Surgery Flashcards
CLEAN procedure
The procedure does not enter a colonised viscus or lumen of the body.
SSI risk entirely due to contaminants from the environment, with a rate of 2-5%.
POTENTIALLY CONTAMINATED procedure
The operative procedure enters into a colonised viscus or body cavity, but under elective or controlled circumstances.
SSI risk is from endogenous bacteria, with a rate of 10%.
What is the most common environmental pathogen causing surgical site infection?
S. aureus
CONTAMINATED procedure
Contamination is present at the surgical site, without obvious infection (e.g. intestinal spillage due to penetrating injury)
SSI risk is from endogenous bacteria, with a rate of 20%.
DIRTY procedure
Surgery performed where active infection is already present (e.g. abdominal exploration for intra-abdominal abscess and perforation.
Infection risk is from already-established pathogens, with a risk of 30%.
Rigid Proctoscopy vs Rigid sigmoidoscopy
PROCTOSCOPY = endoscopic examination of the anal canal using a proctoscope (direct vision).
SIGMOIDOSCOPY = endoscopic examination of the rectum to recto-sigmoid junction using a rigid sigmoidoscope (direct vision)
Indications for rigid proctoscopy/sigmoidoscopy
- Suspicion of colonic neoplasia
- Investigation of IBD
- Biopsies under direct vision
- Treatment of haemorrhoids
- Prior to any ano-rectal operation.
Flexible sigmoidoscopy
= endoscopic examination visualising up to the splenic flexure.
What is haematochezia?
= passage of frank blood per rectum
Indications for tube thoracostomy
Pneumothorax
Pleural effusion / empyema
Post-operative (thoracotomy, oesophagectomy, cardiac surgery)
Where is the triangle of safety?
Between the lateral border of pec major and lat dorsi, superior to the 5th intercostal space, inferior to axillary border.
Thoracostomy - steps
Inject LA to infiltrate skin and parietal pleura
Make 2cm incision near upper border of rib below (avoiding neurovascular bundle) in the triangle of safety
Blunt dissect to parietal pleura, then palpate the lung with gloved finger to free adhesions
Insert drain and attach to underwater seal, suturing in to the chest wall
Apply airtight dressing and sit patient up to 45o.
Check position with CXR and repeat CXR daily.
Indications for urethral catheter
Acute/chronic urinary retention
Output monitoring (in critical illness / perioperative patients)
Incontinence
To aid surgery
Contraindications for urethral catheter
Urethral injury (e.g. pelvic fracture)
Acute prostatitis
Urethral catheter - complications
Retrograde infection
Paraphimosis (if fail to reduce the foreskin post-procedure).
Creation of false passages
Urethral strictures
Bleeding
How should a urine sample be collected from a catheter?
The specimen should be obtained aseptically from a port in the catheter tubing or by aseptic aspiration of the tubing.
NEVER collect a sample from the catheter bag.
Active drains
Involve suction forces provided by vacuumed containers
Used to draw out collections
Passive Drains
Function by differential pressures between the body and the exterior (e.g. using gravity).
Open Drains
Always passive
Lead into a dressing/stoma to provide a conduit around which secretions can flow.
May be tubes or corrugated sheets
Closed Drains
Tube systems that drain directly into a container
With or without suction (active / passive)
Common complications of surgical drains
Damage to structures during insertion
=> Avoided by image-guided insertion.
Damage to structures due to pressure effects of the drain.
Infection
=> Avoided by timely removal of the drain
Failure of the drain
=> Can give a “false sense of security”
Indications for central venous catheter
- Critically ill patients requiring continuous CVP monitoring
- Infusion of irritant substances
- Precise infusion of substances with a very narrow therapeutic window.
- Long-term access for parenteral nutrition, chemotherapy or antibiotics.
- Haemodialysis
- No other venous access available.
Hickman Line
Tunnelled beneath the skin for stability and to prevent infection
Generally at the IJV on the right, however can be either side.
PICC Line
“Peripherally inserted central catheter”
Inserted in the arm (brachial vein) and advanced to the SVC
Portacath
Port installed beneath the skin, and connected to a vein by a catheter
Routine care of central venous lines
Report any signs of infection/bleeding
Do not get the site wet
Avoid contact sports
Swan-Ganz Catheter
A balloon catheter, passed from the femoral vein, through the right side of the heart into the pulmonary artery.
Used to measure pulmonary artery pressures.
Swan-Ganz Catheter - complications
Arrythmias
Valve trauma
Pulmonary infarction / pulmonary artery rupture
Arterial catheterisation
Indications:
- Frequent blood sampling / ABG analysis
- Continuous invasive BP monitoring
Usually inserted into radial artery in the critically ill, after performing Allen’s test
What can be used as a landmark for checking central venous catheter placement in the SVC?
The location of the carina on a CXR
Features of an ileostomy
- Spouted, with prominent mucosal folds
- Tend to be on the RHS
- Bag will have bilious contents
End ileostomy - appearance and indications
One lumen
Generally permanent
Indications = definitive surgery to remove colon
Loop ileostomy - appearance and indications
Two lumens
Often temporary and reversed at a later date;
Indications = to rest distal bowel, to protect distal anastomoses, to provide functional relief from severe incontinence
Features of a colostomy
Usually flush to the skin, with flat mucosal folds.
Tend to be on the LHS
Contents tend to be more faeculant.
Can be loop or end (but end colostomies are far more common)
Urostomy
Formed from a short section of disconnected ileum, into which one or both ureters are directed after a radical urinary tract surgery.
They are indistinguishable from an end ileostomy unless output can be seen.
Gastrostomy - features and indications
A connection from the anterior stomach to the anterior abdominal wall.
Features:
- Narrow in calibre
- Flush to the skin
- Usually in LUQ
- Fitted with indwelling access device.
Indications: for stomach drainage or direct feeding.
Jejunostomy
A connection from the jejunum to the abdominal wall, for direct feeding.
Appearances are the same as a gastrostomy.
Early stoma complications
Infarction / necrosis
Infection
High output from the stoma leading to severe dehydration
Late stoma complications
Parastomal hernia (incisional hernia at the stoma site)
Stoma prolapse (underlying bowel protrudes through the orifice)
Stoma retraction (pulled/drawn below skin level)
Stenosis (narrowing of stomal opening)
Examination of a stoma
- Ask the patient if they have had any pain or issues with their stoma.
- Gently palpate the abdomen for distension / tenderness.
- Ask the patient to cough – observe for parastomal hernia.
- Observe the surrounding skin quality for any signs of infection.
- Determine the type of stoma (define the siting, spouting and contents)
- Observe specifically for any signs of infarction, prolapse, or retraction.
- Listen for bowel sounds
- State that you would like to view the patient’s fluid balance chart.
What are the stages of wound healing and when do they occur?
- Haemostasis (immediate)
- Inflammation (0 – 3 days)
- Proliferation (3 days – 3 weeks)
- Remodelling (3 weeks – 1 year)
Wound Healing - Haemostasis
Platelets aggregate at the site in response to exposed collagen, releasing inflammatory markers and activate clotting and coagulation cascades
Haemostasis is then achieved by vasospasm and thrombus formation.
Wound Healing - Inflammation
Days 0-3
Vasodilatation and increased capillary permeability allow inflammatory cells to enter the wound, leading to oedema.
Neutrophils enter the tissues to debride and kill bacteria, followed by macrophages to phagocytose debris and orchestrate fibroblast migration.
Wound Healing - Proliferation
Day 3 - 21
Fibroblasts migrate in to synthesise collagen, with myofibroblasts secreting actin-containing products to cause wound contraction.
Angiogenesis is stimulated by hypoxia and cytokines => creates granulation tissue.
Wound Healing - Remodelling
3 weeks - 1 year
Re-orientation and maturation of collagen fibres to increase wound strength.
What is granulation tissue?
The combination of capillary loops and myofibroblasts, giving the appearance of small, red foci that bleed easily (commonly seen when a scab is picked).
It is these capillary loops that allow the inflammatory cells to enter the damaged tissue to promote defence and healing.
Infected granulation tissue will be painful; discharging; erythematous & swollen; and the patient may have systemic features.
What is “Epithelialisation” in wound healing?
The covering of a surface with the skin layers removed with epithelial tissue, occurring from the outer edges of the wound after granulation.
Primary Intention Healing
Takes place when there is a close apposition of clean wound edges.
=> Fibrin is able to form a weak framework between the edges, over which the capillaries proliferate and secrete collagen into the fibrin network.
=> The elastic network of the dermis cannot be replaced.
Secondary Intention Healing
Takes place in wounds where skin edges cannot be clearly opposed.
- Phagocytosis removes debris
- Granulation tissue forms to fill the defect.
- Epithelial regeneration then covers the surface
Inflammatory changes in a wound
Occur in a wound or around a suture:
- Heat
- Erythema
- Swelling
- Pain
- Loss of function
Mx of infected surgical wound
Depending on the severity, the patient may need:
- No treatment
- Oral/IV ABX
- Re-intervention on the ward / in theatre to open, drain, debride, rinse and pack the wound
Cultures are always recommended.
Venous Ulcers - Pathophysiology
• Valve incompetence and reflux
• Calf muscle dysfunction
• Toxins accumulate => inflammation and necrosis of tissue.
Venous Ulcers - Features
Generally located below the knee and above the ankle (gaiter area).
• Large and irregular
• Shallow with sloping edges
• Granulation tissue
Venous Ulcers - Leg condition
• Lipodermatosclerosis
• Venous eczema
• Haemosiderin (red/brown colour)
• Atrophie Blanche (smooth, white sclerotic plaques)
• Heavy, aching, pruritis, oedema
Management of venous ulcers
• Dressings +/- antibiotics +/- emollients
• Debridement – surgery/dressings/larvae
• Elevation and compression (EXCLUDE ARTERIAL INSUFFICIENCY FIRST)
=> 1st line = 4-layer bandaging
=> Other = stockings
• Skin graft / superficial venous surgery
Arterial Ulcer - pathophysiology
• Atheromatous changes cause compromised blood flow
• Results in hypoxia and accumulation of toxins => inflammation and necrosis of tissue.
RFs for arterial ulcers
Diabetes, HTN, smoking, arterial disease, cholesterol emboli, Raynaud’s disease, Trauma
Arterial Ulcer - features
Located on bony prominences (usually lateral malleolus and toes)
• Smaller and round
• “Punched out” borders
• Little granulation tissue and dry
• Very painful
Arterial Ulcer - leg condition
• 6Ps – pain, pulseless, pale, paraesthesia, paralysis, perishingly cold
• Claudication/ischaemic rest pain symptoms
• Cool, hairless, dry, shiny skin
Management of arterial ulcers
Dressings +/- antibiotics +/- emollients
Debridement – surgery/dressings/larvae
ABPI to identify severity
Manage vascular risk factors – e.g. antiplatelets, stop smoking
Surgical revascularisation
Neuropathic Ulcers - pathophysiology
Peripheral neuropathy => loss of protective sensation and trauma goes unnoticed
Vascular disease => reduced wound healing
Neuropathic Ulcers - features
• Small, round, deep
• “Punched out” borders
• Thick rim
• PAINLESS
Neuropathic Ulcers - leg condition
• Surrounding callous
• Loss of sensation
• Dry, cracked skin
Neuropathic Ulcers - Management
• Dressings +/- antibiotics +/- emollients
• Debridement – surgery/dressings/larvae
• Optimise glycaemic control
• Treat co-existing arterial disease
• Good foot care
• Offload pressure (therapeutic footwear)
marginal artery of Drummond
an anatomically variable blood vessel that forms a major anastomotic network between the superior and inferior mesenteric arteries
Most common variant of colorectal cancer
Most common variant is Adenocarcinoma
Squamous and adeno-squamous variants can be found in the distal rectum.
