Like costochondritis but with addition of swelling of the costal cartilages], cervical arthritis)
• Management:
o Exclude malignancy – triple assessment
o Cyclical (Reassure, sports bra, anti-inflammatory medication, Evening
Primrose Oil)
o Resistant cyclical pain (Danazol, bromocriptine, Tamoxifen – prescribed by
specialist)
o Non-cyclical - treat cause
Benign lumps:
• Fibroadenosis
o Most common causes of breast lump/thickening – breasts can feel nodular
o Pain and tenderness in premenstrual days with variation during cycle
o Asymmetrical nodular, “lumpy” change needs full assessment
o Surgery not indicated
o Treat symptoms after malignancy excluded
• Fibroadenoma: Usually presents <30yrs but can occur up to menopause. Benign overgrowth of
collagenous mesenchyme of one breast lobule. Firm, smooth, mobile lump. Painless. May be multiple.
o 1⁄3 regress, 1⁄3 stay the same, 1⁄3 get bigger
o Rx: Observation and reassurance, but if in doubt refer for USS (usually conclusive) ± FNA. Surgical
excision if large.
o Large fibroadenoma must be distinguished from Phylloides Tumour
• Breast cysts: Common >35yrs, esp. perimenopausal. Benign, fluid-filled rounded lump. Not fixed to
surrounding tissue. Occasionally painful.
o Rx: Diagnosis confirmed on aspiration under USS guidance
o Discharge if no blood in fluid, cyst disappears and wall looks normal on USS
• Infective mastitis/breast abscesses: Infection of mammary duct often associated with lactation
(usually S. aureus). Abscess presents as painful hot swelling of breast segment. ฀
o Rx: Antibiotics. Open incision or percutaneous drainage if abscess
• Duct ectasia: Typically around menopause and esp. smokers. Ducts become blocked and secretions
stagnate. Present with nipple discharge (green/brown/bloody) ± nipple retraction ± lump w/ pain
behind nipple. Refer for confirmation of diagnosis
o Usually no Rx needed
• Fat necrosis: Fibrosis and calcification after injury to breast tissue. Scarring results in a firm lump. Refer for triple assessment
o No Rx once diagnosis confirmed
Michael Grant
lOMoARcPSD|4776960
Gynaecomastia:
l Hypertrophy of male breast disc (typically: birth, puberty and in the elderly)
l Imbalance between Oestrogen/Androgens
l Examine the Testes!!!! Ensure normal development and exclude obvious malignancy
l Causes:
l Physiological
l Medication (cimetidine, steroids, spironolactone, digoxin)
l Pathological (Liver disease [failure to metabolise estrogens], Testicular tumours)
l Treatment:
l Investigate to exclude pathological conditions (i.e. breast CA)
l Wait for resolution
l ?Surgery – last resort, cosmetic results of scars can be poor
37 Transplant Surgery/Brain Stem Death

Brain stem death:
• Causes:
o Primary causes:
§ Traumatic injury, Intra-cranial haemorrhage
§ Ischaemic stroke
o Secondary causes:
§ Anoxia due to cardiac or respiratory failure, fulminant liver failure
§ Swelling of the brain -> increase of intracranial pressure -> cessation of perfusion -> anoxic cell death
o Irreversibility is key to any concept of death
• Criteria:
o Demonstration of coma
o Evidence for the cause of coma
o Absence of confounding or reversible factors, including hypothermia, drugs, and electrolyte and endocrine disturbances
o Absence of brainstem reflexes
o Absence of motor responses
o Apnoea – removal of ventilation and no effort as PCO2 rises to 6
o A repeat evaluation after a further 6 h is advised.
o 2 experienced docs, not part of Transplant team.
Organ donors:
l Cadaveric – Multiple organ donors
- Heart beating
- Non-heart beating
l Important to consider: Cold Ischaemic Time (CIT) – time organs flushed with cold preservative until re-perfused with
blood in recipient: Heart and lungs 4-6 hr, Liver and Pancreas <12 ideally but up to 20hrs, Kidney <24 but up to 40+
hrs
l Living
- Related
- Unrelated
l Exclusion criteria:
- Malignancy (excluding primary brain tumours – risk of transplanting cancer into immunosupressed recipiant)
- Severe Untreated Systemic Sepsis (exception treated meningitis)
- Viral transmission – Active Hep B/C, HIV, viral encephalitis, Jacob-Creutzfeld disease or recipients human growth hormone
- Organ Specific
- Relative contraindications
l Donor studies:
- ABO blood typing and subsequent HLA studies (tissue typing)
- Viral screening – Hep A, B, C, HIV, CMV, EBV status
- FBC, U&E’s LFTs
- Toxoplasma and syphilis
Transplant terminology:
• Autograft – tissue tx from one part of the body to another in the same individual
• Isograft – graft between 2 genetically identical individuals eg monozygotic twins
• Allograft – graft between 2 individuals of the same species but different genotype
• Xenograft – graft from one species to a different species eg pig to man
• Heterotopic – hetero:other, topos:place. Graft in different anatomical position eg kidney
• Orthotopic – ortho:correct, right, topos: place. Graft in the anatomical position eg liver – OLT
Michael Grant
lOMoARcPSD|4776960
Immunology: Tissue Typing
• Tissue Typing/HLA matching: 6 antigens (major transplant antigens) located on cell surface,
encoded for by HLA genes on chromosome 6p
• 3 groups A, B & DR: inherit one set of 3 or haplotype from each parent.
o Class I antigens (HLA A & B) expressed on cell surface of most nucleated cells
o Class II antigens (HLA DR) are expressed on surface of APC and activated lymphocytes
• Can have 6-0 mismatches – best is 000 mismatches
• 1 in 4 chance of identical match with sibs (share 2 haplotypes)
• Cross-match test: lab test that determines if the potential recipient has pre-formed antibodies to the
donor using donor lymphocytes and recipient serum.
Rejection:
l Normal response to foreign tissue: cell mediated and antibody mediated
l Mediated primarily by T cells: direct and indirect alloantigen presentation
- Direct: MHC peptide complexes on donor APC recognised directly
by recipient T cells
- Indirect: alloantigens processed by recipient APCs and presented
to recipient T cells
l Donor and Host APCs, passenger leucocytes, CD4 and CD8 cells involved
Rejection Classification:
• Hyperacute: <24 hrs, pre-existing Ab’s (ABO), graft loss due to complement
activation, inflammation, endothelial damage and thrombosis
• Acute: days/weeks, cell-mediated (macrophages, cytokines) endothelialitis,
parenchymal cell damage, interstitial inflammation, tubulitis
• Chronic: months or longer, humoral and cell mediated, fibrosis and
scarring, intimal smooth muscle cell proliferation, vessel occlusion
Rejection – clinical:
l Graft dysfunction eg.
- Renal – inc creatinine, tender graft, fever, oliguria
- Liver – increased LFT’s, fever, RUQ discomfort
- Pancreas – hyperglycaemia
- Lung – cough, dyspnoea, sputum
- Heart – heart failure, dysrhythmia
l Investigation Renal/Liver/Pancreas: USS - assess for other
causes
l Graft biopsy for histology
l Banff criteria of rejection
Immunosuppressant:
• Benefits of transplant outweigh risks of chronic immunosuppression
• Multi-drug regimens employed to enhance immunosuppression and decrease side-effects of any one drug
• High doses post transplant,reduced to maintenance therapy
• Required indefinitely
• Classifications:
o Anti-inflammatory: Glucocorticoids (steroids)
o Anti-metabolites: Purine inhibitors
§ Azathioprine (non-selective)
§ Mycophenolate mofetil (lyct selective)
o Immunophilin Binding agents
§ Calcineurin inhibitors: Cyclosporine, Tacrolimus,
§ Calcineurin independent agents: Sirolimus (rapamycin)
o Antibody mediated: polyclonal, monoclonal
§ ATG/ALG, OKT3, Basiliximab (simulect - chimeric mouse-human Figure 5 - Recipient criteria
monoclonal antibody to the α chain of the IL-2 receptor of T cells),
Daclizumab (zenapax - binding to CD25, the alpha subunit of the IL-2 receptor of T-cells)
o Risks:
§ Malignancy : skin cancer, lymphoma (PTLD), solid organ
§ Infection: bacterial, viral (CMV), fungal,
§ Drug side-effects:
• Steroids: hypertension, weight gain, Cushingoid facies, skin- striae, wound healing, osteopenia, glc metabolism,
hyperlipidaemia
• CyA : nephrotoxic, neurotoxic, gingival hyperplasia, hypertension, hirsutism
• Tac : nephro/neuro toxic, impaired glucose metabolism, hypertension
• Aza/MMF : bone marrow suppression, GI disturbance
• Antibody : fever, headache, myalgia, GI, Resp distress/anaphylaxis
Michael Grant
lOMoARcPSD|4776960
38 Ethics and Consent

Valid consent must consider:
• Voluntary
• Informed
o Complications
o Causing harm
• Capacity - Patient has sufficient knowledge and understanding and is able to retain information
o General principle – no one is able to give consent to examination or treatment for an ‘incapable’ adult
o Advance – direction
o Treatment without consent
o Mental health legislation
o Best interests – patient interests / values / relationships / quality of life. Religious / financial interests
o If in doubt/conflict, seek court ruling
Consent for major procedure:

• Written
• Two stage consent
• Process
• Information in advance
• Review at time of procedure
• Written consent serves as evidence of consent
Situation where consent is not given:

• Mental Health Act
• Emergencies
• Best interests
39 Stomas
Types of stoma:
l Colostomy
- Fashioned from large bowel
l End colostomy
l Defunctioning or loop colostomy
l Can be performed quickly even under local
l High risk of prolapse
l Ileostomy
- Will be spouted or “brooked”
- Fashioned from small bowel
l End
l Defunctioning or loop
l If there is an anastomosis distally, giving time to help
e.g. anterior resection
l Urostomy
- Fashioned from small bowel (no longer plumbed into large colon directly due to risk of
cancer, electrolyte imbalance)
- Ureters implanted into ileal bowel segment
- Brought to surface
l Mucous Fistula
nd
- 2 stoma
- Proximal end forms stoma and opens into distal bowel
l Seldom used now-a-days
l Formed part of original Hartmann’s procedure
l May be indicated if possibility of obstruction distal to mucous fistula, e.g. remaining tumour in pelvis
When to use each:

• When normal conduit has been removed:
o End stoma
§ Colostomy Ileostomy Colostomy Urostomy
§ Ileostomy
§ Urostomy Site Usually RIF Usually LIF Usually RIF
• When we are preventing bowel contents passing into Spout or flat Spout Flat Spout
the bowel distal to the stoma
o Loop ileostomy Contents Liquid-soft Soft-Hard Urine
§ Anterior resection
Appliance bag Drainable Not drainable Drainable
§ Constipation
§ Fistula
§ Incontinence
Michael Grant
lOMoARcPSD|4776960
o Loop colostomy
§ Obstructing tumour (and unfit for resection)
§ Fistula
§ inc ontinence
• Choosing a site:
o Poorly sited stoma can result in:
§ Leakage
§ Skin irritation
§ Clothing problems
§ Difficulty applying pouch
§ All leading to confidence issues
o Examine patient with normal clothing on looking at position
of belts, waistband etc
• Complications:
o Ischaemia
§ Not uncommon 24-48 hrs after surgery
§ Always inspect stomas; transparent pouch usually used intially
§ Mucosa only
§ Use proctoscop; if only few cm of ischaemia then conservative management
o Excoriation
§ Poor fitting
§ Leakage
§ Allergic reaction to the base plate
§ Ask stoma nurse to see
o Retraction
o Prolapse
§ Conservative
• Acute - Reduce swelling ice/sugar, manipulate back into cavity
• Chronic - Protective shield +/- Revision surgery
o High output
§ Causes:
• Unexplained
• High stoma (more common in ileostomy)
• Obstruction - Foods to avoid
o Nuts
o Mushrooms
o Oranges
§ Treatment
• Maintain electrolytes
• Antidiarrhoeals
• Celevac (methylcellulose fibre bulking agent)
• Electrolyte replacement solutions +/- Fluid restriction (oral fluids can
increase electrolyte loss)
o Parastomal Hernia
§ Pain, increase risk of obstruction, difficult to apply bag
§ Conservative
• Prevention
• Supports belt/girdle
§ Surgery - Revision/Repair plus mesh
General advice to patients:

• Food
o Advised to take a low residue diet immediately after surgery
o Increase fibre gradually
o Ileostomy may have to avoid certain foods
• Awareness of the pouch
o Clothing will usually cover (site important)
o Pouches with charcoal filters for smell
o Loss of sphincter control, so may be uncontrolled flatus
Michael Grant
lOMoARcPSD|4776960
40 Surgery of the Adrenals

The adrenal glands:
• The adrenal cortex produces steroids:
o Glucocorticoids (eg cortisol), which affect
carbohydrate, lipid and protein metabolism
o Mineralocorticoids, which control sodium and
potassium balance
o Androgens, sex hormones which have weak effect
until peripheral conversion to testosterone and
dihydrotestosterone
• Corticotropin-releasing factor (CRF) from the
hypothalamus stimulates ACTH secretion from the
pituitary, which in turn stimulates cortisol and
androgen production by the adrenal cortex
• Cortisol is excreted as urinary free cortisol and various
17-oxogenic steroids
• Mineralocorticoids are a class of corticosteroids,
which are a class of steroid hormones.
Mineralocorticoids are corticosteroids that influence
salt and water balances (electrolyte balance and fluid
balance)
o The primary endogenous mineralocorticoid is
aldosterone, although a number of other
endogenous hormones (including progesterone
and deoxycorticosterone) have mineralocorticoid function
o Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as well
as the active secretion of potassium in the principal cells of the cortical collecting tubule and active secretion of protons via proton
ATPases in the lumenal membrane of the intercalated cells
Cholesterol
of the collecting tubule
• Steroidogenesis:
o Steroidogenesis is the biological process by which Pregnenolone
steroids are generated from cholesterol and changed into
other steroids. Progesterone 17-OH Pregnenolone DHEA
o Progestogens are the precursors of all other human
steroids, and all human tissues which produce steroids
Deoxycortisol 17-OH Progesterone Androstenedione
must first convert cholesterol to pregnenolone. This
conversion is the rate-limiting step of steroid synthesis,
which occurs inside the mitochondrion of the respective Corticosterone 11-OH Deoxycortisol
tissue.
• Catecholamine Synthesis: Aldosterone Cortisol
o A catecholamine is a monoamine, an organic compound
that has a catechol (benzene with two hydroxyl side groups at
Catechol
carbons 1 and 2) and a side-chain amine
o Catecholamines are derived from the amino acid tyrosine, which is
Tyrosine
derived from dietary sources as well as synthesis of phenylalanine
o Catecholamines are water-soluble and are 50%-bound to plasma
Dopa
proteins in circulation
o Two catecholamines, norepinephrine and dopamine, act as Dopamine
neuromodulators in the central nervous system and as hormones in
the blood circulation. The catecholamine norepinephrine is a Noradrenaline
neuromodulator of the peripheral sympathetic nervous system but
is also present in the blood (mostly through "spillover" from the Adrenaline
synapses of the sympathetic system)
o Some typical effects are increases in heart rate, blood pressure, blood glucose levels, and a general reaction of the sympathetic
nervous system.
Adrenal Pathology:
l Underactivity
- Adrenal Failure; Addison’s
l Loss of glucocorticoid effects and mineralocorticcoid effects
l Remember suppressive effects of therapeutic steroid use – patients may experience Addison's if treatment stopped or have
physiological stress on Rx
l Overactivity – mostly hormone-secreting benign or malignant tumours
- Mineralocorticoids
- Glucocorticoids
- Adrenal Androgens
- Catecholamines
Michael Grant
lOMoARcPSD|4776960
l Normal Hormonal Secretion
- Incidental Adrenal lesions
Addison’s disease:
• Features:
o Hypotension/ Postural hypotension
o Electrolyte disturbance
§ Hyponatraemia
§ Hyperkalaemia
§ Hypercalcaemia
o Fatigue/lethargy
o Gastro-intestinal upset
o Hyperpigmentation
• Causes:
o 80% are due to autoimmunity in the UK
o Other causes:
§ Infective: TB (commonest cause worldwide), opportunistic infections in HIV (eg
CMV, Mycobacterium avium)
§ Adrenal haemorrhage: Waterhouse–Friderichsen syndrome (haemorrhage
into 1 or both adrenal glands secondary to severe infection +/- DIC; esp. Meningococcal); antiphospholipid syndrome; SLE;
anticoagulants
§ Malignant: Adrenal metastases (eg from lung, breast, renal cancer), lymphoma
• Treatment:
o Replace steroids: ~15–25mg hydrocortisone daily, in 2–3 doses, eg 10mg on waking, 5mg lunchtime. Avoid giving late (may cause
insomnia). Mineralocorticoids to correct postural hypotension (increase Na, decreased K+): fludrocortisone PO from 50–200μg daily.
§ If there is a poor response, suspect an associated autoimmune disease (check thyroid, do coeliac serology)
Conn’s syndrome:
l Hyperaldosteronism
l Features:
- Hypertension
- Electrolyte disturbance
l Hypokalaemia
Sodium and water retention – feeding
l
hypertension
l Benign Adenoma within one adrenal
Cushing’s syndrome:
l Adrenal adenoma
l Adrenocortical carcinoma
l Ectopic ACTH secretion
- ACTH-producing tumours (e.g. Neuroendocrine; pancreas and bronchial ca)
l Cushing’s Disease – ACTH dependent Cushing’s (“Pituitary Cushing’s”)
Virilizing Tumours:
l 30% malignant
l Peripheral conversion of weaker adrenal androgens to testosterone
l Features
- Male pattern baldness
- Hirsutism esp. in female
- Very rare
Phaeochromocytoma:
l Produce adrenaline, noradrenaline or dopamine
l “10% rule”
- 10% bilateral
- 10% familial
- 10% extra-adrenal (adjacent to great vessels, arising from cervical chain)
- <10% malignant
l May be part of MEN syndrome
l Symptoms:
- Headache
- Hypertension with Associated postural hypotension
- May be paroxysmal
- Palpitations/Anxiety and fear of impending death
- Chest pain/cardiac events (Type 2 MI)
- Congestive cardiac failure
- Hypertensive crisis:
Michael Grant
lOMoARcPSD|4776960
l Increased risk intra-operatively/ under anaesthesia even if
surgery is for other pathology
l Requires urgent treatment with intravenous sodium
nitroprusside or magnesium
l Always arrange resection of phaeochromocytoma before
anaesthetic for other pathology
Adrenal “Incidentaloma”:
• Adrenal mass on CT or MRI scan performed to investigate an unrelated problem
• Affects 3-5% of the population
• <3cm - rarely malignant
• >6cm - 10% malignant
• Require tests to exclude hormone secretion
Assessment of Adrenal Lesions:

• 24 hr urine collections (4 collections in total – 2 of each):
o Catecholamines/ vanillylmandelic acid (VMA)/ metanephrines
(metabolites of catecholamines)
o Cortisol
• a.m. + p.m. serum cortisol (?loss of diurnal variation)
• Overnight low dose dexamethasone suppression test (look for a normal
reduction in cortisol)
• Urea + electrolytes + blood pressure. If abnormal Renin/Aldosterone activity
41 Carotid Artery Disease

Risk factors:
l Old Age
l Male gender (vs female)
l Hypertension, Dyslipdaemia, Smoking
l Diabetes
l Race (Asian/Black versus Caucasian)
l Arrythmia (Atrial Fibrillation)
l Carotid Stenosis
Definitions:
Stroke (also known as Cerebrovascular Accident (CVA))
l Episode of focal neurological dysfunction of >24 hrs duration presumed vascular aetiology
l 80% are ischaemic
l 50% due to atheroembolism from Carotid Stenosis
Transient Ischaemic Attack (TIA)
l Episode of focal neurological dysfunction of <24 hrs duration presumed
vascular aetiology
Amaurosis Fugax
l Transient loss of vision in one eye due to occlusion of branch of retinal
artery by emboli
Carotid artery disease:

• Internal Carotid Artery
o Progressive Stenosis
o Microemboli
o Plaque rupture
o Occlusion
• Asymptomatic (>50%)
o 5-10% >65 yr have Carotid Stenosis >50%
o Rises to 12% if PVD
o Rises to 25% if hypertensive Degree of Primary Additional
Stenosis Parameters Parameters
• Symptomatic
o Atheroemboli to Opthalmic Artery leads to Amaurosis Fugax or Monocular ICA PSV ICA/CCA PSV ICA EDV
Blindness (cm/sec) ratio (cm/sec)
o Atheroemboli to Middle Cerebral Artery leads to Hemiparesis and
<50% <125 <2.0 <40
Hemisensory loss (contralateral side)
§ If dominant hemisphere > Dysphasia
≥70% >230 >4.0 >100
• Examination
Michael Grant
lOMoARcPSD|4776960
o Neurological Exam
o Cardiovascular Exam
o Carotid Bruit
• Investigations:
o Carotid Duplex Ultrasound
B-mode (real-time) imaging
§ Waveform analysis (PWD)
§ Strandness Criteria (PSV, EDV, Spectral)
o Complementary Tests
§ Magnetic Resonance Angiography (MRA)
§ Computed Tomographic Angiography (CTA)
§ Catheter Angiography
• Treatments:
o Medical
§ Optimisation
• Manage risk-factors (SALAD)
• Exclude co-morbidity
§ Medication
• Aspirin (25% reduction risk CVA)
• Aspirin + Dipyridamole (added benefit)
• Clopidogrel vs Aspirin (NO added benefit in reduction ischaemic CVA),
however reduced cardiovascular events.
o Surgical
§ Endarterectomy
• LA or GA with heparin
• Plastic shunt to maintain blood supply during (although if under LA, then
patient level of conscioness can be used to judge perfusion)
• Endarterectomy – remove plague
• Can sew closed or use patch Angioplasty (to increase diameter)
§ Endovascular repair
• Carotid Angioplasty & Stenting
• Balloon expandable stent via PCI (femoral)
• Higher peri-operative risk of stroke
• Alternative to CEA, should be reserved for patients deemed at
too high risk for CEA.
42 Pancreatic Cancer & the Spleen