Risk Factors for colorectal cancer
Family History (+ FAP / HNPCC)
Age
Western Diet (low in dietary fibre, high in fats)
UC
Smoking
Heavy alcohol consumption
Protective factors for colorectal cancer
Fruit and veg / fibre consumption
Exercise
HRT
Aspirin/NSAIDs
Familial Adenomatous Polyposis (FAP)
Autosomal dominant defect in tumour-suppressor APC gene.
Develop hundreds of adenomas throughout colon, CRC in 100% if untreated (~36y).
Hereditary Non-polyposis Colorectal cancer (HNPCC)
“Lynch Syndrome”
Responsible for <5% of all cancers
Arises from autosomal dominant mutations affecting various mismatch repair genes
Predisposes to cancers of colon, ovaries, endometrium, stomach, bladder, brain and skin
Young onset and aggressive
Spread of CRC
Initially by direct infiltration through the bowel wall.
It then involves lymphatics and blood vessels with subsequent spread – primarily to the liver (also lung, bone).
Transcoelomic spread can occur
Appearance of colorectal adenocarcinoma on investigations
Usually as a polypoid mass with ulceration
Characteristic “signet ring cells” on histology.
Where do colorectal cancers usually occur?
Recto-sigmoid region
Rectum ~45%
Sigmoid colon ~25%
Descending colon ~5%
Transverse colon ~10%
Caecum & ascending colon ~15%
Symptoms of CRC
Right-sided tumours:
=> Often asymptomatic; may present with weight loss/iron-deficiency anaemia; can present with abdominal discomfort and change in bowel habit.
Left-sided tumours:
=> PR bleeding/mucous, altered bowel habit, tenesmus, obstruction, mass on PR examination.
Rectal tumours:
=> PR bleeding, pain, changes in bowel habit, masses/stricture
2WW referral for ?bowel cancer
In patients >40 years
- Rectal bleeding or change in bowel habit >6 weeks
- Persistent rectal bleeding in those >45, with no obvious cause of benign anal disease
- Iron deficiency anaemia, without an obvious cause
- Palpable abdo/PR mass
Colorectal cancer - screening
HIGH RISK GROUPS
Routine regular colonoscopy – in high-risk groups with positive family history (FAP, HNPCC, MUTYH-associated polyposis).
AVERAGE-RISK POPULATION – faecal occult blood (FOB) testing
- FOB test is done every 2 years between the ages of 50 and 74, and a single flexible sigmoidoscopy is performed at age 55.
- A colonoscopy is performed if there is a positive FOB test.
Colorectal cancer - Ix
History, Abdo Exam + DRE
Blood tests
=> FBC, U&E, LFT, Magnesium, Calcium
=> Carcinoembryonic antigen (CEA) – tumour marker, can be used to monitor disease.
=> Coagulation
=> G&S/XM
Colonoscopy +/- biopsy = gold-standard
Imaging for staging
- CT colon – “virtual colonoscopy”
- CT CAP
What tumour marker is useful for monitoring of colorectal cancer?
Carcinoembryonic antigen (CEA)
CRC - Duke’s stage A
Tumour invades submucosa +/- muscularis propria
CRC - Duke’s stage B
Tumour invades past the muscularis propria (into subserosa / directly into other organs, but no LN involvement)
CRC - Duke’s stage C
Regional LN involvement
CRC - Duke’s stage D
Distant metastases
(= advanced bowel cancer)
CRC treatment
Involves a wide resection of the mass and regional lymphatics and blood supply
Surgical procedure depends on location of tumour
What is an anterior resection?
What are the indications?
Removal of the rectum and sigmoid colon
Almost always performed due to a sigmoid or rectal cancer
Can be high vs. low - depending on how much of the rectum is removed
Sigmoid colectomy
Removal of sigmoid colon
What is a left hemicolectomy?
What are the indications?
Removal of the splenic flexure, descending colon, and a portion of the sigmoid colon.
- bowel malignancy (most common)
- diverticular disease,
- bowel ischaemia
- bowel perforation.
What is a right hemicolectomy?
What are the indications?
Removal of the terminal ileum, caecum (including the appendix), ascending colon, and hepatic flexure.
An EXTENDED right hemicolectomy further involves the removal of the transverse colon as well.
- bowel malignancy (most common)
- diverticular disease,
- bowel ischaemia
- bowel perforation.
What is an Abdominoperineal Resection?
What are the indications?
Removal of perineal skin, anal sphincters, rectum, and sigmoid colon.
- very low rectal cancers
- anal cancers refractory to chemoradiotherapy
- severe perianal Crohn’s disease
Total proctocolectomy
Removal of entire colon and rectum
Used in ulcerative colitis
Subtotal colectomy
Removal of the large bowl, but leaving the sigmoid colon and rectum
CRC - radiotherapy
Used pre-operatively in rectal cancer to reduce recurrence and increase survival.
Higher risks of post-operative complications (DVT, pathological fractures, fistula formation).
Post-operative radiotherapy is used only if high risk of local recurrence.
CRC - chemotherapy
Adjuvant chemotherapy – usually oxaplatin or 5-FU based.
May be used in palliation of metastatic disease.
Management of an obstructing colorectal cancer
- ABCDE Approach
- Analgesia & NG tube decompression
- AXR & erect CXR – confirm Dx and check for perforation
- CT to determine level of obstruction
- Surgery once the patient is adequately hydrated (or endoscopic stenting for palliation).
What is the most common variant of anal cancer?
Squamous cell carcinoma (80%)
RFs for anal cancer
- Ano-receptive sex
- Syphilis infection
- Anal warts/cervical cancer (HPV)
- Immunosuppression
Pectinate Line
= an embryological division between the upper 2/3rds and the lower 1/3rd of the anal canal
Anal cancer ABOVE pectinate line
Columnar epithelium
Lymph draining to internal iliac nodes
Portal venous drainage (thus hepatic metastases).
More common in women, worse prognosis.
Anal cancer BELOW pectinate line
Squamous epithelium
Lymph drainage to superficial inguinal nodes.
Caval venous drainage (thus pulmonary metastases)
More common in men, better prognosis.
Anal cancer - presentation
Bleeding, discharge
Pain, fistula
Changes in bowel habits
Pruritis ani
Masses or stricture, ulcer
2WW referral for ?anal cancer
Unexplained anal mass
Anal ulceration.
Anal cancer - pattern of spread
- Spreads locally (rectum, sphincter, scrotum, vagina).
- Inguinal LNs involved in 10-20% at presentation.
- Metastases to liver, lung, bone.
Anal Cancer - Tx
Radiotherapy plus chemotherapy = mainstay of treatment
Small tumours at anal margin = local excision alone
Anal Cancer - Ix
Examination under general anaesthetic (PR + proctoscopy)
Imaging
Biopsy
What is the definition of bowel obstruction?
The mechanical or functional blockage of the bowel, resulting in absolute constipation.
- Mechanical – physical blockage of the passage of intestinal contents.
- Functional – decreased bowel motility.
Bowel Obstruction - Sx
Vomiting
(Bilious vomiting = upper small bowel obstruction; Faeculent vomiting = more distal small bowel obstruction)
Pain
(initially colicky, then constant; NO pain in functional obstruction)
Constipation
What is absolute constipation?
What does this suggest?
= when the patient is not passing flatus or faeces rectally.
Suggests complete obstruction of the bowel
Bowel obstruction - signs
Abdo Distension
=> Due to fluid and air accumulation in the bowel.
Tinkling Bowel Sounds (or NO bowel sounds if paralytic ileus)
Dehydration
=> Caused by:
1. Vomiting,
2. Lack of fluid intake
3. “Third spacing”
Central resonance to percussion, dull flanks
Scars (previous surgery => Adhesions)
Palpable mass (causing the obstruction)
NO abdominal tenderness (unless strangulation)
Large Bowel obstruction presentation
Absolute constipation and pain are more prominent early, vomiting often late.
Symptoms are generally more gradual due to the large volume of colon.
Pain tends to be lower (suprapubic)
Small Bowel obstruction presentation
Vomiting is the predominant early feature, constipation often late.
Pain tends to be peri-umbilical.
Fluid sequestration in bowel obstruction
There will be dilatation of proximal bowel with sequestration of fluid into the intestinal lumen.
The fluid sequestered into the bowel tends to be very electrolyte rich – patients will typically have an AKI and hypokalaemia.
SBO - mechanical causes
Adhesions (80%)
Hernias
Crohn’s Disease
Intussusception
LBO - mechanical causes
Carcinoma of the colon UNTIL PROVEN OTHERWISE
Diverticular disease
Sigmoid volvulus
Constipation
Bowel obstruction - complications
- The bowel wall becomes oedematous and distends.
- Bacteria proliferate in the obstructed bowel.
- As the bowel distends, vessels become stretched and the blood supply is compromised, leading to strangulation (=> ischaemia and necrosis).
- Eventually the bowel will perforate (=> peritonitis).
Strangulation of bowel - presentation
Most common with volvulus or hernia, however can occur in any obstruction.
Increasing pain/tenderness, with leucocytosis and systemic upset.
May progress to perforation and peritonism, with absent bowel sounds.
Volvulus
= a twisting of a loop of bowel around its mesenteric axis, resulting in obstruction together with venous occlusion at the base of the mesentery.
The bowel stretches, becomes ischaemic and is more likely to perforate.
Sigmoid volvulus - cause, appearance, Tx
Most common in elderly, constipated patients.
Classic “coffee bean” appearance on X-ray.
Tx = insertion of a long flatus tube advanced into the sigmoid, which often untwists the volvulus (releases large amounts of faeces/gas).
If this is unsuccessful, there will be an emergency laparotomy.
Caecal volvulus - cause, appearance, Tx
Due to congenital malrotation
Gives the classic “embryo” appearance of an ectopically placed caecum on AXR.
Treatment is untwisting during laparotomy.
Paralytic ileus
= temporary disruption of normal peristaltic activity, without mechanical blockage.
Functional Bowel obstruction
There will be NO BOWEL SOUNDS, and an identifiable cause:
- Post-surgery (normally up to 4 days)
- Due to anastomotic leak / intra-abdominal sepsis
- Electrolyte disturbances
- Critically unwell patients on ITU with multiple injuries
Pseudo-obstruction of bowel
LBO when no identifiable cause can be found (a form of paralytic ileus).
SBO vs Paralytic Ileus
Air in the colon in paralytic ileus, none in SBO
Bowel sounds present in SBO, absent in ileus.
Bowel Obstruction - Ix
BEDSIDE
Basic observations
Abdominal Exam, PR, hernial orifices
BLOODS
FBC, U&E, LFT, Amylase
CRP, ABG/VBG
IMAGING
Supine AXR
Erect CXR (if perforation suspected)
CT CAP
Contrast enema (differentiates obstruction and pseudo-obstruction)
Gastrograffin
Used for contrast in a contrast enema, but may also have a therapeutic effect in bowel obstruction!
SBO features on AXR
Dilated loops of bowel are >3cm in diameter.
Dilated loops of bowel are more central in the abdomen.
Valvulae conniventes/plicae circulares present (full crossings).
LBO features on AXR
Dilated loops of bowel are >6cm in diameter (>9cm at caecum).