Pancreatic 62physiology:
• Exocrine:
o Secretion of water and electrolytes originates in the centroacinar
and intercalated duct cells
o Pancreatic enzymes originate in the acinar cells
o Final product is a colourless, odourless, and isosmotic alkaline (ductal
epithelium secrete bicarb) fluid (1-2L a day) that contains digestive enzymes
(amylase, lipase, and trypsinogen; of which only amylase is in an active form)
o Alkaline pH results from secreted bicarbonate which serves to neutralize
gastric acid and regulate the pH of the intestine
• Endocrine:
o Insulin
§ Synthesized in the B cells of the islets of Langerhans
§ 80% of the islet cell mass must be surgically removed before diabetes
becomes clinically apparent
§ Proinsulin, is transported from the endoplasmic reticulum to the Golgi
complex where it is packaged into granules and cleaved into insulin and
a residual connecting peptide, or C peptide
§ Major stimulants
• Glucose, amino acids, glucagon, GIP, CCK, sulfonylurea compounds,
β-Sympathetic fibers
§ Major inhibitors
• Somatostatin, amylin, pancreastatin, α-sympathetic fibers
o Glucagon
§ Secreted by the A cells of the islet
§ Glucagon elevates blood glucose levels through the stimulation of
glycogenolysis and gluconeogenesis
§ Major stimulants: Aminoacids, Cholinergic fibers, β-Sympathetic fibers
§ Major inhibitors: Glucose, insulin, somatostatin, α-sympathetic fibers
Michael Grant
lOMoARcPSD|4776960
o Somatostatin
§ Secreted by the D cells of the islet
§ Inhibits the release of growth hormone
§ Inhibits the release of almost all peptide hormones
§ Inhibits gastric, pancreatic, and biliary secretion
§ Used to treat both endocrine and exocrine disorders
• Aetiology:
o Cause unknown
o Smoking & alcohol?
o Diabetes? (5 years greater than 2x increase)
o Hereditary pancreatic cancer – susceptibility locus has been found in relation to
chromosome 4q32-34
o Familial breast cancer gene (BRCA2) + Accuracy of 60%-80 % by imaging alone.
o Chronic pancreatitis - 5%-10% complication rate.
• Presentation:
o Weight loss
o Anorexia/Cachexia
Double duct
o Nausea & vomiting sign
o Abdominal pain Dilation of CBD and Pancreatic ducts
o Obstructive jaundice (head lesions)

• Diagnosis:
o Ultrasound (consider endoscopic)
Tissue/Brushings
o CT scan + Diagnostic yield in the range of 40% to 50%.
Distal CBD stricture
o MRI & MRCP - Up to 11% and 21% complication rate
o ERCP
§ Diagnostic and therapeutic:
• Brushings/cholangiography/biopsy
• Balloon sphincterotomy/stent
§ “Double duct sign” - simultaneous dilatation of the common bile and
pancreatic ducts; likely causes by pancreatic cancer
o CT-PET (Used to rule out extra-pancreatic disease – esp. the liver)
o Tumour marker: CA 19.9
• Treatment:
o Resection possible in only approx 20%
§ Local invasion
§ Proximity to portal vein
§ Metastases
§ Advanced cachexia
o Resection – Whipple procedure
o Unresectable – biliary bypass + gastric bypass
• Complications:
o Up to 30%
o Include: pancreatic fistula
o intraabdominal sepsis
o delayed gastric emptying
o Mortality < 5%
Pancreatic cancer:
• Typical patient: >60yrs old
• Risk factors: Smoking, alcohol, carcinogens, DM, chronic pancreatitis, increased waist circumference (ie adiposity) and possibly a high fat
and red or processed meat diet
• Pathology: Mostly ductal adenocarcinoma (metastasize early; present late)
o 60% arise in the pancreas head, 25% in the body, 15% tail.
o A few arise in the ampulla of Vater (ampullary tumour) or pancreatic islet cells (insulinoma, gastrinoma, glucagonomas,
somatostatinomas, VIPomas); both have a better prognosis
• Genetics: ~95% have mutations in the KRAS2 gene.
Cystic lesions:
• Types:
o Pseudocyst
o Serous cystadenoma
o Mucinous cystadenoma
o Intraductal papillary mucinous neoplasm (IPMN)
o Pseudopapillary cystic tumours
• All mucinous pancreatic neoplasms are (believed) to malignant or
pre-malignant
Michael Grant
lOMoARcPSD|4776960
• Intraductal papillary mucinous neoplasm (IPMN) is a type of tumor that grows within
the pancreatic ducts (intraductal) and is characterized by the production of thick fluid
by the tumor cells.
• Frankly malignant (invasive + CIS) among resected:
o Main duct IPMN ≈25-80%
o Branch duct IPMN ≈0-30% (series at high end do not have assx pts)
o Mucinous cystadenoma ≈5-20%
• Treatment:
o Main duct IPMN - resect
o Branch duct IPMN
§ Resect if symptomatic, > 3cm, mural nodules, + cytology, jaundice, ductal
dilatation
§ Observe if ≤3 cm, no sx, nor worrisome features
o Mucinous cystadenoma - generally resect (younger women, usually left sided resection with < morbidity)
Pancreatic Endocrine Tumours are rare tumours which may give rise to overproduction of peptide products
• Insulinoma (B cells)
• Glucagonoma (A cells)
• Gastrinoma
• VIPoma
o Verner–Morrison syndrome, usually (about 90%)
originating from non-β islet cell of the pancreas,
that produce vasoactive intestinal peptide
§ Profound and chronic watery diarrhea and
resultant dehydration, hypokalemia,
achlorhydria
Spleen trauma:
• Predisposing factors:
o Splenomegaly
o Pathological spleen
• Causes:
o Closed trauma
o Open trauma
o Iatrogenic
• Pathology:
o Subcapsular hecatomb.
o Superficial tears
o Deep lacerations
o Avulsion of a pole
o Crush of spleen
o Complete avulsion from its pedicle
• Clinical presentations:
o Fatal type
o Classic type – signs of hypovolaemic shock
o Delayed type – delayed rupture
• Management:
o Non operative - esp. in paeds if:
§ Hemodynamic stability
§ Absence of peritonitis
§ CT scan – w/ no contrast extravasation and absence of other injuries
§ Transfusions - <2 PRBC’s
§ Management:
• Observe in HDU (CVP monitoring)
• Bed rest for 48 hours
• Restrict activity for 6 weeks
• Avoid contact sports for 6 months
o Operative:
§ Cautery, local hemostatic agents
§ Splenopexy - Suturing
• Mesh Splenorrhaphy
• Autotransplantation
§ Partial splenectomy
§ Wrapping in haemostatic agents
§ Splenectomy, ?transplants
Michael Grant
lOMoARcPSD|4776960
Splenic Cysts:
l Splenic Pseudocysts
- Lack epithelial lining
- Account for most splenic cysts
l Pancreatic pseudocyst
l Posttraumatic
- Splenectomy is indicated when:
l Size >10 cm or
l Symptomatic
l Simple congenital cysts
- Epithelium-lined cysts
- Epidermoid cysts – most common
- Mostly asymptomatic
- Young children + young adults
- LUQ pain, N/V, early satiety
- Dx: CT scan
- Complications
l Infection, bleeding, rupture
l Tx: Splenectomy (complete or partial)
Splenic Abscess
l Uncommon, but fatal
- Erode into adjacent structures
l Most are secondary in etiology
- Bacterial endocarditis
- Intrabdominal infections (pyelo-, etc)
- Infected splenic haematoma
- Infected splenic infarctions (embolizations, ischemia, etc)
l Staphylococcus & Streptococcus, E.coli, Salmonella, anaerobes
l Treatment
- Splenectomy + IV Antibiotics
- Percutaneous drainage
Spleen Tumors
Malignant:
l Spleen - mostly secondary involvement
l Non-Hodgkin’s Lymphoma - most common malignancy
l Spleen is the primary site
- 10% Hodgkin’s disease
- 30% of resected spleens (staging procedure) have (+) histology
l Hairy cell leukaemia
- Resect for symptomatic splenomegaly
l CML & CLL
- symptomatic splenomegaly (hypersplenism when it beings to affect WBC and platelets) = splenectomy
Benign:
l Hemangioma
- Risk of rupture + platelet sequestration
- No treatment unless symptomatic
l Hamartoma
l Lymphangioma
Indications for splenectomy:

1. Spleen trauma
2. Hematological diseases
1. Hereditary spherocytosis
2. ITP
3. Thalassemia
4. Sickle cell anaemia
3. Lymphomas
4. During surgery
5. In ileao-renal shunts (splenic vein is attached to the left renal vein in Rx of portal hypertension)
6. Hypersplenism
7. Splenic cyst
8. Splenic abscess
9. Splenic tumors
Michael Grant
lOMoARcPSD|4776960
43 The Dyspeptic Patient