Dilated loops are more peripheral.
Haustra present (incomplete crossings).
May be small bowel dilatation, depending on
duration of obstruction and incompetence of the ileocaecal valve
Management of SBO
ABCDE resuscitation (IV fluids to replace losses, catheter for fluid balance, bloods)
NBM + NG decompression of the stomach (Ryle’s tube)
If no signs of strangulation, delay operative Mx by 48 hours
If signs of strangulation or severe obstruction, then surgical management of the cause of obstruction.
=> ABX therapy will be commenced if there are signs of strangulation.
Management of LBO
Generally requires operative management (Hartmann’s)
If due to faecal impaction, enemas or manual evacuation will be tried.
Causes of Intestinal Obstruction in children
Intussusception
Incarcerated hernia
Malrotation of the bowel
Hirschsprung’s disease
Meconium ileus
Faecal impactation - causes
General Factors:
Poor diet, dehydration, lack of exercise, IBS, old age, pain
Anorectal Disease:
Fissure, stricture, rectal prolapse
Metabolic/endocrine:
Hypercalcaemia, hypothyroidism, hypokalaemia
Drugs:
Opiates, anticholinergics, iron, aluminium-based antacids, diuretics
Neuromuscular:
Spinal/pelvic nerve injury, diabetic neuropathy, Hirschsprung’s disease
Faecal impactation - Ix
Bloods (FBC, ESR, U&Es, Calcium, TFTs).
Not required in mildly affected individuals.
Role of Anal Sphincters in Faecal Continence
The internal anal sphincter is an involuntary sphincter, surrounding the upper 2/3rds of the anal canal
Tonic contraction is stimulated by sympathetic fibres from the superior rectal/hypogastric plexus.
Parasympathetic fibres inhibit this tonic contraction, thus requiring contraction of the puborectalis/the external anal sphincter to maintain continence.
Physiological nipple discharge
Tends to be clear/yellow/milky and bilateral.
Milky - due to pregnancy/hyperprolactinaemia
Green nipple discharge
Can be physiological around the menopause, due to duct ectasia.
Can be due to fibrocystic disease
What nipple discharge warrants urgent referral to breast unit?
Blood-stained discharge
Unilateral discharge
ANY colour discharge with symptom suspicion of underlying disease
Management of nipple discharge
Treatment will be based on the cause of discharge.
Periductal mastitis
An infection of the ducts beneath the nipple
More common in smokers and those with nipple piercings.
Symptoms:
- Tender, hot/red breast
- Nipple discharge – can be bloody/non-bloody
Tx = analgesia +/- ABX
Tail of Spence
The extension of the breast towards the axilla
What do the breasts consist of?
Mammary glands = modified sweat glands; ~15-20 secretory lobules
Connective tissue – condenses to form suspensory ligaments (of Cooper).
Fatty tissue
Arterial supply to the breast
Internal thoracic artery (a branch of the subclavian artery) => medial part of breast
Lateral thoracic and lateral mammary arteries => lateral part of breast
Venous drainage of breast
via the corresponding veins to the arteries, into the axillary and internal thoracic veins.
Lymphatic drainage of breast
75% of the lymph drains into the ipsilateral axilla
25% goes via the internal mammary lymph nodes, draining to the contralateral axilla.
Some drainage to inferior deep cervical and infraclavicular nodes
Benign breast lumps
Fibroadenoma
Fibrocystic disease
Breast cysts
Breast abscess
Fat necrosis
Phylloides Tumour
Typical characteristics of a benign breast change
Tend to be smooth and mobile structures
Typical characteristics of a malignant breast change
Tend to be irregular, craggy and fixed.
Who normally gets fibroadenomas?
Mostly seen in young females of reproductive age.
Tend to shrink after menopause
Fibroadenoma - presentation
Painless (or very localised pain)
Rubbery, well-demarcated lump.
Highly mobile (sometimes called a “breast mouse”) and not tethered to the skin.
Can be multiple and bilateral.
Not associated with any lymphadenopathy
Outcome of fibroadenoma
1/3 regress, 1/3 remain the same, 1/3 get bigger
Tx:
- Mostly need no treatment, as they have very low malignant potential.
- Can be excised if large (>4cm)
What is fibrocystic disease?
Due to a combination of localised fibrosis, inflammation, cyst formation and hormone-driven (cyclical) breast pain.
Presents exclusively between menarche and the menopause.
Fibrocystic disease - presentation
Lumpy, rope-like texture in the breast.
Cyclical swelling and tenderness
Pain in the armpit
Greenish/dark brown nipple discharge, that’s free of blood.
Fibrocystic disease - management
Supportive bra
Combined OCP
Evening primrose oil
What is a breast cyst?
A benign, fluid-filled cyst of the breast.
Typically seen in perimenopausal women.
Can be associated with fibrocystic change, or occur alone.
Breast cyst - presentation
Sudden onset swelling.
Symmetrical smooth round lump
Usually painless and solitary
Not associated with lymphadenopathy
Breast cyst - Ix
Drainage under USS guidance – usually straw-coloured liquid (if suspicious – e.g. blood-stained – then should be sent for cytology)
Then the breast is re-examined, as it can co-exist with cancer.
Who is normally affected by fat necrosis of the breast?
Usually seen in females of BMI >30
Generally occurs following a history of trauma to the breast.
Fat necrosis of breast - presentation
Presents as a firm, painless lump
Can be tender around it
Irregular outline
May be associated with skin thickening/retraction
Can be red or bruised
Fat necrosis of breast - Investigation
Must undergo triple assessment
Fat necrosis of breast - Mx
Will resorb naturally, give simple analgesia.
Types of breast abscess
- Lactational – caused by staph. aureus in breast feeding women.
- Non-lactational – caused by gram-negative bacteria in diabetics and smokers.
Breast abscess - presentation
Hot, red, swollen lump.
Can lead to systemic upset – pyrexia, sepsis.
Breast abscess - Mx
USS-guided aspiration
Antibiotics
Rest the breast from breastfeeding – use breast pump and dump contents.
Phylloides Tumour
= a rapidly growing tumour of the stroma
=> 75% benign, 25% malignant
Presentation:
- Smooth, firm lump
- Usually painless
Investigations:
- Triple assessment with core needle biopsy
- Sometimes excisional biopsy needed to fully rule out malignancy
What does triple assessment of a breast lump involve?
- Clinical assessment – Hx and Examination
- Radiological imaging
- Tissue biopsy
Triple Assessment - Imaging
Mammogram – not typically used for younger patients due to dense breast tissue.
USS Breast
(all women will also have an ultrasound of the axilla)
Triple Assessment - biopsy options
- Fine needle aspiration – collects a sample of cells
- Core needle biopsy – collects a core of tissue, USS or MRI guides process
- Open (surgical) biopsy – removes all/part of an abnormality.
Breast carcinoma - epidemiology
Carries a lifetime risk of 1 in 8 for a woman in the UK.
Incidence increases with age
1% of cases are in males
5-10% are associated with gene errors.
Types of breast carcinoma
Most tumours are invasive adenocarcinomas,
of which:
- Invasive Ductal Carcinoma (90%)
- Invasive Lobular Carcinoma (5%)
- Other (5%)
Can be either oestrogen-receptor/progesterone-receptor/HER-2 positive or negative
prognosis of oestrogen-receptor positive breast cancer
better prognosis
prognosis of HER-2 positive breast cancer
worse prognosis
Risk factors for breast cancer
25% genetic factors (PMHx, FHx, BRCA positive)
75% environmental factors
(mostly to do with increased oestrogen exposure)
• Early menarche/late menopause
• Nulliparity
• Not breastfeeding
• HRT / COCP
• Obesity
• Smoking
BRCA1
Autosomal dominantly inherited gene, chromosome 17
Lifetime risk of breast cancer – 60-90%
Lifetime risk of ovarian cancer – 40-60%
Also associated with prostate and colon cancer
BRCA2
Autosomal dominantly inherited gene, chromosome 13
Lifetime risk of breast cancer – 45-85%
Lifetime risk of ovarian cancer – 10-30%
Lifetime risk of MALE breast cancer – 5-10%
Breast cancer - presentation
Feeling a thick area/bump/hard lump
Skin changes – sores, dimple, peau d’orange, Paget’s disease of the nipple, Engorged veins
Nipple changes – crust, sunken, discharge.
New shape/size/asymmetry between breast.
Palpable lump in axilla
Paget’s disease of the nipple
= Rare but highly associated with underlying neoplasm.
Often mistaken for eczema of the nipple
Clinical features are reddening, rough/flaking skin, itching and ulceration of the nipple.
MUST do skin biopsy to confirm diagnosis
Spread of breast cancer
LOCAL
= into overlying skin (causes tethering/nipple retraction), into pectoral muscles (causes deep fixation of tumour).
LYMPHATICS
= nodal involvement common in axilla as well as clavicular nodes; can block lymphatics and prevent lymphatic drainage (causing Peau d’orange)
DISTAL DISSEMINATION
= commonly to the bone, lung, liver and brain.
Breast carcinoma in situ
= a pre-cancerous lesion:
Normally ductal (DCIS) but can be lobular (LCIS)
Abnormal cells that haven’t yet developed the ability to breach the basement membrane.
If left, it will become cancerous, therefore offered similar treatments as breast cancer
TNM staging of breast cancer
T1 <2cm
T3 >5cm
T4 = fixed to chest or peau d’orange
N0 = no nodes
N1 = mobile ipsilateral nodes
N2 = fixed nodes
M0 = no distant metastases
M1 = distant metastases
If metastases are suspected, the patient will have a liver USS, CXR & bone scan
Breast Cancer - Mx
All patients are treated surgically, if they are fit for surgery.
=> Wide local excision or Mastectomy
Regional lymph nodes must also be managed – sentinel node biopsy is performed
Most breast surgery is combined with adjuvant RADIOTHERAPY for invasive disease
If there is nodal disease, or high-grade tumours, CHEMOTHERAPY is considered
If the tumour is ER/HER2 positive, adjuvant hormonal/biologic treatment is given for 5 years.
Wide local Excision vs Simple Mastectomy for breast cancer
Wide Local Excision = Breast-conserving surgery
=> can be used providing the breast if of adequate size and the tumour location is not central/retro-areolar.
=> Margins are checked to ensure they are clear of disease
Simple Mastectomy
=> Preferred for large tumours (or small breasts), central location of the tumour or late presentation with complications.
How is a Sentinel node biopsy performed?
- Inject dye into/around the tumour bulk to identify the first 1-2 nodes that drain the tumour, which are removed and analysed histologically.
- If negative, it can be assumed that there is no nodal involvement.
- If positive, full axillary clearance is required (20% risk of lymphoedema)
Hormonal/biologic Tx for breast cancer
Tamoxifen if pre-/perimenopausal (breast-selective ER-antagonist
Aromatase inhibitors (e.g. letrazole, aromisin, exemestone) if post-menopausal, to stop peripheral oestrogen production.
Herceptin (traztuzumab) if HER2 positive (this is always combined with chemotherapy).
Nottingham Prognostic Index (NPI) for breast cancer
NPI = (tumour size x 0.2) + histological grade + nodal status
If treated with surgery alone, 10-year survival rates are:
- NPI <2.4 = 95%
- NPI 2-4 – 3.4 = 85%
- NPI 3.4 – 4.4 = 70%
- NPI 4.4 – 5.4 = 50%
- NPI >5.4 = 20%
What are the anal vascular cushions?