Causes:
• Non ulcer (functional) dyspepsia (60%)
• Duodenal ulcer
• Gastric ulcer
• Duodenitis
• Gastroesophageal reflux disease
• Gastric cancer
• Rarer: Chronic pancreatitis, pancreatic cancer, small intestinal stricture, mesenteric ischaemia,
myocardial ischaemia
History:
• Epigastric, central upper abdominal or retrosternal discomfort related to eating, specific foods,
hunger or time of day
• Heaviness, unease, postprandial fullness, early satiety, flatulence, borborygmi (rumbling)
• Heartburn and acid brash are more likely to indicate underlying gastroesophageal reflux
disease than dyspepsia but may be overlap of both conditions
• Review medication that may cause dyspepsia, eg
o Calcium antagonists – relax smooth muscle
o Nitrates – dilate sphincter
o Theophyllines
o Biphosphonates – irritation
o Steroids
o NSAIDs including Aspirin loss of protective secretions
• Red flag symptoms:
o Unintentional weight loss
o Dysphagia
o Recurrent vomiting
o Gastrointestinal blood loss
o Iron deficiency anaemia
o Epigastric pain severe enough to hospitalise patient
Helicobacter Pylori
• Gram -ve, spiral, Giemsa stain +ve
• Infects antrum; sometimes fundus, body and duodenal cap
• May increase gastric acidity
• Associated with:
o DU, GU
o Menetrier’s (rare, acquired, premalignant disease of the stomach characterized by
massive gastric folds, excessive mucous production with resultant protein loss, and little
or no acid production)
o Cancer: MALToma, Gastric
• Long term infection may cause atrophy
• Metronidazole resistance 35% in UK
• Infection detected by urease (breath test, biopsy kit), histology, culture, serology, stool
antigen test
• Eradication detected by breath test or biopsy or stool antigen test; after triple therapy
Endoscopy
• Indications:
o Gastrointestinal bleeding
o Unintentional weight loss
o Dysphagia
o Persistent vomiting
o Iron deficiency anaemia
o Epigastric mass
o Suspicious barium meal
o Patients over 55, when symptoms persist despite H pylori testing and acid
suppression
o Previous gastric ulcer or surgery
o Continuing need for NSAID treatment
o Increased risk of gastric cancer
o Anxiety about cancer
Non ulcer disease:

• Refers to relapsing or chronic dyspepsia in patients who lack an identifiable cause for
symptoms after a routine clinical diagnostic work up
Michael Grant
lOMoARcPSD|4776960
• Gastritis or duodenitis can be included in non-ulcer dyspepsia as a definite link between these abnormalities and symptoms has not been
established
• Management:
o Make a positive clinical diagnosis based on history and examination
o Minimise invasive investigations and avoid giving “mixed messages” – do not repeat tests eg OGD without good indication
o Reassurance – benign prognosis
o Education about the condition
o Lifestyle changes – eg avoid stress, regular meals, less alcohol, stop smoking
o Dietary modification – avoid foods that precipitate symptoms, low fat diet, small meals, exclusion diets, etc
o Prescribe drugs sparingly – target symptoms of most concern
l Dysmotility type – domperidone, metoclopramide (both D2 antagonists), hyoscine (antimuscarinic)
l Ulcer type – proton pump inhibitors
l Reflux type – proton pump inhibitors
l H pylori eradication if positive
Gastric ulcers:
• H pylori – 60%
• Drug related – NSAIDs, aspirin
• Smoking
• ?Environmental stress – weak association
• Physiological stress”
o Cushing’s ulcer (ssociated with elevated intracranial pressure causing ulcer via increased vagal tone) after neurosurgery
o Curling’s ulcer (acute gastric erosion resulting as a complication from sever e burns when reduced plasma volume leads to ischemia
and cell necrosis) after burns
• Management:
o Eradicate H pylori if present Duodenal ulcers Gastric ulcers
o Proton pump inhibitor (PPI) therapy for 4 weeks or until repeat Age * Young Elderly
endoscopy Gender * Male Either
o Repeat endoscopy after 8 – 12 weeks to ensure ulcer healing Pain * Nocturnal, before meals Soon after eating
o Consider stopping aspirin, NSAIDs or clopidrogel but need Vomiting * Unusual Anorexia
to balance benefit and risk of stopping Weight * Stable Loss
§ If can’t be stopped, co-prescribe PPIs Endoscopy For diagnosis Repeat till healed
o Lifestyle – stop smoking, reduce alcohol Biopsies Antral for H pylori Multiple
Treatment H pylori eradication Acid suppression if H pylori –ve or on NSAIDs
o Surgery – rarely done, only for complications, eg intractable
Maintenance Failed H pylori eradication, Failed H pylori eradication, NSAIDs, surgery risk
bleeding, perforation complications, NSAIDs, aspirin
Surgery Intractable bleed, perforation, pyloric Suspicion of malignancy, complications, eg bleed or
stenosis perforation
Duodenal ulcers:
• H pylori – 90%
• Drugs – aspirin, NSAIDS
• Genetic predisposition
• Blood group O
• Smoking – slows healing and increases likelihood of relapse
• Management:
o Eradicate H pylori if present
o Proton pump inhibitors for 4 – 8 weeks if complicated, eg bleeding
o Consider stopping aspirin, NSAIDs or clopidrogel but need to balance benefit and risk
of stopping
§ If can’t be stopped, co-prescribe PPIs
o Lifestyle – stop smoking, reduce alcohol
o Surgery – rarely done, only for complications, eg intractable bleeding, perforation
Michael Grant
lOMoARcPSD|4776960
44 Tumour markers/Screening/Staging
WHO - Principles of Screening: Currently recommended clinical recommendations
• World Health Organization guidelines were Tumour marker Relevant Screening Diagnosis Prognosis Detecting Monitoring
published in 1968, but are still applicable cancer or early or case (with recurrence treatment
detection finding other
today
factors)
• The condition for screening should be an Α-fetoprotein Germ No Yes Yes Yes Yes
important health problem cell/testicular
• There should be a treatment for the tumour
condition Hepatocellular Yes Yes Yes Yes Yes
• Facilities for diagnosis and treatment should carcinoma
Calcitonin Medullary No Yes No Yes Yes
be available
thyroid
• There should be a latent stage of the disease carcinoma
• There should be a test or examination for the Cancer antigen Ovarian Under Yes Yes Yes Yes
condition 125 (CA125) cancer evaluation
• The screening test should be acceptable to Cancer antigen Breast cancer No No No Yes Yes
the population 15-3 (CA15-3)
Cancer antigen Pancreatic No Yes Yes Yes Yes
• The natural history of the disease should be
19-9 (CA19-9) cancer
adequately understood Carcinoembryonic Colorectal No No Yes Yes Yes
• There should be an agreed policy on who to antigen (CEA) cancer
treat Human chorionic Germ cell and No Yes Yes Yes Yes
• The total cost of finding a case should be gonadotrophin testicular
economically balanced in relation to medical cancers;
gestational
expenditure as a whole
trophoblastic
• Case-finding should be a continuous process, neoplasia
not just a "once and for all" project Paraproteins (M B cell No Yes No Yes Yes
protein/Bence proliferative
Serum Tumour Markers: Jones protein); disorders
• Tumour markers can contribute to patient also measured in (such as
urine8 multiple
management but be aware of their limitations myeloma)
• The main application of tumour markers is in Prostate specific No Prostate
Yes Yes Yes Yes
monitoring of disease response to antigen cancer
treatment
• Measurement of α-fetoprotein and human chorionic gonadotrophin is mandatory in the management of germ cell tumours
• Carcinoembryonic antigen (CEA) is recommended for postoperative follow-up of patients with stage II and III colorectal cancer
• Prostate specific antigen (PSA) may be used for detecting disease recurrence and monitoring treatment in patients with prostate cancer
• In some high risk patients, measurement of α-fetoprotein, CA125, or CA19-9 may aid early detection of primary liver (hepatocellular)
cancer, ovarian cancer, or pancreatic cancer respectively
• Measurement of CA125 in men or PSA in women is inappropriate
45 Burns & the Reconstructive Ladder

“Indications” for referral to burn service
• Airway burns Flaps - ‘free’
• Big burns complex
• (>5% TBSA partial thickness burn in child )
• (> 10% TBSA partial thickness burn in adult )
• Deep burns (full thickness > 1%) Flaps - loco regional
• Special burns (electrical,chemical, non- Flap is piece of tissue with a blood supply
accidental)
• Special areas (face, hands, perineum, feet,
circumferential, inhalation)
• Special people (children esp. < 5yr, elderly, co Skin grafting
morbidites) No blood supply, relay on
angiogenesis at site
Suturing
less complex
Conservative Mx
Michael Grant
lOMoARcPSD|4776960
46 Common Hand Conditions

Peripheral Nerve Injuries:
Muscle innervation:
• Median:
o Lateral two lumbricals
o Opponens pollicis
o Abductor pollicis brevis
o Flexor pollicis brevis
• Ulnar:
o all small muscles of hand apart from
those supplied by median nerve
• Radial:
o Extensor muscles
Nerve compression:
Ulnar:
• ‘Ulnar Claw Hand’
o Hyperextension MCP joints
o Flexion IP joints
o Little/ring fingers
• Ulnar paradox:
o 'The closer to the Paw, the worse the
Claw'
o Ulnar nerve also innervates the medial aspect of digitorum profundus (FDP), so if lesion
occurs more proximally the flexor digitorum profundus muscle may also be denervated,
which reduces the claw-like appearance of the hand
o Treatment is usually conservative (rest, nighttime splinting) but medial epicondylectomies,
intra- & submuscular nerve transpositions in severe
o Froment’s sign tests the palsy of the ulnar nerve. The patients is asked to hold a piece of
paper between thumb and index finger, while the examiner tries to pull it out. If the ulnar
nerve is damaged, the patient will have difficulties and flex the interphalangeal articulation
(flexion of the thumb allowed by median nerve).
o Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little)
finger, caused by unopposed action of the extensor digiti minimi (radial nerve)
Radial:
• Wrist drop
Median:
• Hand of benediction
• Carpel tunnel syndrome
o Female > Male (smaller wrist)
o 50 – 60’s
o Aetiology
§ Pregnancy
§ Arthritis
§ Trauma (and Colles’ splint following #)
§ Diabetes
§ Swellings
o Signs:
§ Thenar wasting
Michael Grant
lOMoARcPSD|4776960
§ Loss of sensation in median distribution; however, sensation over the thenar muscle is
actually spared as palmer branch of median nerve branches off before passing under the
flexor retinaculum
o Special tests:
§ Tinels – Tap on retinaculum
§ Phalens – Maximal wrist flexion for 1 min to elicit symptoms
o Investigations
§ Radiological – esp. if suspicion of mass
§ Nerve conduction studies
o Management:
§ Conservative – splints, underlying cause, phsyio
§ Medical – steroid injections
§ Surgical – Longitudinal division of the flexor retinaculum
Dupuytrens Disease:
• A hereditary, palmar fibromatosis of the palmar fascia that may begin with nodules
and lead to the in ability to extend fingers – may take years to progress or can be
aggressive (dupuytren’s diathesis)
• Northern Europeans
• Increases with age
• M>F
• Hueston table top test
• Exact aetiology unknown; Associations:
o Peyronie’s disease (penile fibromatosis)/ Ledderhose syndrome (plantar
fibromatosis/Garrod’s pads (a.k.a. violinist’s pads - dorsal aspect IPJ
fibromatosis)
o Smoking
o Diabetics
o Alcohol
o Liver disease
o Anti-epileptic medication
• Management:
o Conservative – splints, phsyio
o Medical – control associated disease
o Surgical
§ Fasciotomy – cut in palm, finger or both using small knife or needle
§ Segmental Fasciectomy – small sections of cord removed
§ Regional Fasciectomy – entire cord removed
§ Dermofasciectomy – cord and overlaying skin is removed, skin grafts applied from arm or groin; used for
recurrent or in advanced disease in young (photos to right)
47 Day Case Surgery

Patient selection:
l Suitability of both patient and procedure for day surgery
l Consider:
1. Social factors
l Patient accompanied home by responsible adult
l Present for 24 hours post-procedure
l Patients not to drive home
l < 1 hour from hospital
l Telephone available
l Toilet and washing facilities
Patient
2. Age
3. Body Mass Index (BMI)
4. Smoking
General practitioner
l Smokers increased complications
l Impaired gas exchange Outreach nurse Outpatient clinic
Fast track or
l Increased secretions outreach clinic
l Bronchospasm
l Chest infections Discharge Inpatient admission Pre-assessment
l Wound complications Unsuitable
l Smoking cessation - Temporary (12 hours pre- Unplanned

admission
surgery) allows decreased Recovery Day surgery admission
carboxyhaemoglobin and improved peri-
operative lung function Operating theatre
Michael Grant
lOMoARcPSD|4776960
5. Medical co-morbidities
ASA Grade:
I. Fit healthy patient
II. Mild to moderate systemic disease caused by the surgical condition to be treated or another disease process with no functional
limitation
III. Severe systemic disease with some functional limitation
IV. Severe systemic disease that is a constant threat to life
V. Moribund patient not expected to survive
*In general ASA I& II patients suitable +/- selected ASA III*
Anaesthesia:
l Sedation
- Defined as ‘a technique in which a drug(s) are used producing CNS depression enabling treatment, but where verbal contact is
maintained with the patient’
- ‘Simple’ – IV midazolam titrated 0.07mg/kg (care in the elderly patient)
- Addition of analgesic agent - Pethidine/Morphine/Fentanyl (Sedo-analgesia)
l Local and regional anaesthesia
- Local – loss of sensation from the surgical field
- Regional – nerves blocked at a distance from site of surgery
l Variety of agents
- Lignocaine, Bupivacaine, Ropivacaine (+/- adrenaline)
- Toxicity – circumoral tingling, tinnitus, deafness
- Adrenaline contraindicated – end artery (penis, digits) Operating theatre
l Local or regional techniques can be used in conjunction with sedation
or general anaesthesia
1st stage recovery
l General anaesthesia
No
- Defined as ‘a technique where a drug or combination of Direct transfer for
selected patients after
drugs produces loss of sensation and consciousness with or Vital signs stable Local anaesthesia
Protective reflexes present
without relaxation’ Obey commands
- Techniques and drugs usually permit up to 90 minutes of Yes
anaesthetic time 2nd stage recovery
- Use of laryngeal mask cf. ET tube
l Ease of use
Discharge criteria fulfilled
l No need for muscle relaxation ( case dependent)
Yes
l Use of propofol for induction and maintenance of Unplanned overnight Home
anaesthesia admission
E.g. post op NV and pain
- IV fluids to reduce post operative nausea and vomiting
(PONV)
- Multimodal pain management – Local/regional block, paracetamol, NSAIDs & opiods
Day case surgeries:

l General surgical procedures:
- Circumcision
- Inguinal hernia repair
- Minor anorectal procedures (Haemorrhoids, skin tags, fistula)
- Varicose veins
- Ganglion excision
- Dupuytren’s contracture
- Minor breast lesions
- Upper and lower gastrointestinal endoscopy
- Laparoscopic cholecystectomy
l Gynaecology
- Laparoscopy, D+C / hysteroscopy
l Otorhinolaryngology
- Tonsillectomy, myringotomy, bat ears, reduction nasal fracture
Michael Grant
lOMoARcPSD|4776960
l Orthopaedic
- Arthroscopy, bunion, removal of metalwork
48 Cardiac Surgery
Prognostic indications:
• Left main stem stenosis >50%
• Three vessel disease (LAD, Circumflex, RCA) with ejection fraction <50%
• Three vessel disease with ejection fraction >50% and significant inducible
ischaemia
• One and two vessel disease with extensive myocardium in jeopardy but
lesions not amenable to PCI
• Symptomatic:
o New York Class 3-4 angina
o Ischaemic pulmonary oedema Vein graphs harvest long saphenous
o Strongly positive stress test prior to non-cardiac major surgery
• Concomitant surgery for other cardio-pathology; e.g. Valvular heart disease, Postinfarction
mechanical defects
Cardiopulmonary bypass circuit are required for CABG:

• Aortic cross-clamp prevents blood returning from CPB circuit entering heart
• Cardioplegia (containing potassium) used to hyperpolarize cardiac myocytes, stop
myocardial activity and reduce cardiac metabolism
Non-surgical options:
• Medication
• Percutaneous / Stent
o Bare-metal vs Drug eluting
o Reintervention rate higher with stents
Surgical considerations:
• On-pump (Cardiopulmonary bypass) vs OPCAB (beating heart surgery)
• Standard access (median sternotomy) vs minimal access (may be possible for
single vessel disease)
• LIMA and Vein grafts vs Total/Multiple Arterial Revascularisation
Valvular Heart Disease

• Aortic Stenosis
o Symptoms: angina, heart failure, syncope
o Critical AS <0.7cm2
o Preop investigations
§ Coronary angiography
§ Dental assessment
o Transfemoral / transapical aortic valve insertion (TAVI) – reserved for those not fit
• Aortic Incompetence
o Pathophysiology
§ Volume overload
§ Acute:
• left ventricular failure and pulmonary oedema
§ Chronic:
• progressive left ventricular dilation and symptoms of left heart failure
• Mitral Stenosis
o Rheumatic fever
o Elevated left atrial and pulmonary venous pressure leading to heart failure
§ Atrial fibrillation (due to increase in L. atrial size) may further decrease ventricular
filling
o Pulmonary hypertension may lead to right heart failure and functional tricuspid
regurgitation
Michael Grant
lOMoARcPSD|4776960
o Indications:
§ Severe symptoms
2
§ Valve area <1cm
§ Systemic thromboembolism from LA thrombus
o Surgical options:
§ Mitral valvuloplasty
• Percutaneous balloon vs closed
• Open (Standard vs minimal access)
§ Mitral valve replacement
• Mechanical (younger, chronic af) vs tissue
§ Concomitant tricuspid annuloplasty
• Mitral Regurgitation
o Mitral valve apparatus
§ Leaflets, chords, papillary muscle, ventricle, annulus
o Carpentier classification
§ Type 1: normal leaflet motion
§ Type 2: leaflet prolapse
§ Type 3: restricted leaftlet
o Acute vs chronic
o Surgical options:
§ Mitral valve repair - Procedure of choice for degenerative mitral valve
disease
§ Mitral valve replacement - Mechanical vs tissue
§ Concomitant tricuspid annuloplasty
49 Urological Cancer
Bladder cancer:
• Aetiology:
Shadow caused by cancer mass
o Smoking 4x
o Occupational – analine dye & rubber industry (hydrocarbons, aromatic amines)
o Chronic infection – esp. parasites (schistosomiasis, assoc. aggressive form)
o Drugs (cyclophosphamide)
o Genetic/Familial
• HISTOPATHOLOGY
o Transitional Cell – overwhelming cell of origin – Form wart like lesions (photos)
o Squamous Cell – more aggressive and assoc. with chronic infection
o Adenocarcinoma – rarer type, typically seen in dome of bladder
• PRESENTATION
o Haematuria (70-80%; frank or micro)
o Infection (Esp. Recurrent in man)
o Mass
• INVESTIGATION
o Cystoscopy - Flexy cyst is outpaitent
o Staging: CT and MRI
• TREATMENT
o SUPERFICIAL Ca
§ Transurethral Resection (electro cautary)
§ Intravesical Chemo (Mytomycin)/Immunotherapy (BCG)
§ >80% 5-year survival
o INVASIVE
§ Radical Surgery (cystourethrectomy with urostomy)
§ Radiotherapy
§ Systemic Chemotherapy (usualy just for metastatic)
§ 25-50% 5-year survival
Prostate cancer:
• AETIOLOGY:
o Testosterone (basically unseen in those that are castrated)
o Race (Afro-carribeans – younger age and more aggressive)
o Family History
o Diet (Selenium and Vit D are protective, animal fats are risk)
o Smoking
• HISTOPATHOLOGY
o Peripheral zone most common
§ Transition zone is 2nd
o Local spread
§ Perineural
Michael Grant
lOMoARcPSD|4776960
§ Seminal vesicle
o Metastatic spread
§ Regional lymph nodes
§ Bones, lungs, viscera
o Adenocarcinoma
o Prostatic Intraepithelial Neoplasia
§ Grade: Gleason Score 2-10
• Degree of glandular tissue
• Higher number, higher grade
o Stage T1-4, N0-1, M0-1
• PRESENTATION:
o ASYMPTOMATIC
§ Raised Prostate Specific Antigen
§ Abnormal Digital Rectal Examination
§ Screening annually in >50 in America – no such program here yet pending evidence
o LOCAL SYMPTOMS
§ Haematuria
§ Haematospermia
§ Bladder Outlet Obstruction
o ADVANCED SYMPTOMS
§ Lymphoedema
§ Pathological Fracture/Spinal Cord Compression
§ Anaemia
§ Ureteric Obstruction
o INVESTIGATIONS
§ PSA (not specific – raised after instrumentation, infection, benign disease)
§ Transrectal Ultrasound Biopsy
§ Isotope Bone Scan
§ CT
§ MRI
o TREATMENT
§ CONSERVATIVE
• Watchful Waiting – if older, asymptomatic or confined disease
• Active Surveillance – in younger with confined disease, regular biopsy
§ CURATIVE
• Radical Prostatectomy (plus seminal vesicles)
• Radiotherapy
o External beam
o Brachytherapy
§ ADVANCED DISEASE
• Endocrine Therapy – anti-testoterone
treatments mainly for symptom relief
• Chemotherapy
• Corticosteroids
• Palliation
Renal cancer
• AETIOLOGY
o Inherited (younger patients, multifocal, aggressive):
§ Von Hippel-Lindau Syndrome
§ Hereditary Papillary Renal Cell Carcinoma Syndrome
o Smoking
o Obesity
o Polycystic renal disease
• HISTOPATHOLOGY
o Solid/Cystic
Michael Grant
lOMoARcPSD|4776960
o Clear cell 75%
§ Papillary 10%
§ Chromophobe 10%
o Oncocytoma (essentially bengin)
o Collecting duct tumours
• PRESENTATION Tubule
o 40% Incidental
o TRIAD OF: Haematuria, Mass, Pain Clear Cell Tumour
o LATE:
§ Paraneoplastic phenomena Glomerulus
§ Secretion of active compounds can present with fever, hypertension,
polycythemia (increased haemoglobin from EPO secretion)
§ Metastatic – e.g. bony met’
§ Varicocoele – backpressure from renal vein occlusion
leads to pressure in gonadal vein leading to left
varicocoele
• INVESTIGATIONS
o Ultrasound
o CT
o MRI
• TREATMENT
o Organ-Confined
§ Radical Nephrectomy – tumour, kindey and renal fascia
are removed en bloc
§ Nephron Sparing Surgery – partial nephrectomy, used in
those with 1 kidney or those with Von Hipple Lindau (likely to have more in future)
Testicular cancer
• RISK FACTORS
o Cryptorchidism (4-8x if intra-abdominal)
o Previous personal or family history
• HISTOPATHOLOGY
o 95% Germ Cell:
§ Seminoma
§ Teratoma (Non Seminoma)
o Lymphoma (most common in older men)
o Sertoli
o Leydig Cell (may be seen with feminisation from LH production)
o Metastases
• PRESENTATION
o Most present early
o Painless mass
o Hydrocoele
o Undescended – inguinal or pelvic mass
• INVESTIGATION
o Tumour Markers:
§ a-FetoProtein
§ b-Human Chorionic Gonadotrophin
§ Lactate Dehydrogenase; non-specific but coorelates to prognosis
o Pathology
o Ultrasound
o CT
o MRI
• TREATMENT
o Radical Orchidectomy via an inguinal approach
o Adjuvant Therapy
§ Seminoma
• Radiotherapy
• Chemotherapy
§ Non Seminomatous Germ Cell Tumour (Teratoma)
• Combination Chemotherapy (Bleomycin [risk of pulmonary fibrosis] and cisplatin [peripheral neuropathy])
• Retroperitoneal Lymph Node Dissection of remaining matches
Michael Grant
lOMoARcPSD|4776960
50 Paediatric Acute Abdomen