Formed of smooth muscle with subepithelial anastomoses of the rectal arteries/veins (i.e. highly vascular areas)
They act to assist the anal sphincter in maintaining continence.
There are three, positioned at the 3-, 7- and 11 o’clock positions when viewed from the lithotomy position.
What are haemorrhoids?
= disrupted/dilated anal vascular cushions
How are haemorrhoids classified?
According to their size:
1st Degree - Remain in the rectum
2nd Degree - Prolapse through the anus on defecation but spontaneously reduce
3rd Degree - Prolapse through the anus on defecation but require digital reduction
4th Degree - Remain persistently prolapsed
Causes/RFs for developing haemorrhoids
Idiopathic
Excessive straining/increased anal tone – chronic constipation, low-fibre diet.
Increasing age
Factors that cause congestion of superior rectal veins – cardiac failure, rectal carcinoma, portal hypertension, any raised IAP
Drainage of superior and inferior rectal veins
superior rectal veins = into the inferior mesenteric vein (portal drainage),
middle/inferior rectal veins = into the IVC.
Haemorrhoids - Presentation
Often asymptomatic
Painless rectal bleeding
- Usually bright red blood on the paper
- Only seen on the surface of the stool (not mixed in).
Prolapse
Mucous discharge
Pruritis ani
Impaired continence
Rectal fullness/anal lump
Pain if the haemorrhoids are thrombosed.
Haemorrhoids - Complications
Anaemia – if severe/continuous bleed.
Thrombosis
Ulceration/gangrene (secondary to thrombosis).
Perianal sepsis.
Thrombosis of haemorrhoid
Occurs when prolapsing haemorrhoids are gripped by the anal sphincter (“strangulated”).
Venous return is occluded, leading to thrombosis.
Haemorrhoids swell, become purple/blue and tense, cause significant pain/distress.
Often fibrose within 2-3 weeks, giving spontaneous cure.
Management is conservative – cold compresses, opioids and rest.
Haemorrhoids - Investigations
It is important to exclude other causes of rectal bleeding – malignancy, IBD, diverticular disease.
Investigations:
- PR exam – prolapsing haemorrhoids are obvious.
- Proctoscopy – can visualise the haemorrhoids and assess for any lesion higher in the rectum.
- Abdominal exam – palpable mass, enlarged liver.
- Colonoscopy/flexi-sigmoidoscopy – if symptoms suggest a different pathology (e.g. malignancy).
If significant/prolonged bleeding – FBC and coagulation screen.
Haemorrhoids - Management
Conservative/medical management
Sclerotherapy (1st and 2nd degree)
Banding (1st to 3rd degree)
Surgical (reserved for 3rd and 4th degree)
Conservative management of haemorrhoids
Advice to patient – plenty of fluids, lots of fibre, try not to strain.
Ice packs
Topical analgesia (e.g. instillagel)
Bulk forming laxative
Sclerotherapy for haemorrhoids
- 5% phenol in almond oil is injected above each haemorrhoid as a sclerosing injection.
- Suitable for 1st and 2nd degree haemorrhoids
- Painless, as placed high in anal canal above the dentate line.
Banding for hameorrhoids
= applicaton of small rubber band to the protruding mucosa to cause strangulation.
Can be done to 1st to 3rd degree haemorrhoids
Band must be above dentate line
Surgical Mx of haemorrhoids
Reserved for 3rd and 4th degree haemorrhoids
Stapled haemorrhoidopexy
Haemorrhoid artery ligation operation (HALO)
Surgical haemorrhoidectomy (now less commonly used)
Which muscles maintain anal continence?
Levator Ani
Internal anal sphincter = Thickening of the involuntary smooth muscle of bowel
External anal sphincter = voluntary muscle
Anatomical changes to the mucosa around the dentate line
the mucosa gathers into longitudinal folds containing the anal glands.
Anal glands secrete mucous to help with propulsion of faeces.
ABOVE dentate line
from embryological hindgut.
Columnar epithelium.
Blood supply from superior rectal artery (from inferior mesenteric artery).
Venous drainage by superior rectal vein (branch of inferior mesenteric vein).
Internal iliac lymph nodes
Innervated by inferior hypogastric plexus – sensitive to stretch only.
Rectum - BELOW dentate line
- epithelial type
- vasculature
- innervation
from ectoderm.
Non-keratinising stratified squamous epithelium.
Blood supply from the inferior rectal artery (from pudendal a., a branch of internal iliac a.)
Venous drainage by inferior rectal vein (branch of internal pudendal vein).
Superficial inguinal lymph nodes.
Innervated by pudendal nerve – sensitive to pain, temperature, touch and pressure.
What should be done for anyone with palpable inguinal lymph nodes?
anyone with palpable inguinal lymph nodes should also have a PR exam (?anal cancer)
What happens at the anal verge?
the epithelial cells become keratinised squamous (“true skin”)
Perianal haematoma
= “thrombosed external haemorrhoid”
however, unlike internal haemorrhoids it is covered by squamous epithelium supplied by somatic nerves, and thus is painful
Onset is acute, with sudden pain and a lump at the anal verge.
Perianal haematoma - Mx
Left untreated, they will either subside over a few days to leave a fibrous tag, or rupture to discharge clotted blood.
In the acute phase they can be incised and drained under LA.
If they are already discharging/being resorbed, hot baths and reassurance is all that is necessary.
Where is the most common site of perianal infection?
Anal sinuses/crypts are most common site of infection
Anorectal abscess
Usually caused by gut organisms
Associated with Crohn’s, DM and malignancy
Tx = incision and drainage under GA, to prevent rupture/formation of a fistula.
What is a pilonidal Sinus?
Obstruction of natal cleft hair follicles around 6cm above the anus, with ingrowing of hair leading to a foreign body reaction.
This can lead to abscess formation or tracks to the skin as a pilonidal sinus with foul discharge.
Pilonidal sinus - Tx
= excision of the sinus tract and primary closure, with pre-op ABX.
=> Hygiene and hair removal advise should be given.
What is a fistula-in-ano?
= an abnormal connection between the anal canal and the skin.
Presents as intermittent or continuous discharge of pus/blood/mucous from the perineum.
Causes of fistula-in-ano
Usually the result of an abscess (1 in 3 abscess patients have a fistula).
- IBD
- Diverticular disease
- Rectal Carcinoma
- TB
- Immunocompromised individuals
Fistula-in-ano - Investigations
Examination of the tract (VERY painful, only done under anaesthetic)
MRI
Endoanal USS
Goodsall’s Rule for anal fistulae
the position of the external opening can give you clues as to the tract of the fistula.
Anterior to transverse line – short, direct radicular tract to the interior opening.
Posterior to transverse line – curved/horseshoe tract to the interior opening.
The exception to this rule is anterior fistulas that lie >3cm from the anus, which may drain like posterior fistulas with a curved track to the posterior midline
Fistula-in-ano - Management
Superficial and low-level fistulae => laid open to heal by secondary intention (fistulotomy).
High fistulae (involving the continence muscles of the anus) may be injected with fibrin glue or a “fistula plug”.
If these methods fail, a “seton suture” gradually tightened over time can be used to maintain continence (ensures the sphincter is fixed by scar tissue before the tract is divided by tightening the suture).
Recurrent fistulae associated with Crohn’s may respond to metronidazole.
Anal fissure
An anal fissure is a longitudinal tear in the sensitive anal canal mucosa, distal to the dentate line.
Usually at 6 o’clock (90%) or 12 o’clock (10%, due to parturition).
Can be acute (present <6 weeks) or chronic (present >6 weeks).
Anal fissure - Causes
Mainly constipation.
Parturition – causing anterior/12 o’clock tears.
Rarer causes:
- Infections (syphilis/herpes)
- Trauma
- Crohn’s
- Anal cancer
- Psoriasis
Anal fissure - Presentation
SYMPTOMS
Pain, worse on defecation, lasting for hours afterwards
Associated constipation
Pruritis Ani
PR bleeding on defecation (fresh red)
O/E:
Midline longitudinal tear in the rectal mucosa
PR may not be possible due to pain/sphincter spasm
Anal fissure - Investigations
Proctoscopy and sigmoidoscopy should be performed under anaesthesia to exclude other anorectal diseases.
Enlarged nodes in the groin suggest a complicating factor.
Anal fissure - Management
Early small fissures may heal spontaneously, with symptomatic relief and a high fibre diet.
=> Local anaesthetic ointments and a lubricant laxative
If chronic, 0.4% GTN cream is used to relax the anal sphincter and allow the torn epithelium to heal.
=> SEs of GTN = headaches
Botox injection has the same effect and can last up to 8 weeks (but small risk of incontinence afterwards).
Intractable fissures/recurrent cases may require a sphincterotomy (submucosal division of the external sphincter under GA).
What are diverticula?
Where can they occur?
= outpouchings of bowel wall
can occur anywhere in the GI tract but are more common in the sigmoid (95% of cases) and descending colon.
Why are diverticula more common in the sigmoid colon?
Sigmoid has smallest lumen and highest pressures, therefore more prone to diverticulum formation
Pathophysiology of diverticula
Weakened bowel => stool movement increases intraluminal pressure => outpouching of the bowel wall.
True vs. False diverticula
True (involving all layers of the intestine – serosa, muscle, submucosa, mucosa).
False (does not contain all layers – often mucosa pushed through muscle defect).
RFs for diverticulosis
• Western/low fibre diet
• Age >50 years
• Male
• Obesity
• Connective tissue disorders – e.g Marfans, Ehler-danlos; predisposition to weakened GI wall.
• Smoking
• Family history
• NSAID use
What is diverticulosis?
= the presence of diverticula
What is diverticular disease?
= the presence of diverticula + symptomatic
What is diverticulitis?
= bacterial overgrowth within the gut causes inflammation of the diverticula.
Prevalence of diverticulosis
Highest prevalence = Europe and the USA (rare in Africa and Asia).
Age:
=> 50% of over 50s
=> 80% of over 80s in the UK.
Diverticulosis - Presentation
most commonly (95% of cases) asymptomatic and discovered incidentally
If symptomatic, they exactly mimic Sx of carcinoma of the colon:
- Left-sided colic, relieved by defecation
- Altered bowel habit (including PR blood/mucous)
- Nausea
- Flatulence
- Severe pain and constipation if severe (causing luminal narrowing)
Diverticular Disease - Investigations
PR (to r/o DDx of abscess/cancer)
Sigmoidoscopy/colonoscopy
Barium enema
CT
Diverticular Disease - Mx
Mebeverine is 1st line
Surgery may be considered if recurrent/very severe (rarely resorted to due to compications)
Asymptomatic Diverticula - Mx
Dietary Advice only for asymptomatic diverticulae (increase dietary fibre and balanced diet).
Diverticulitis - Presentation
SYMPTOMS
Severe left-sided colic
Constipation (or overflow diarrhoea)
Symptoms mimicking appendicitis, but on the left.
Systemically unwell
If there is extensive inflammation, the diverticula can perforate, and the patient can present with localised/generalised peritonitis.
SIGNS
Fever & tachycardia
Tenderness, guarding & rigidity on LHS
Can be a palpable mass in LIF
Raised WCC & inflammatory markers
What can sometimes mask the symptoms of diverticulitis?
If a patient is taking corticosteroids or immunosuppressants, this can mask symptoms of diverticulitis.
Simple vs. Complicated diverticulitis
Complicated – presence of abscess, formation of fistula, stricture, free perforation.
Simple – inflammation without any of these features.
Diverticular bleed
Diverticulitis is NOT typically associated with bleeding, as blood vessels become scarred from the inflammation.
However, diverticular bleeds occur when the diverticulum erodes into a submucosal blood vessel.
This causes haematochezia (the passage of bright red blood in the stool). This is generally large-scale and painless.
Diverticulitis - Mx in mild or severe attacks
Mild Attacks (uncomplicated, low-grade fever):
- Bowel rest (fluids only) at home
- Oral co-amoxiclav +/- metronidazole
Severe Attacks (complicated, high-grade fever):
- Admit if pain cannot be controlled, or oral fluids cannot be tolerated
- Give analgesia, IV fluids, IV cefuroxime & metronidazole & keep NBM
- Order erect CXR, AXR and contrast CT to assess for complications
- DO NOT SCOPE in acute attack
- Further management depends on degree of complications.
Complications of diverticulitis
Perforation
Abscess Formation
Bleeding
Fistula Formation
Intestinal Obstruction
Perforation in diverticulitis
Usually acute diverticulitis
Can lead to formation of a paracolic/pelvic abscess, fistulae or generalised peritonitis
Presents with ileus & peritonitis +/- shock
Mortality is up to 40%
Mx = Laparotomy +/- Hartmann’s procedure
Abscess formation in diverticulitis
Presents with swinging fever, leucocytosis and localising signs (e.g. boggy rectal mass)
Mx = drainage under CT guidance
Fistula formation in diverticulitis
Colovesical (=> UTI and pneumaturia)
Colovaginal (=> foul discharge)
Intestinal obstruction in diverticulitis
Most commonly sigmoid after repeated episodes of diverticulitis.
Chronic inflammation leads to scarring and the formation of a diverticular mass, which causes obstruction and may mimic colonic carcinoma.
Meckel’s Diverticulum
= An outpouching in the lower part of the small intestine.
A congenital abnormality - a remnant of the vitello-intestinal duct.
Approx. 2% of population have them, most are asymptomatic.
What is the most common GI congenital abnormality?
= Meckel’s Diverticulum
Meckel’s Rule of 2s
Affects 2% of population
2 years old
2:1 M:F ratio
2 inches long
2 feet proximal to ileocaecal valve
2 types of ectopic tissue (gastric/pancreatic)
Meckel’s Diverticulum - Presentation
Most commonly presents in young (<2 years old) children with painless melaena, then followed by obstruction / intussusception.
HOWEVER: can mimic appendicitis and present very similarly.
What is “Acute Abdomen”?
= sudden onset, severe abdominal pain which may indicate potentially life-threatening intra-abdominal pathology that requires urgent surgical intervention.
Painless acute abdomen
occurs particularly in older people, in children, in the immunocompromised, and in the last trimester of pregnancy.
Causes of abdo pain - right hypochondriac region
Gallstones
Cholangitis
Hepatitis
Liver abscess
Cardiac causes
Lower lobe pneumonia
Causes of abdo pain - left hypochondriac region
Spleen Abscess
Acute splenomegaly
Spleen rupture
Lower lobe pneumonia
Cardiac causes
Causes of abdo pain - epigastric region
Oesophagitis
Peptic Ulcer
Perforated Ulcer
Pancreatitis
MI
Causes of abdo pain - right lumbar region
Renal stones
Pyelonephritis
Causes of abdo pain - left lumbar region
Renal stones
Pyelonephritis
Causes of abdo pain - umbilical region
AAA rupture
Appendicitis (early)
Meckel’s diverticulitis
Small bowel obstruction
Ischaemic bowel
Peritonitis
DKA
Causes of abdo pain - left Iliac region
Diverticulitis
IBD
Constipation
Ovarian Cyst
Ectopic pregnancy
Hernias
Causes of abdo pain - right Iliac region
Appendicitis
IBD
Caecum obstruction
Ovarian cyst/torsion
Ectopic pregnancy
Hernias
Causes of abdo pain - hypogastric/suprapubic region
Testicular Torsion
Urinary retention
Cystitis
Placental Abruption
Large bowel obstruction
PID
Endometriosis
Acute abdomen - bleeding
AAA rupture – most serious cause, requires immediate surgical intervention.
Ruptured ectopic pregnancy
Bleeding from organ
Gastric ulcer
Trauma
What is peritonitis?
= Inflammation of the peritoneum.
Localised – when the inflammation is in a limited area (e.g. adjacent to inflamed appendix/diverticulum prior to rupture).
Generalised – when the inflammation is widespread (e.g. after the rupture of an abdominal organ).
Peritonitis - presentation
Patients lay completely still, with shallow breathing.
=> Pain is made worse by movement/ coughing/ inspiration
Tachycardia and potentially hypotension/pyrexia.
Percussion/rebound tenderness
Involuntary guarding (reflex contraction of abdominal muscles on examination of the inflamed area) and rigidty (increased tone at rest).
Reduced or absent bowel sounds.
Ischaemic bowel - Presentation
Any patient who has severe pain out of proportion to the clinical signs has ischaemic bowel until proven otherwise.
- Diffuse and constant abdominal pain reported.
- Examination may be unremarkable.
- Acidaemia with raised lactate on blood gases (due to impaired blood supply resulting in anaerobic respiration of the tissues)
Ischaemic bowel - Dx and Mx
Definitive diagnosis of ischaemic bowel is via a CT scan with IV contrast.
These patients require early surgical involvement to prevent perforation of the bowel and subsequent peritonitis and potential sepsis.
Abdo pain - inflammatory
Constant pain, supported by a raised temperature, pulse and leucocytosis.
Includes peritonitis
Abdo pain - Obstructive
Colicky pain
=> Crescendos to become very severe and then completely goes away (except biliary colic)
Patients often agitated.
Pain may become constant with superimposed inflammation.
Abdo pain - Referred Visceral Pain
Foregut (oesophagus to D2) pain is referred to the upper abdomen.
Midgut (D2 to transverse colon) pain is referred to the middle abdomen
Hindgut pain is referred to the lower abdomen.
Initial Management of acute abdomen
A to E assessment
(Pregnancy test if female)
Certain presentations require an urgent laparotomy:
1. Rupture of an organ (spleen, aorta, ectopic)
2. Peritonitis
Keep NBM if for theatre
Acute Abdo - Investigations
Basic observations
ECG (exclude MI)
Urine dip
Pregnancy test
BM (?DKA)
Bloods - FBC, U&E, LFTs, Amylase/lipase, ABG/VBG, CRP, Coagulation, Group and save/ XM, ?Blood cultures
Imaging - depending on DDx
What amylase result is likely to indicate pancreatitis?
What else can cause raised amylase?
Amylase 3x higher than upper limit to be diagnostic of pancreatitis
Values lower than this suggests other pathology – e.g. perforated bowel, ectopic pregnancy, DKA.
Acute Abdo - imaging choice
Erect CXR – evidence of bowel perforation
Abdominal X-Ray
=> Bowel obstruction, Toxic megacolon, Foreign body ingestion (if radio-opaque)
Abdominal Ultrasound
=> Biliary pathologies, KUB, Gynae pathologies, Appendix
In a patient who is very unwell, a CT is a good option
What is the most common cause of acute abdomen?
Appendicitis
(occurs in ~6-10% of population)
Causes of appendicitis
= inflammation of the appendix, usually caused by blockage within the lumen.
This can be due to:
- Faecolith (a stone made of faeces) – most common.
- Swollen lymphoid tissue in the wall – common in adolescence
- Parasites
- Tumours
Bacteria can proliferate in the closed loop of bowel, eventually leading to ischaemia & necrosis. The appendix can eventually perforate due to the raised intraluminal pressure, releasing bacteria into the abdominal cavity.
Appendicitis - Presentation
Abdominal pain
- Starts dull and central
- Then becomes localised and sharp in the RIF at McBurney’s point
- Pain may not be severe until the appendix has ruptured!
Constipation (or sometimes diarrhoea).
Anorexia
Nausea and vomiting (after the pain starts).
Where is McBurney’s Point?
1/3 of the way between the ASIS and the umbilicus
Appendicitis - signs
Rebound and percussion tenderness in RIF (maximum at McBurney’s point)
Guarding (especially if perforated)
Rovsing’s Sign
Tachycardia, tachypnoea
Mild pyrexia
Psoas sign – pain on R hip extension: retroperitoneal retrocaecal appendix.
Obturator sign – pain on internal rotation of R hip: pelvic appendix.
Rovsing’s Sign
more painful in RIF than LIF when LIF pressed
Appendicitis - Investigations
Abdominal exam and PR
Pelvic examination in females
Pregnancy test
Bloods – FBC, U&E, CRP/ESR
Urinalysis
USS/CT – if diagnostic uncertainty
AXR/erect CXR – if questioning perforation.
Appendicitis - Mx
If confirmed
- NBM ready for appendectomy.
- Resuscitation – IV fluids and IV metronidazole/cephalosporin pre-op
- Appendectomy (laparoscopic is gold standard)
- If ruptured appendix – remove the appendix and do a wash out (using large volumes of sterile fluid).
Appendectomy - early complications
Haematoma; surgical site infections
Appendectomy - late complications
SBO (adhesions); incisional hernia.
Appendicitis - Complications
Perforation
Surgical site infection
Appendix mass
Pelvic abscess
Surgical damage to other organs
Universal post-op complications – DVT/PE, bleeding, ileus, etc.
Adhesions – small bowel obstruction due to scarring.
What is an appendix mass?
when an inflamed appendix becomes covered with omentum and forms a mass
Who is more likely to get IBD?
More common in Caucasians, and Ashkenazi Jews.
Types of IBD
- Ulcerative colitis
- Crohn’s disease
- Indeterminate colitis – when it is not possible to distinguish between UC and Crohn’s.
RFs for Crohn’s Disease
poor diet,
FHx,
smoking,
altered immune states
Rose-thorn ulcers
deep penetrating linear ulcers or fissuring typically seen within stenosed terminal ileum with a thickened wall.
They appear as thorn-like extraluminal projections on barium studies
One of the typical signs of Crohn’s disease
Cobblestone appearance on CT
due to a combination of extensive, broad, linear transverse and longitudinal ulcerations/fissures within an inflamed mucosal surface
=> gives an appearance reminiscent of cobblestones.
Often seen in Crohn’s disease
Crohn’s disease - Pathophysiology
Inflammation affects any part of the GI tract (mouth to anus).
=> Most commonly terminal ileum and proximal ascending colon
Can affect just one area, or multiple areas leaving normal bowel in between (“skip lesions”).
Involved bowel is narrowed due to thickened wall, with deep ulcers
Due to inflammation, a lot of fat wrapping/stranding is seen around the intestine.
Inflammation extends through ALL layers of the bowel, so fistulas and strictures are common.
Crohn’s disease - Presentation
Abdominal pain (varying in character)
Diarrhoea
- Steatorrhoea in ileal disease
- Bloody in colonic disease
Weight loss (or FTT) – due to malnutrition
Severe aphthous ulceration of the mouth (early sign)
Anal complications – fissure, fistula, haemorrhoids, skin tags, abscesses
Extra-GI manifestations of IBD
Can present with RIF pain/mass
Ulcerative Colitis - Pathophysiology
thought to be autoimmune in nature.
The inflammation only affects the mucosa (i.e. superficial ulceration).
Ulceration is extensive and continuous.
Mucosa is reddened, inflamed and bleeds easily.
Only very small portions of normal mucosa.
Inflammation leads to loss of the colonic haustra.
Gives the adjacent mucosa the appearance of inflammatory polyps.