SEE PAEDS NOTES
51 ATLS Principles
SEE POEM NOTES ON ABC
52 Endoscopy
ERCP:
• Indications:
o Biliary obstruction
o Pancreatic obstruction
o Stent placement
§ Strictures (benign or malignant)
§ Fistulae
§ Post-op bile leak
§ patients with large, unremovable common duct stones Sphincterotomy Biliary stent
o Balloon dilatation of strictures
o Pancreatic pseudocyst drainage
o Brushings from biliary or pancreatic duct
• Complications:
o Pancreatitis 3-5%
o Bleeding 1 %
o Cholangitis 1%
o Perforation 0.5%
o Sedation
Capsule endoscopy:
• Capsule
• Ambulatory recorder on a belt
• Software for processing and viewing
• Indications:
o Obscure GI bleeding
o Evaluation of Crohn’s disease
o Evaluation of Coeliac disease
o Chronic diarrhoea
o Abnormal imaging of the small intestine
Double Balloon Enteroscopy:

• View whole GI tract – sequential inflation of balloons allows scope to along the length of bowel
• Per oral & per rectum
• Allows therapy:
o Biopsy
o Bleeding lesions
o Removal of polyps
Colonoscopy:
• Examination of the colon +/- terminal ileum
• ‘Conscious sedation’
• Bowel preparation & dietary restriction
Michael Grant
lOMoARcPSD|4776960
• Public will become more aware with
Bowel Cancer Screening
programme introduced in April
2010
• Sigmoidoscopy - no sedation, up to
splenic flexure
• Complications:
o Bleeding 1:100-200
o Perforation 1:1000 – 2000,
increases with therapy
o Sedation
o Incomplete procedure, missed
pathology
53 Thoracic Surgery
Scope of Thoracic Surgery:

• Surgery for Benign, malignant disease affecting the thorax, including:
o The chest wall, major airways, mediastinum, lungs and oesophagus.
o Cosmetic procedures for chest wall deformities such as pectus excavatum
o Trauma to the chest
• Does not include heart and aorta usually
• Examples:
o Correction of Pectus Excavatum
o Lobectomy or Pneumonectomy
o Mediastinoscopy
o Repair of Ruptured Diaphragm
o Pleural Biopsy
o VATS (Video Assisted) Pleurectomy
Lung cancer:
M M
o
r o
e r
l
u
t
n a
g
r
l
e i
m t
o
v y
e
d
54 Neurosurgery
Intracranial Contents:
l Intracranial Compartments:
- Supratentorial: frontal, parietal, temporal, occipital lobes; hypothalamus,
thalamus.
- Infratentorial: brainstem (midbrain, pons, medulla) and cerebellum.
l Craniospinal fluid (CSF) pathways: Ventricular system and subarachnoid space
CSF pathway:
• CSF is made by the choroid plexus in the ventricles (500 ml/day with 120ml at any
one given time) by modified ependymal cells that line the ventricular system (lateral,
third and fourth ventricles) and flows into the subarachnoid space via the foramina of
luschka and magendie
Michael Grant
lOMoARcPSD|4776960
• CSF removes waste (e.g. toxins, beta amyloid) and provide buoyancy from within the subarachnoid space
• Normal ICP is approximately 10
mmHg in the resting state
• This can be monitored using a variety
of devices (image to right) and can
help calculate Cerebral perfusion
pressure (CPP = MAP – ICP)
• Absorption occurs at the arachnoid
granulations into sagittal sinus
Key neurological symptoms

• Global:
o Headache (sudden/gradual/ progressive)
o Confusion
o Drowsiness
o Seizures
• Local:
o Motor (posterior frontal)
o Sensory (anterior parietal)
o Dyscoordination (cerebellum)
o Visual (optic pathway)
Common pathologies in neurosurgery:

l Trauma
- Head (open/closed, fracture, haematoma)
- Spine (stable / unstable)
l Intracranial vascular disorders
- Aneurysms, arteriovenous malformations, Cavernomas
- Subarachnoid haemorrhage, intracerebral haemorrhage
l Tumours
- Intrinsic / extrinsic
- Primary / secondary (metastases)
l Hydrocephalus
- Communicating (impaired absoprtion) / non-communicating (obstruction)
l Infection
- Meningitis, brain abscess, subdural empyema
l Cauda Equina Syndrome (loss of function of the lumbar
plexus nerve roots of the spinal canal below the
termination, i.e. below conus medullaris)
- Disc prolapse
- Tumour compression
Trauma
• Diffuse axonal injury is widespread axon damage from
acceleration force (e.g. car accident)
o Leads to tearing of axons and damage to white
matter leading to oedema – with most tearing happening at the grey-white matter junction due to the differences in density
allowing different
o No lucid interval and may enter coma from the time of injury - 90% of patients with severe DAI never regaining consciousness
o Axonal swelling can be seen by staining for beta-amyloid precursor protein
• Extradural haemorrhage where blood collects between the skull and the dura, which is normally the result of a
skull fracture tearing a meningeal artery (esp. the middle meningeal artery, underlying the pterion with weak
squamous temporal bone)
Michael Grant
lOMoARcPSD|4776960
o Often associated with a “lucid” interval of hours to days between
initial impact and onset of neurological deterioration as ICP slowly
rises – be suspicious in head injury with little or no immediate LOC
o Underlying brain can retain function in treated promptly
o CT scan shows high density biconvex shape (formed by dura peeling
off bone) adjacent to the skull seen on imaging
o Presents with reduced GCS, headache, vomiting followed by fits and
upper motor neuron signs
§ Severe signs: ipsilateral pupil dilation, cushing’s triad
(bradycardia, raised blood pressure, altered breathing) and
death occurs via cerebral compression and herniation
o Management:
§ ABCDE, stabilize, intubation, mannitol IVI (decreases ICP)
§ Emergency neurosurgical unit transfer for clot evacuation ±
ligation of the bleeding vessel
• Subdural haemorrhage
o Tearing of bridging veins that empty into the superior sagittal sinus
with resulting blood between the dura and arachnoid – which are
vulnerable to deceleration injury
§ Usually trauma (may be minor and up to 9 months prior – blood
baby) but occasionally from reduced ICP or mets
§ Elderly are at risk as brain atrophy makes bridging veins
vulnerable
o Consider this very treatable condition in all whose conscious level
fluctuates, and also in those having an ‘evolving stroke’ (esp. if
anticoag)
o Gradually raises ICP, shifting midline structures away from the side of
the clot and, if untreated, eventual tentorial herniation and coning
§ Localizing neurological symptoms (e.g. unequal pupils,
hemiparesis) occur late and often long after the injury (mean=63 days)
o CT scan shows crescentic mass of increased attenuation adjacent to inner table of skull
o Management: Irrigation/evacuation, e.g. via burr twist drill and burr hole craniostomy
• Cerebral contusions are superficial bruises of the brain that tend to occur over bony prominences (seen in alcoholics and elderly due to
increased fall risk) are classified as coup (with injury at site of impact) or contrecoup (with bruising at the
opposite point of skull to impact due to the momentium of brain tissue in recoil after impact)
• Skull Fractures:
o Open (scalp laceration)
o Depressed (lies below adjacent bone)
o Comminuted (multiple fragments)
Intracranial vascular disorders