Extent of ulcerative colitis
Inflammation that starts at the rectum, extending proximally along the colon
Proctitis – affects the rectum alone
Proctosigmoiditis
Distal colitis
Extensive colitis
Pancolitis – whole colon is affected
How common are obstructions/fistulae/strictures in IBD?
Common in Crohn’s as all layers of the bowel are affected
Uncommon in UC, as inflammation is mostly superficial
What is backwash ileitis?
inflammation of the distal terminal ileum in ulcerative colitis patients
What is a protective factor in UC?
Smoking!
Ulcerative Colitis - Presentation
Crampy lower abdominal discomfort
Gradual onset diarrhoea (often bloody)
Urgency and tenesmus if disease confined to rectum
Extra-GI manifestations.
AXR – may show dilated colon, with thumb-printing of the bowel wall.
What does “thumb-printing” of the bowel wall on an AXR suggest?
Indicates inflammation and thickening.
Extra-colonic manifestations of IBD
During Active phase of IBD:
• Skin disorders – erythema nodosum, pyoderma gangrenosum
• Joints – arthralgia of large joints
• Eye manifestations – conjunctivitis/episcleritis/iritis
• Venous thrombosis
• Fatty liver
Unrelated to disease activity:
• Autoimmune hepatitis
• Gallstones
• Renal calculi
• Primary sclerosing cholangitis
• Cholangiocarcinoma
• Ankylosing spondylitis
Histological differences between Crohn’s and UC
Crohn’s – transmural inflammation, lymphoid hyperplasia, granulomas.
UC – mucosal inflammation, crypt abscesses, goblet cell depletion.
HOWEVER it may not be possible to distinguish between IBDs if the biopsy is taken in the acute phase – “indeterminate inflammatory colitis”.
IBD - Investigations
Bloods
=> FBC, U&E, LFT, CRP/ESR, Serum iron, B12, folate
Stool Studies
=> Stool chart; MCS x3 to exclude infective causes; Calprotectin
Radiology
=> AXR/CXR in acute disease
=> CT in Crohn’s
Endoscopy
=> Rigid/flexi-sigmoidoscopy
=> Colonoscopy
=> Endoscopic rectal biopsy
=> Biopsies
What is the aim of treatment of IBD?
to prolong the remission phase and prevent relapses with maintenance therapy
Acute Crohn’s Flare - Mx of Mild attack
Mild attack (= symptomatic but systemically well):
- Oral prednisolone
- Tapered steroids and review in clinic
Acute Crohn’s Flare - Mx of severe attack
Severe attack (= symptomatic + systemic upset)
- Raised temp, HR, CRP/ESR and low albumin warrant admission
- Start IV steroids (hydrocortisone 100mg/6h)
- NBM, parenteral nutrition
- High level monitoring
- Thiopurines (e.g. Azathioprine or 6-mercaptopurine) are 2nd line
- Biological agents (infliximab) used in refractory disease not responding to medical treatment
- Once improving, transfer to oral prednisolone as per mild attack
If unable to control, surgical advice should be sought.
Acute UC flare - Mx of mild/moderate attack
Proctitis/proctosigmoiditis – topical aminosalicylate (e.g. mesalazine suppository/enema) +/- oral mesalazine
More extensive disease – loading dose oral mesalazine +/- oral beclomethasone and topical mesalazine
2nd line (after 4 weeks of unsuccessful 1st line Tx) – add oral prednisolone
3rd line – tacrolimus after a further 2-4 weeks
4th line – biological agents, considered by a specialist
Acute UC flare - Mx of severe/fulminating UC
MDT management
1st line =
Start IV corticosteroids
Assess the patient with regard to surgical intervention
SC LMWH
Avoid any anti-motility drugs
2nd line – IV ciclosporin if symptoms worsen or no improvement within 72h of steroids
3rd line – biological agents, considered by a specialist
What factors increase the likelihood of surgical intervention in UC?
Likelihood of surgery is suggested by:
> 8 motions/day,
pyrexia, tachycardia,
colonic dilatation,
low albumin, low Hb,
CRP <45
UC Maintenance Tx
5-ASA derivatives are 1st line (topical if proctosigmoiditis, oral if left-sided)
=> Sulfasalazine, mesalazine
Oral thiopurines are 2nd line
=> Azathioprine, mercaptopurine
Surgical Mx of IBD
UC – colectomy provides cure.
Crohn’s - surgery is never curative and patients still tend to develop recurrent disease.
=> Temporary ileostomies can be used to rest the distal diseased bowel
=> Can perform limited resection of the small bowel (but must keep it above 1m long to prevent malabsorption)
Surgical options for UC
EMERGENCY PROCEDURES:
• Subtotal colectomy & end ileostomy (leaves rectal stump, so still a proctitis/cancer risk)
• Proctocolectomy & end ileostomy (rectal stump also removed)
ELECTIVE PROCEDURES:
• Completion proctocolectomy & ileoanal pouch reconstruction (faecal continence maintained)
• Colectomy and ileorectal anastomosis
General complications of IBD
Bowel perforation
Lower GI haemorrhage
Toxic dilatation (more common in UC)
Colonic carcinoma
=> Higher risk in Crohn’s than UC
What is the colorectal cancer risk in UC?
UC patients with pancolitis for 20 years have 15% risk (surveillance required)
Toxic Dilatation of the colon
Features – persistent fever, tachycardia, loose blood-stained stools.
Investigations:
Falling albumin/potassium.
AXR – dilated (>6cm) colon with mucosal islands.
Perforation is imminent – surgery often required
Complications specific to Crohn’s Disease
SBO
Fistulae
Abscess formation
B12/folate/iron deficiencies
What is the definition of a hernia?
= the protrusion of viscus through a defect in the walls of its containing cavity into an abnormal position.
Reducible vs irreducible hernias
- Reducible – contents can be manipulated back to its original position through the defect.
- Irreducible – cannot be reduced without surgery.
What is an incarcerated hernia?
= an irreducible hernia, with the contents trapped due to adhesions.
What is a strangulated hernia?
= Compression of bowel => obstructed venous return => ischaemia
Can lead to necrosis, gangrene and perforation if left untreated
What is an obstructed hernia?
= Bowel contents cannot pass through the herniated bowel
Presents as abdominal pain and distension; absolute constipation; N&V.
RFs for developing a hernia
Male (increased risk of central obesity)
Increasing age, protein deficiencies (less collagen for tensile strength)
Heavy lifting, chronic cough, chronic constipation, obesity (Increased intra-abdominal pressure)
Spigelian Hernia
Due to natural weakness in semilunar space between two muscle groups.
Inguinal Hernia
= most common type of hernia
Occurs through the inguinal canal
=> Can be direct/indirect
Femoral hernia
when abdominal viscera or omentum pass through the femoral ring into the potential space of the femoral canal.
Hernia - principles of Mx
Try to reduce the hernia to prevent obstruction/strangulation
If the hernia is irreducible, elective surgery is considered.
=> Open or laparoscopic
=> Generally done as a day case
If obstructed/strangulated, an emergency Hartmann’s procedure is performed.
How are congenital inguinal hernias managed?
Treated with herniotomy and ligation of the processus vaginalis at about the age of one year.
Inguinal canal anatomy
Extends inferiorly and medially through the inferior part of the abdominal wall.
Is about 4cm long
Embryologically, was used to allow the descent of the testes into the scrotum
Contains:
- Spermatic cord (if male) / round ligament (if female)
- Nerves
- Arteries
Has a deep and superficial inguinal ring
Deep inguinal ring - location
found ~1cm above the midpoint of the inguinal ligament (lateral to the epigastric vessels).
How can you located the midpoint of the inguinal ligament
= halfway from ASIS to pubic tubercle
Superficial inguinal ring - location
found just superior to the pubic tubercle.
What are the borders of the inguinal canal?
ROOF = transversalis fascia; internal oblique; transversus abdominis
ANTERIOR = aponeurosis of external oblique; internal oblique
POSTERIOR = Transversalis fascia
FLOOR = Inguinal ligament
Which type of inguinal hernia is more common?
Indirect Inguinal Hernia (~80%)
Indirect inguinal hernia
The hernia goes through in the deep ring, through the inguinal canal and out through the superficial ring.
Accounts for ~80% of inguinal hernias
More likely to strangulate
Direct inguinal hernia
Hernia goes through a defect in the posterior wall. It exits through the superficial ring.
Accounts for ~20% of inguinal hernias
Reduce easily, rarely strangulate.
What is Hesselbach’s Triangle?
= a triangular region in the anterior abdominal wall, which is a particular area of potential weakness.
Inferior border = the inguinal ligament
Lateral border = inferior epigastric vessels
Medial border = rectus abdominis muscle.
Inguinal hernia - clinical features
Painless swelling in the groin
Often asymptomatic
May come and go, or emerge suddenly – e.g. after heavy lifting
They can become symptomatic and the common features of this are:
- Pain – particularly when coughing or stooping
- Change in bowel habit
- Burning sensation in the groin
- Scrotal swelling (in males)
Inguinal hernia - differentiation between direct/indirect on examination
To differentiate between indirect/direct on examination:
- Reduce the hernia
- Press over the deep ring (just above the midpoint of the inguinal ligament.
- Ask the patient to cough.
- If the hernia reappears – it is a DIRECT hernia.
Absolute differentiation can ONLY be achieved via surgical exploration – the inferior epigastric vessels are used as the landmark.
=> Indirect inguinal hernias are lateral to the inferior epigastric vessels.
=> Direct inguinal hernias are medial to the inferior epigastric vessels.
Femoral canal anatomy and purpose
= an anatomical compartment, in the anterior thigh.
Normally lies medial to the femoral vein ( N A V [Y] )
Its purpose is allow space for the vein to expand.
Normally contains a small amount of fatty tissue and lymph nodes.
RFs for femoral hernias
• Female (due to wider anatomy of pelvis)
• Pregnancy
• Raised intra-abdominal pressure
• Increasing age
What is there a risk of with femoral hernias?
There is a HIGH risk of strangulation due to the narrow neck of the femoral canal and strong borders.
=> 50% present as a surgical emergency with an obstructed or strangulated hernia
Femoral Hernia - Presentation
50% present as a surgical emergency with an obstructed or strangulated hernia
Otherwise present as painless groin lump
Inguinal vs femoral hernia
Inguinal hernias are SUPERIOMEDIAL to the pubic tubercle
Femoral hernias are INFEROLATERAL to the pubic tubercle
Richter’s Hernia
= a hernia involving only one side wall of the bowel, and not the bowel lumen, which can result in bowel strangulation and perforation without causing obstruction or any of its warning signs.
They are particularly likely in the femoral sac.
Cause of umbilical Hernia and RFs
Due to a defect in transversalis fascia = umbilical ring, where the umbilical vessels passed in-utero
Occur in babies
More common in black, male, premature babies
Cause of Paraumbilical Hernia and RFs
Occur adjacent to the umbilicus due to a weakness in the linea alba
More common in 35-50 year old women
Usually caused by raised IAP.
Umbilical hernia - presentation
Generally asymptomatic, more prominent on coughing/laughing.
Low strangulation risk, very rarely become obstructed.
Paraumbilical hernia - presentation
Localised dragging pain and enlarging hernia over time.
High risk of strangulation as the weakness is not a natural occurrence.
Umbilical hernia - Mx
90% retract by the age of 2 (consider surgical repair in a child >2)
Paraumbilical hernia - Mx
Early operative management advised
=> excision of the sac and stitching of the rectus sheath; with mesh repairs for larger defects
What is an incisional hernia ?
= a hernia that occurs through a previously made incision in the abdominal wall, i.e. the scar left from a previous surgical operation.
An incisional hernia should form part of the consent process along with a scar in abdominal surgery.
RFs for incisional hernia
• Emergency surgery – 2x risk of hernia
• Type of incision used – e.g. midline.
• Poor surgical technique
• Absorbable stitches
• Anything that may affect the ability of the wound to heal:
- Immunosuppression
- Wound infection
- Smoking
- Diabetes
- Vascular disease
- Pre-op chemo
Incisional hernia - presentation
Bulge in the scar and local discomfort
Subacute bowel obstruction is common as the hernia enlarges
Usually a wide neck, so strangulation uncommon (but becomes more likely the longer it’s there, as adhesions begins to make it irreducible)
Incisional hernia - Mx
Usually repaired with mesh, but often reoccur after repair as the risk factors are still there.
=> Weight loss and smoking cessation will increase likelihood of successful repair.
=> Recurrence risk of 2-5% for small incisions, and 10-20% for large ones.
Epigastric hernia
= Herniation of FAT which overlies the bowel through the linea alba, above the umbilicus.
Usually small – 1cm diameter
Epigastric hernia - presentation
Over 75% asymptomatic, but can cause pain/discomfort
Varies from mild epigastric pain to a deep burning pain, radiating to the back or lower abdomen.
=> Aggravated be exercise/eating
=> Relieved by reclining
Can also have symptoms of abdominal bloating, N&V.
Epigastric hernia - Mx
If there are symptoms of pain, then the defect is often surgically repaired
Divarification of recti / Diastasis recti
= separation of rectus abdominus due to linea alba laxity
Appears as a bulge in the upper abdomen, worse when sitting up and retracts when lying down.
RFs for divarification of recti
- Men – weight gain (truncal obesity)
- Women – pregnancy
- Repeated midline operations
- Chronically raised intra-abdominal pressure
Divarification of recti - Ix
Diagnosis through USS.
Divarification of recti - Mx
Physiotherapy to strengthen the rectus abdominus (no indication for surgical management)
What can cause upper GI haemorrhage?
Peptic ulceration ~40%
Gastroduodenal erosions ~15%
Oesophagitis ~15%
Mallory-Weiss syndrome ~15%
Varices ~10%
Upper GI malignancy ~1%
What is Mallory-Weiss Syndrome?
partial-thickness tear of the oesophagus after repeated vomiting, causing haemorrhage
Upper GI haemorrhage - presentation
Symptoms:
- Haematemesis
- Melaena (blood altered by bacteria)
- Haematochezia (unaltered PR blood, can occur in massive upper GI bleeds)
- Abdo pain
Signs will be of any underlying cause, and of shock.
Iron-deficiency anaemia (if chronic blood loss)
Management of upper GI haemorrhage
Managed as per haemorrhagic shock
- Assess using Glasgow-Blatchford score
- Endoscopy should occur within 4 hours if indicated, generally as soon as stabilised
=> Can identify the site of bleeding and administer treatment (adrenaline injection/ diathermy/ banding of varices) - IV Omeprazole to reduce the risk of rebleed (high mortality)
- High level monitoring to assess for signs of a rebleed
- Definitive surgery (laparotomy) or angiographic embolisation may be needed
Indications for surgery in upper GI bleed
If bleeding recurs after endoscopy
If it is persistent despite endoscopic treatment
If bleeding is torrential and obscuring adequate visualisation
Glasgow-Blatchford score
= a scoring system for UGIB
Includes:
- SBP,
- pulse,
- Hb,
- blood urea level,
- evidence of melaena
- recent syncope
- hepatic disease
- cardiac failure
Scores >6 indicate mortality >50%, thus urgent intervention is required
Rockall Score
= a score for prediction of mortality in UGIB
includes age, shock, co-morbidity AND endoscopy findings
What are oesophageal varices?
= extremely dilated sub-mucosal veins in the lower third of the oesophagus.
most often a consequence of portal hypertension, following cirrhosis of the liver.
Management of acute variceal bleeding
ABCDE Resuscitation
Vitamin K & FFP (if needed) to correct clotting
IV Terlipressin (or somatostatin analogues)
IV antibiotic prophylaxis
=> Significantly reduces mortality
If still bleeding, attempt endoscopic banding and adrenaline injection under GA
=> As a last line, balloon tamponade devices can be used to temporarily compress varices.
Transjugular Intrahepatic Portosystemic Shunting (TIPSS) = the definitive procedure for varices resistant to banding, carried out by interventional radiology.
Use of IV Terlipressin in Acute Variceal Bleed
Treatment should be stopped after definitive haemostasis has been achieved, or after five days, unless there is another indication for its use.
Transjugular Intrahepatic Portosystemic Shunting (TIPSS)
= a shunt between portal and hepatic veins
the definitive procedure for varices resistant to banding, carried out by interventional radiology.
Variceal Bleed - secondary prophylaxis
Following an initial bleed, endoscopy is indicated as soon as haemodynamically stable
=> to identify the site of bleeding, estimate the risk of rebleeding and administer ADRENALINE AND BAND THERAPY. (Sclerotherapy is 2nd line)
Following endoscopy, non-selective beta-blockers (e.g. propranolol) are used.
What percentage of varices rebleed within 2 years?
80% of varices rebleed within 2 years.
Primary prophylaxis for varices
Primary prophylaxis should be implemented (beta-blockers and endoscopic banding) if asymptomatic varices are found.
Causes of dysphagia
Diseases of the mouth/tongue – e.g. tonsilitis
Neuromuscular disorders – MG, MND, bulbar palsy
Oesophageal motility disorders – achalasia, scleroderma, diabetes
Extrinsic pressure – goitre, lymph nodes, enlarged left atrium
Intrinsic lesion – foreign body, benign/malignant stricture, pharyngeal pouch, oesophageal web (Plummer-Vinson Syndrome)
What are the two “types” of dysphagia?
Oropharyngeal Dysphagia
=> Difficulty initiating swallow +/- choking/aspiration
Oesophageal Dysphagia
=> Food “sticks” after swallowing +/- regurgitation
Oropharyngeal Dysphagia - cause and Ix
Caused by neurological disease
Investigations:
• Neuro exam
• Videofluoroscopic swallowing assessment
Oesophageal Dysphagia - cause and Ix
Caused by:
• Dysmotility,
• Stricture (e.g. intrinsic oesophageal malignancy or extrinsic bronchial ca.)
• Oesophagitis (reflux, candidiasis)
• Pharyngeal pouch
Investigations:
• Barium swallow
• Endoscopy (OGD)
• Biopsy
Typical presentation of dysphagia caused by malignancy
Malignant strictures have a SHORT history of progressive dysphagia, associated with severe weight loss in elderly patients.
If the history strongly suggests malignancy, endoscopy & biopsy is 1st line.
Plummer-Vinson Syndrome
A triad of dysphagia, as well as koilonychia and glossitis (both signs of IDA)
It is a pre-malignant condition due to hyperkeratinisation of the oesophagus causing an oesophageal web.
Tx = iron supplementation and dilation of the web via OGD
What is achalasia?
Due to a lack of coordinated muscle contraction and relaxation at the lower end of the oesophagus, leading to retention of the food bolus.
Over time, the oesophagus becomes markedly dilated (megaoesophagus), with a classic “rat tail” appearance below the megaoesophagus seen on barium studies.
Achalasia - presentation
typically in younger/middle-aged patients (30s)
- Dysphagia
- Regurgitation
- Substernal cramps
- Nocturnal cough
Achalasia - diagnosis
Barium swallows
OGD – dilated oesophagus with a pond of stagnant food/fluid
Oesophageal manometry – increased lower oesophageal sphincter pressure
Achalasia - management
Conservative/lifestyle measures – chew food well, always eat upright, drink lots with meals, etc.
Botulinum toxin injection (provides temporary relief; done if unsuitable for invasive procedures)
Endoscopic balloon dilation (risk of oesophageal rupture)
Heller’s cardiomyotomy
What happens during a Heller’s cardiomyopathy ?
the muscles of the cardia are divided, and the upper wall of the stomach is sutured onto the lower oesophagus
What is there a risk of with endoscopic balloon dilation for achalasia?
Risk of oesophageal rupture
What is a pharyngeal pouch?
= an outpouching of posterior pharyngeal wall
Typically seen around C5-6 level.
Seen mostly in 60-80 year olds, and more common in males (5:1)
Clinical features of pharyngeal pouch?
• Dysphagia => Solids AND liquids
• Regurgitation
• Chronic cough
• Gurgling on drinking
• Halitosis
• Globus
Pharyngeal pouch - Ix
Initial investigation is with barium swallow.
Pharyngeal pouch - Mx
It may not require treatment, but if symptomatic then consider endoscopic repair/open surgery.
Oesophageal Malignancy - who normally gets it?
Generally occurs in those aged >60
Although becoming more common in younger age groups!!!
Oesophageal Malignancy - clinical features
!!!! Initially asymptomatic
Progressive dysphagia – starting with solids, progressing to liquids and eventually difficulty swallowing saliva
Weight loss and anorexia
Retrosternal chest pain
Coughing/aspiration
Occasional lymphadenopathy
Oesophageal cancer - pathology
Most are now in the lower 1/3rd of oesophagus, mainly adenocarcinomas
The remainder are mainly SCCs
Oesophageal cancer - adenocarcinoma
- where does it occur?
- what are the risk factors?
- how does it spread?
More common in UK and western Europe
Typically lower 1/3 of oesophagus
Risk factors:
• GORD – obesity/alcohol/medications
• Barrett’s Oesophagus
• Smoking
Metastasise earlier via lymphatics
Oesophageal cancer - SCC
More common worldwide
Typically middle and upper 1/3 oesophagus
Risk factors:
• Alcohol and Smoking
• Diet – high nitrates/nitrosamines
• Chronic inflammation (e.g. Achalasia)
Regional lymph node spread.
Oesophageal malignancy - prognosis
Prognosis is poor – <10% 5-year survival
(SCC has a slightly better prognosis as it is more responsive to radiotherapy)
Oesophageal malignancy - spread
Metastases (to liver/lungs/bone) are common at diagnosis (25%) as presents late
Oesophageal malignancy - diagnosis
If suspected oesophageal malignancy – urgent OGD and biopsy.
Staging:
- CT CAP
- PET-CT scan
- Laparoscopy to exclude peritoneal mets
Oesophageal malignancy - Management
Radical curative oesophagectomy for T1/T2 localised disease
=> Pre-op chemotherapy improves survival, but causes morbidity
Chemoradiotherapy combinations can be used if surgery is not indicated
Palliation can involve oesophageal stenting to restore swallowing
(many cases treated as palliative as advanced disease at presentation)
Gastric cancer - who does it affect?
Most commonly affects people age 50-70
Especially in Japanese populations.
Gastric cancer - pathology
Most are adenocarcinomas and most occur in the antrum.
More rarely stromal tumours (more slow growing/benign)
Gastric cancer - potential findings on endoscopy
Tend to appear as polypoids or ulcerating lesions with rolled edges
“Leather bottle stomach” occurs when there is submucosal infiltration of tumour with marked fibrous reaction, producing a small but thickened & contracted stomach
Gastric Cancer - RFs
- H. pylori infection leading to metaplasia
- High salt/nitrate diet
- Smoking
- Genetic factors – blood group A / HNPCC, Japanese
- Pernicious anaemia
- Adenomatous polyps
- Low socio-economic status
Gastric Cancer - Spread
Direct invasion of abdominal viscera
Lymphatic spread (Virchow’s node)
Portal dissemination to the liver
Transcoelomic spread can cause peritoneal metastases (including bilateral ovarian tumours)
Gastric Cancer - Symptoms
Often non-specific!