• Subarachnoid haemorrhage is the spontaneous (although
rarely can be caused by extreme lacerations) bleeding
typically caused by:
§ Berry aneurysms; 85% of cases; saccular
aneurysms linked to polycystic kidneys,
coarctation of aorta, ethler-danlos, marfan’s
§ Ateriovenous malformations; 15%; abnormal
arteriovenous connection that bypass capillaries
• A subtype of this is the carotid cavernous
fistula: a dural AV fistula between ICA and the
cavernous sinus as it travels through it, either
spontaneous or post- trauma
o Orbital bruit, Exophthalmos, ocular pulsation, chemosis, pulsatile tinnitus
o Risk factors: smoking, alcohol, hypertension, bleeding disorders, mycotic aneurysm, close
relative with SAH (3-5x risk – thus screening is offered)
o Symptoms: thunderclap, occipital headache; following by vomiting, collapse, seizures, coma
§ Onset may be proceeded by “sentinel headache” perhaps due to a small warning leak
o Signs: Neck stiffness, Kernig's sign (pain on flexed knee, hip extension), Terson’s syndrome
(vitreous haemorrhage assoc. w/ 5x mortality), focal neurology (e.g. pupil changes from IIIrd
nerve palsy with a post. communicating aneurysm)
o Tests: CT Head will reveal >90% in first 48hrs
§ If negative and no contraindications of lumbar puncture for >12hr, then perform:
§ LP: position patient on side with knees to chest, palpate the iliac crest at L4, clean area, LA
administered, needle inserted aiming for umbilicus
• Frank blood may be seen early (<4 hr) but broken down into oxyhaemoglobin (4-10hrs)
and then bilirubin (>10hr) causing a yellowish appearance of CSF (Xanthochromia);
given that bilirubin produced in vivo, this proves result is not just a “bloody tap”
• Send sample urgently to be spun w/in 30mins and protect from light
Michael Grant
lOMoARcPSD|4776960
• Contraindications: focal neurology, spinal cord compression, coagulopathy, infection at ideal puncture site
o Management:
§ Maintain perfusion: aim for >160mmHg
§ Nimodipine is a CCB that effectively provides chemical
angioplasty thus reducing 2dary vasospasm and maintain
perfusion
§ Endovascular coiling is preferred to surgical clipping where
possible (7% increase in independent survival over 7yrs
follow-up, but higher risk of rebleeding)
• Perform CT angiography to identify single vs multiple
aneurysms before intervening
§ AVM Management:
• Surgery, embolization
• Stereotactic radiosurgery - radiation induced endothelial damage with smooth muscle proliferation, occluding vessel
lumen
o Complications:
§ Rebleeding is most common
causes of death (20%) and
often occurs in the first few
days
§ Vasospasm leading to
ischaemia is most common
cause permanent CNS deficit –
prevented by nimodipine
§ Hydrocephalus due to
blockage of arachnoid
granulations – requires
ventricular drain
§ Hyponatraemia is common
but such not be managed with
fluid restriction – seek expert
help
• Intracerebral hemorrhage (ICH), is a
type of intracranial bleed that occurs
within the brain tissue or ventricles.
o Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital admissions for stroke
o Symptoms can include headache, one sided weakness, vomiting, seizures, decreased level of consciousness, neck stiffness +/fever
and often get worse over time
o Causes:
§ Hypertension – most common cause of ICH
• Large vessel – accelerated atherosclerosis
• Small vessel – hyaline artheriosclerosis
• Charcot–Bouchard aneurysms are aneurysms of the
brain vasculature which occur in small blood vessels (less
than 300 micrometre diameter) vessels of the basal
ganglia
§ Vascular lesions
• Aneurysm rupture
• AVM
§ Neoplastic
§ Coagulation disorders
§ Cerebral venous thrombosis (Haemorrhagic transformation
of ischaemic stroke)
§ Vasculitis
§ Warfarin
§ Substance abuse (esp. cocaine)
§ Amyloid angiopathy - second most common of ICH
• Associated with age, Down’s (extra copy of beta amyloid
precursor gene on Ch.21) and Alzhiemer’s
• Tunica media is replaced by amyloid (seen on congo red stain)
weakening the vessel
o Prognosis poor if:
§ Poor initial conscious level (GCS <9)
§ Haematoma volume >60ml (30 day mortality - 90%)
§ Intraventricular haemorrhage on CT
§ Increasing age
o Management as SAH + rehab
§ Better outcome if superficial and craniotomy can be performed
Michael Grant
lOMoARcPSD|4776960
Tumours
• A 2/3rds of patients with space occupying lesions have the classical triad of
headache, papilledema and vomiting
o Headache: Waking disperses within 1-2hrs (may disappear for days
or even weeks) and usually not of great intensity, throbbing or bursting,
aggravated by coughing, sneezing, stooping down or exertion
o Vomiting: Usually before breakfast frequently as an accompaniment
of headache and described as projectile, although usually occurs
without nausea and therefore appears without warning.
o Papilloedema: Enlargement of blind spot and late peripheral
constriction of the fields, Intermittent loss of vision more common
than steady deterioration eg amaurosis fugax bilaterally and usually
lasting less than 1 min usually precipitated by getting up or lying
down eg morning
• Secondary brain tumours are the most common type and account for over
50%
o Typically, metastases from lung, breast, prostate, renal, melanoma or GI
o Clinical signs are usually new onset epilepsy, focal signs, hydrocephaly and raised ICP (headache, pappiloedma)
• Primary brain tumours arise from the cells of brain itself; i.e. neurones and the neuroglia cell – oligodendrocytes, astrocytes (electrical
insulator, metabolic function and repair and scar formation), ependymal cells, microglia (fixed macrophage system)
o Majority arise from neuroglia and are known as gliomas (astrocytoma, oligodenroglioma, ependymona and glioblastoma [grade 4 –
most common]), however other types include neuroblastomas, meningiomas, schwannomas and neurofibromas.
o Primary tumours are usually supratentorial in adults and in the posterior fossa in
children
th th
o Astrocytomas are usually found in the cerebral hemispheres in the 4 to 6 decades of
life
§ Males>Females
§ Graded based on: nuclear atypia, mitotic figures, necrosis, endothelial proliferation
§ Treatment: Surgery if operable, otherwise chemo/radio
• Temozolomide is an oral alkylating agent used with radiotherapy for Grade 4
and recurrent Grade 3 Glioma. Some countries using for Oligodendroglioma
§ Grade 4 known as glioblastomas, which have a diffuse nature and a median
survival of 13 months
th th
o Oligoddendroglioma are usually found in the cerebral hemispheres in the 4 to 5
decades of life and are associated with calcification that may be visible on plane XR
§ Better prognonsis – 5-10 years
o Ependymonas tend to affect children and teens, arising from the ependymal cells and
thus found in relation to the ventricular system
th
§ Can occur in the 4 ventricle causing a non-communicating hydrocephalus
§ Meningeal gliomatosis describes the spread of cancer via CSF
§ Average survival is 4 years with treatment
o Meningioma is a slow-growing and benign tumour that is link to mutations of 22q12, that originate
from meninges (arachnoid)
§ 90% occur above the tentorium
§ Slow growth allows them to achieve a large size before onset of symptoms (Monro-Kellie doctrine)
§ Majority are benign (Grade 1) and completely resectable, Grade 2 have a propensity for local
recurrence and Grade 3 are frankly malignant
§ Associated with:
• Previous radiotherapy
• Neurofibromatosis type 2
• Breast and endometrial carcinoma (meningioma may also express ER)
§ Surgical excision is primary goal
• High recurrence rates can be treated with repeat surgery or radiation
o Pituitary Adenomas:
§ Large tumours (macroadenomas)
• Compression of adjacent structures e.g. optic nerves resulting in classical
bitemporal hemianopia presentation
§ Small tumours (microadenomas)
• Prolactinoma
• GH-secreting (acromegaly)
• ACTH (Cushing’s disease)
o Vestibular schwannomas are slow-growing benign nerve
sheath tumours arising on the vestibular nerve
§ Presentation:
• Hearing loss
• Tinnitus
• Balance problems
Michael Grant
lOMoARcPSD|4776960
§ Association with Neurofibromatosis
• Internal herniation can be causes by any form of mass effect (tumour, abscess, etc.)
o Supracallosal/subfalcine herniation is when the cingulate gyrus herniate
under the falx cerebri
o Uncal/tentorial herniation is when the temporal lobe is forced down through
the tentorial incisura, leading to:
§ CN III compression – pupil dilation and loss of movement
§ Post. Cerebral artery compression
§ Haemorrhage in midbrain
o Tonsillar herniation is when the cerebellar tonsil are displaced down through
the foramen magnum leading to brainstem compression and coma/death
Hydrocephalus can be seen as a dilation of ventricles and compressed white matter due
to increased cranial pressure
• Clinical signs: Headache, vomiting, confusion, reduced GCS, sexiure, papilloedema,
coning (tonsillar herniation leading to dysfunction of the centers in the brain responsible
for controlling respiratory and cardiac function in the medulla oblongata)
• Stages:
o Compensation – reduction in other brain contents (e.g. venous blood) as CSF
increases
o Compensatory exhaustion – cushing’s response
o Tipping point – rapid increase in CSF
o Cerebral vasomotor paralysis – ICP has matched or exceeded MAP causing a cessation
in cerebral circulation
• Hydrocephalus can be congenital (e.g. Spinabifida, aqueduct stenosis) or acquired (eg
Infection, tumour, subarachnoid haemorrhage)
• Communicating hydrocephalus has CSF circulation is blocked at level of arachnoid granulations or if
there is overproduction
o Can be caused by infection (e.g. previous meningitis), haemorhage (e.g. SAH), high protein states
(e.g. Multiple Myeloma) , sinus thrombosis
o Fourth Ventricle is “open”
o Malabsorption of CSF is primary problem
• Non-Communicating Hydrocephalus is seen with enlargement of Ventricles proximal to
blockage.
o Block is proximal to arachnoid granulations.
o Caused by mass lesions (tumour, abscess), chiari malformations (downward displacement of
cerebellum can cause herniation and CSF obstruction in the foramen magnum – associated with
spinabifida), Dandy-Walker syndrome (enlargement of the fourth ventricle due to complete
absence of the cerebellar vermis), A colloid cyst (contains gelatinous material & almost always
found post. to the foramen of Monro)
• Normal pressure hydrocephalus (NPH) is a particular form of communicating hydrocephalus, characterized by enlarged cerebral
ventricles, with only intermittently elevated cerebrospinal fluid pressure. The diagnosis of NPH can be established only with the help of
continuous intraventricular pressure recordings (over 24 hours or even longer
• Hydrocephalus ex vacuo is a unique form of compensatory hydrocephalus that affects the elderly due to atrophy of brain tissue in
conditions such as dementia and schizophrenia
• Idiopathic intracranial hypertension is markedly raised pressure (60mmHg) in the absence of any pathology on scans
o Deteriorating vision
o Responds to shunting
• Hydrocephalus in Children is typical seen with macrocephaly, vomiting, sunsetting eyes (indicates urgency of
management)
o Causes:
§ Post Germinal Matrix haemorrhage (Prematurity)
§ Spinabifida
§ Aqueduct stenosis
o Hydra-anencephaly is when the cerebral hemispheres are absent and replaced by CSF due to infection or
carotid artery occlusion – thalami and cerebellum are usually spared
o Benign External Hydrocephalus defined as a rapid increase in head circumference, combined with enlarged
subarachnoid spaces and normal/moderately enlarged ventricles; as seen on neuroimaging
§ Occurs during infancy and subarachnoid enlargement gradually decreases and disappears over the next
yeay; but temporary psycho motor delay is common
§ Often a history of familial macrocephaly
o Without treatment, 80% will be dead within the year and survirors will have severe learning difficulties
• Treatments for all forms of hydrocephalus:
o Endoscopic third ventriculostomy in which an opening is created in the floor of the third ventricle using an
endoscope placed within the ventricular system through a burr hole to allows the CSF to flow directly to the basal cisterns
§ Primarily used for non-communicating (e.g. bypass aqueduct stenosis)
o Ventricular shunt
§ A Mechanical device to divert CSF from brain to:
• Peritoneum
Michael Grant
lOMoARcPSD|4776960
• Heart/ Atria
• Pleural space
§ 30-40% failure rate in first year
• 50% failure in two years
• 10-15% recurrent failures
• If concerned about failure, perform CSF Infusion test (injecting fluid into CSF spaces and measuring increase in pressure as
this is proportional to resistance – introduce ICP transfucer and 60min Hartmans infusion)
Infection
• Cerebral abscesses are formed when infection comes to the brain:
§ Haematogenous (most common)
• Arterial (endocarditis, IV drug use, sepsis)
• Venous (e.g. any facial infection in the
danger triangle due to the ophthalmic
vein connecting the facial vein to the
cavernous sinus)
§ Direct implantation
• Trauma
• Lumber puncture
§ Local extension
• Otitis media (spreads to temporal lobe)
• Paranasal sinus (frontal lobe)
• Infected tooth/dental root (spreads to
anterior pariental)
• Osteomyelitis
o Symptoms are similar to that of raised ICP plus
septic signs and swinging temperatures
o Management:
§ IV ABx
§ Treat source of infection
§ If >2cm Surgery:
• Aspiration via burr hole
• If this fails, Craniotomy
• Subdural Empyema is a collection of pus in the
subdural space – usually arising from direct spread of
intra cranial infection (e.g. sinusistis, osteomyelitis, otitis media)
o Symptoms same as abscess but with particular likelihood of seizures
• Treatment of intracranial infection:
o Urgent surgical drainage / evacuation.
o Prolonged course of anti-microbials based on sensitivities of organisms cultured.
o Regular clinical, serological (CRP, WCC) and imaging surveillance until infection has
resolved.
Cauda Equina syndrome

l Cauda Equina syndrome is a neurosurgical emergency due to
sphincter dysfunction
l Compression of nerve roots in lumbosacral spine leads to
radicular pain, paraesthesia, weakness, perianal numbness,
bladder and anal sphincter disturbance
l Emergency surgery is usually needed within 24hrs to save
sphincter function
l Underlying Pathologies include:
- Tumours
- Degenerative disease; e.g. disc herniation (most
common)
- Infection
- Trauma
l Management:
- Immobilise the spine if CES is due to trauma.
- Surgery is indicated to remove blood, bone
fragments, tumour, herniated disc or abnormal bone
growth.
- Lesion debulking is required for space-occupying
lesions - eg, tumours, abscess.
- If surgery cannot be performed, radiotherapy may relieve cord compression caused by malignant disease.
- Other treatment options may be useful in certain patients, depending on the underlying cause of the CES:
Michael Grant
lOMoARcPSD|4776960
l Anti-inflammatory agents, including steroids, can be effective in patients with
inflammatory causes - eg, ankylosing spondylitis.
l Infection causes should be treated with appropriate antibiotic therapy.
l Patients with spinal neoplasms should be evaluated for chemotherapy and
radiation therapy.
55 The Diabetic Foot

Peripheral Neuropathy:
• Affects 20 – 50% of diabetics
• Related to elevated Blood Glucose levels
• Neurovascular factors
• Auto-immune component
• Nerves affected:
o Nerves to the foot - Longest in body, thus most likely to be effected
§ Sensation – Pain, Proprioception
• Dry cracked skin, Callus on wt bearing areas
• Abnormal foot posture – pressure points
• Unrecognised injury
• Interdigital ulcers
• Pressure points:
st
o 1 MTP joint
th
o 5 Metatarsal head
o Heel
§ Motor – muscle wasting
§ Autonomic
Peripheral Vascular Disease (PVD):

• Diabetics often have a different pattern of disease
• Macro and microvascular disease
• Medial Clacification of vessels common – inaccurate BAPI
Immunocompromise:
• Blood glucose levels cause bacterial growth
• Migration and Chemotaxis inhibited
• White Blood cells phagocytosis defective (macrophage defect)
Signs
• Examine feet regularly to distinguish between ischaemia (critical toes ± absent dorsalis pedis pulses and worse outcome) and peripheral
neuropathy
• Neuropathy:
o Sensation decreased in ‘stocking’ distribution (test sensation with a 10g mono-filament fibre applied with
just suffcient force to bend it), absent ankle jerks, neuropathic deformity: pes cavus, claw toes, loss of
transverse arch, rocker-bottom sole
• Ischaemia:
o If the foot pulses cannot be felt, do Doppler pressure measurements
o Educate (daily foot inspection with a mirror to inspect sole; comfortable/therapeutic shoes (Pressure Relief Walkers®))
o Recommend regular chiropody to remove callus, as ulcers may form and be concealed underneath
o Treat fungal infections
o Surgery (including endovascular angioplasty balloons, stents, and subintimal recanalization)
Foot ulceration
Typically, painless, punched-out ulcer in an area of thick callus ± superadded infection. Causes cellulitis, abscess ± osteomyelitis.
• Assess degree of:
o Neuropathy (clinically).
o Ischaemia (clinically + Doppler ± angiography).
o Bony deformity, eg Charcot joint (clinically + X-ray)
§ Refers to progressive degeneration of a weight bearing joint (bony destruction > bone resorption > deformity)
o Infection (swabs, blood culture, X-ray for osteomyelitis, probe ulcer to reveal depth).
Michael Grant
lOMoARcPSD|4776960
Management:
• Absolute indications for surgery: Abscess or deep infection; spreading anaerobic infection; gangrene/rest
pain; suppurative arthritis.
• Diabetic neuropathies: Symmetric sensory polyneuropathy: (‘glove & stocking’ numbness, tingling, and
pain, eg worse at night).
o Treatment: (in order) paracetamol > tricyclic (e.g. amitriptyline) > duloxetine, gabapentin, or pregabalin
> opiates
• Autonomic neuropathy: Postural BP drop; decreased cerebrovascular autoregulation; loss of respiratory
sinus arrhythmia (vagal neuropathy); gastroparesis;
o Gastroparesis (early satiety, post-prandial bloating, nausea/vomiting) is diag- nosed by gastric
scintigraphy with a 99technetium-labelled meal. It may respond to anti-emetics, erythromycin
o Postural hypotension may respond to fludrocortisone 50–300μg/24h PO (SE: oedema, increased BP)
OSCE:
• Inspection  
o General: gait, shoes (flat heel, pattern of wear)  
o Skin: vascular insufficiency (hair, pallor), rubor/corns/callous at pressure points, texture, fissures, skin
breaks/lesions/ulcers,  diabetic dermopathy, infection (swelling, erythema, gangrene, cellulitis),
oedema, venous eczema/lipodermatosclerosis  
o Nails: dystrophic, ingrown  
o Webspaces: cracked, infected, ulcers, maceration  
o Deformity: claw toes, bony prominency, Charcot’s joints (joint swelling, collapse of medial longitudinal
arch – due to “loss  protective pain sensation”)  
o Describe any ulcer: size and site, characteristics (shape, edge, colour), secondary features.  
• Palpation (ARTERIOPATHY)  
o Temperature: use dorsum of each hand to feel up legs  
o Pulses: femoral, popliteal, pos tibial, dorsalis pedis  
o Capillary refill  
Palpation (NEUROPATHY)  
• Sensory: show patient how each feels on sternum before and get them to close their
eyes 
o Monofilament - use monofilament fully out and use enough force to make it
bend. Touch foot in multiple places. 
o 128Hz Tuning fork - use fingers to twang end with prongs and hold circular base
on the patient’s joint. Start over big  toe joint first and move proximally if patient
can’t feel it. Ask patient to tell you when they feel a vibration, and ask  them to say
when it stops (manually stop it)
o Proprioception - hold distil phalanx of big toe with a finger each side (while
stabilising proximal phalanx with other  hand). Ask the patient to look and show
them the up and down positions. Now, ask them to close their eyes and wiggle
up and down a few times, then stop and ask patient if it’s up or down. If no
proprioception, move to proximal joints until they can.
• Motor: muscle wasting, pes planus, pes cavus, Charcot joints  
• Reflexes: ankle jerk  
• Autonomic: sweaty, dry cracked skin  
To Complete exam  
• Thank patient and cover them  
• “To complete my exam, I would examine do a full neurovascular examination and educate
the patient”  
• Summarise and suggest further investigations you would do after a full history  
• ABPI  
• Doppler arterial pulses
• Blood glucose 
• HbA1C  
Michael Grant

Surgery Revision PDF

Hochgeladen von

Dokumentinformationen

Originaltitel

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Surgery Revision PDF

Hochgeladen von

Copyright:

Verfügbare Formate

lOMoARcPSD|4776960

Surgery revision pdf

Medicine (Queen's University Belfast)

StuDocu is not sponsored or endorsed by any college or university

3 Fluids and Electrolytes

Superior wall (roof):

A thorough assessment will include:

Pre operative Management:

Definition: Acute circulatory failure with

Hypoperfusion can arise from: Inadequate energy Anaerobic Lactic acid

Compensated Uncompensated Irreversible

Management and treatment: Palliative • Metastatic disease

• Blood supply • Right hemi-colectomy

• Site tumour • Sigmoid colectomy

• Anastomosis • Anterior resection (upper 2/3 or rectum)

9 Abdominal Aortic Aneurysm

WHO Analgesia ladder:

Deep vein thrombosis occur in 25–50% of surgical patients, however 65% of

14 Haematemesis and melaena

Peptic ulcer/erosive disease:

The great saphenous

Presentation can be either: Oedema

§ Can lead to “champagne bottle leg” or can present acutely as a pseudo-cellulitis

Assessment should include:

Treatment can include:

Overtransfusion is considered as: “Transfusing to a haemoglobin level more

Maximum Surgical Blood Ordering Schedule ( MSBOS)

General Surgery Operation Tariff

Open Cholecystectomy/Laproscopic Cholec ystectomy G+S

Management of minor reaction:

18 Malnutrition and Nutrition Support

Why are so many hospital patients malnourished?

Overnutrition and its’ consequences:

Identifying the malnourished patient

Indications for Artificial NS:

How many calories? 15-18 17.6 x W + 656 13.3 x W + 690

Bluffer’s guide to PN prescription: 60

19 Benign and Malignant Thyroid disease

20 Peripheral Arterial Disease

Clinical manifestation depends on:

The cardinal feature of PAD is intermittent claudication:

Types of breast cancer:

The Lumen Bleeding

Cardinal signs of obstruction:

Systemic Inflammatory response syndrome (SIRS):

General supportive measures:

l Non catecholamine drugs

form of human activated protein C (serine protease)

CRP/ESR, a tender colon ± localized or generalized peritonism.

• Drug: omission; comission

• Drug not available

• Drug: omission; comission

An incident is defined as:

28 Level of care and monitoring

32 Neck swellings/Salivary glands

o Radiotherapy +/- chemotherapy if malignant

33 Skin cancer & common 'lumps

Non Melanoma Skin cancer:

Inner circular muscle Thickening of

Outer longitudinal muscle

trigeminal, facial and hypoglossal nerves Auerbachs plexus

Inner circular muscle

5 key questions to ask