Epigastric pain, as with gastric ulcer
Nausea & vomiting (vomiting more frequent if tumour is near the fundus)
Dysphagia (if tumour is near the fundus)
Anorexia / weight loss
Gastric Cancer - Signs
Usually completely absent until late disease
Palpable epigastric mass (50%)
Large left supraclavicular node (Virchow’s)
Hepatomegaly, jaundice & ascites
Acanthosis nigricans
Anaemia
Gastric Cancer - Investigations
History & Examination
Bloods – FBC, U&E, LFT
OGD and multiple ulcer edge biopsy
STAGING:
- Endoscopic USS and CT
- Staging laparoscopy
Gastric Cancer - Management
Gastrectomy:
=> Partial gastrectomy for tumours in the distal 2/3rds of the stomach, otherwise total gastrectomy.
=> Associated with many complications
Combination chemotherapy can increase survival in advanced disease
Endoscopic mucosal resection for tumours confined to the mucosa.
Wide local excision for stromal tumours
Stenting of the pylorus can be palliative to relieve gastric outlet obstruction in patients with pyloric tumours.
Gastric Cancer - Prognosis
Only ~1/3 have curable disease at presentation, the remainder are treated palliatively.
<10% 5-year survival
<20% for those undergoing radical surgery
Complications associated with gastrectomy
MANY COMPLICATIONS
Chronic diarrhoea/vomiting,
Dumping syndrome,
Bacterial overgrowth
Malabsorption,
Anaemia,
Osteomalacia
Carcinoma of the gallbladder - who gets it?
= an uncommon adenocarcinoma
Occurs in the elderly, associated with long-standing gallstones
Carcinoma of the gallbladder - spread
Direct invasion of the liver
Lymphatic spread
Carcinoma of the gallbladder - symptoms
(resembles chronic cholecystitis)
- RUQ pain
- N&V
- Weight loss
- Obstructive jaundice
- Palpable mass
Carcinoma of the gallbladder - management
Staging CT CAP, staging laparoscopy for peritoneal mets
Treatment = surgical:
=> Radical cholecystectomy +/- liver resection if caught incidentally
Most tumours present too late for surgical therapy (survival is short)
Cholangiocarcinoma - pathophysiology
Adenocarcinoma arising from the epithelium of the bile duct/ampulla
Common sites = at the confluence of the ducts in the biliary tree
Slow growing and metastasise late, but are often advanced at presentation with low long-term survival.
Cholangiocarcinoma - who gets it?
More likely to occur in patients with primary sclerosing cholangitis or IBD
Cholangiocarcinoma - Presentation
Painless progressive jaundice (as with cancer of the head of the pancreas)
Can present like HCC (if arising from the cells of the intrahepatic ducts)
Cholangiocarcinoma - Management
Extra-hepatic or periampullary tumours may be treated by curative resection (Whipple’s procedure)
Palliative stenting (ERCP) may be used in advanced disease
hepatopancreatic Duct/Ampulla of Vater
= formed by the joining of the pancreatic duct and common bile duct.
The Sphincter of Oddi
Prevents the reflux of duodenal contents into the biliary tree
Located between the ampulla of Vater and the wall of the 2nd part of the duodenum.
What does bile contain?
water,
cholesterol,
bile salts,
conjugated bilirubin,
phospholipids.
Physiology of bile production
- Produced by the liver
- Stored and concentrated in the gallbladder
- Lipid-rich food in the duodenum stimulates CCK release
- CCK causes the gallbladder to contract and the sphincter of Oddi to relax.
- Bile passes from the GB into the duodenum.
What is cholelithiasis?
= formation of stones in the gallbladder
What is choledocholithiasis?
= stone impaction in the common bile duct.
What is Cholestasis?
= reduction/stoppage of bile flow.
What factors predispose to gallstone formation?
- Cholesterol Supersaturation
- Stasis of Bile
- Increased Hb breakdown
Gallstone formation - what can cause cholesterol supersaturation?
Caused by:
1) increased plasma oestrogen (obesity, pregnancy, OCP, female)
2) depletion of the bile acid pool (terminal ileal resection/disease)
Blood cholesterol levels have very little influence on bile cholesterol
Gallstone formation - what can cause stasis of bile?
Lack of stimulus to GB emptying – fasting, TPN
Gallstone formation - what can cause increased Hb breakdown?
Haemolytic disorders – e.g. spherocytosis, sickle cell disease, malaria
Composition of gallstones
20% are cholesterol
75% are mixed (predominantly cholesterol)
5% are bile pigments
Cholesterol gallstones - cause, appearance and RFs
Generally caused by cholesterol supersaturation and bile stasis.
Often solitary, Large (>2.5cm), Smooth
RFs:
• Increasing age
• Obesity, high fat diet, rapid weight loss
• Female sex, multiparity, pregnancy, OCP
• DM
• Ileal disease (e.g. Crohn’s) / resection
• Liver cirrhosis
Mixed gallstones
Multiple stones
“Generations” – a range of colours and shapes
Bile pigment gallstones
Multiple, Small
Black (associated with haemolytic conditions) or brown (due to bile stasis/infection)
Gallstones - presentation
MAJORITY ARE ASYMPTOMATIC
If they are symptomatic, the symptoms depend on the location of the stone:
=> Biliary Colic/Acute cholecystitis
=> Choledocholithiasis
=> Mirizzi’s Syndrome
=> Gallstone Ileus
How do gallstones cause choledocholithiasis ?
stone impaction in the common bile duct, which can cause biliary colic if temporary, or painful obstructive jaundice if more prolonged.
This can predispose to ascending cholangitis or acute pancreatitis
How do gallstones cause Mirizzi’s Syndrome?
gallstone impacted in the cystic duct / Hartmann’s pouch (at the neck of the gallbladder); causes extrinsic compression of the common hepatic duct.
This leads to obstructive jaundice, without dilation of the cystic/common bile duct
How do gallstones cause gallstone ileus?
(UNCOMMON)
a large gallstone erodes through to the gallbladder lumen to create a fistula into the adjacent duodenum.
This can then produce an obstruction if it impacts in a narrow segment of bowel.
Biliary Colic - typical presentation
Severe, constant epigastric/RUQ pain
Crescendo characteristic (peaks around 2 hours after eating, due to CCK peak at this time).
May radiate to the back or right shoulder/subscapular region
Worse upon food consumption (especially fatty foods)
Worst mid-evening, lasting until the early hours (often wakes the patient)
Can be associated with N&V
Pain often resolves after analgesia, or spontaneously if the stone becomes unblocked and passes down the bile duct.
The patient will be systemically well
Acute cholecystitis - pathophysiology
An obstruction of gallbladder emptying, leading to gallbladder distension.
There is ongoing water reabsorption from the retained bile, which becomes highly concentrated, leading to a secondary inflammatory response in the wall of the gallbladder.
Acute cholecystitis - presentation
Initial features are similar to biliary colic, until the inflammatory component develops, leading to:
- Severe localised RUQ pain (as inflamed GB touches the peritoneum), with guarding and rigidity
- Vomiting & systemic upset (fever & leucocytosis)
- Palpable gallbladder (Murphy’s sign positive)
- Rarely the gallbladder can become gangrenous and perforate, leading to generalised peritonitis.
Murphy’s Sign
Whilst applying pressure in the RUQ, ask the patient to inspire deeply.
Murphy’s sign is POSITIVE when there is a halt in inspiration due to pain.
A similar manoeuvre in the LUQ should not elicit discomfort
Murphy’s sign is specific (if found, it is likely that the diagnosis is cholecystitis), but it is not sensitive (not everyone with cholecystitis will have a positive Murphy’s sign).
Chronic Cholecystitis
= Repeated episodes of inflammation due to gallstones lead to fibrosis and thickening of the gallbladder wall.
Features:
- Recurrent bouts of abdominal pain due to mild cholecystitis
- Discomfort and flatulence after fatty meals
CBD obstruction - Presentation
Obstructive jaundice and biliary colic
Attacks last for hours to days, ceasing when the stone passes through the Sphincter of Oddi or disimpacts and falls back into the dilated common bile duct.
If the obstruction is not relieved, the chronic back pressure can lead to secondary biliary cirrhosis and liver failure.
Courvoisier’s Sign/Law
In a patient with painless jaundice and an enlarged gallbladder the cause is unlikely to be gallstones and therefore presumes the cause to be an obstructing MALIGNANCY until proved otherwise.
What is Ascending Cholangitis?
= an infection of the common bile duct, usually caused by bacteria ascending from the duodenum.
Usually occurs following obstruction due to choledocholithiasis
Ascending Cholangitis - symptoms
Classic symptoms = Charcot’s Triad:
1. Fever (+/- rigors)
2. Jaundice
3. RUQ Pain
What is Charcot’s Triad
Charcot’s Triad:
1. Fever (+/- rigors)
2. Jaundice
3. RUQ Pain
=> Suggestive of ascending cholangitis
Gallstone/gallbladder disease - Investigations
Observations
Abdo exam
BLOODS - WBC, LFTs, Amylase/lipase, prothrombin time
Abdo USS
MRCP/ERCP
What is the 1st line imaging in ?gallstone disease
Abdo USS
Can show sludge/stones
Shows thickened gallbladder wall in acute/chronic inflammation
Shows increased diameter of common bile duct in obstruction
when is MRCP indicated in gallstone disease?
(Magnetic Resonance Cholangiopancreatography)
Any patients with an inconclusive USS/CT scan and symptoms of gallstones should undergo an MRCP
Gives detailed information about the biliary tract anatomy of the patient and can detect stones.
What is ERCP ?
= endoscopic retrograde cholangiopancreatography
Gold standard for cholangitis – both diagnostic and therapeutic.
Endoscope is passed via oesophagus into duodenum, fine catheter is passed into the common bile duct.
What is the gold-standard investigation for cholangitis?
ERCP - it is both diagnostic and therapeutic
Asymptomatic Gallstones - Mx
Cholecystectomy only indicated if the patient is at significant risk of complications due to co-morbidities (e.g. diabetes or chronic renal failure)
Gallstones with Biliary Colic - Mx
Admit for bed rest, with fluids and analgesia (keep NBM)
Elective laparoscopic cholecystectomy
=> Preferably during the first 72 hours (“hot cholecystectomy”)
=> Otherwise scheduled for 6 weeks later (“cold cholecystectomy”)
Medical Tx involve oral bile salts (chenodeoxycholic acid) for small, non-calcified stones in a minority of patients unfit for surgery
Cold vs Hot cholecystectomy
Hot = within 72 hours
Cold = 6 weeks later
Cholecystectomy - Complications
Bile leakage;
Jaundice due to ductal injury
Missed stones in the CBD.
Patients may complain of intolerance to fatty meals post-surgery
Management of acute cholecystitis
As per biliary colic, but also IV co-amoxiclav
Management of chronic cholecystitis
Laparoscopic cholecystectomy, with cholangiogram to ensure no stones remain in the common bile duct (if so, removed at ERCP)
Management of Obstructive Jaundice due to stones
ERCP for sphincterotomy and to remove the stones, as an emergency if there is a high fever
Any intervention is preceded with vitamin K, as a lack of bile salts mean this may not have been absorbed well
Elective laparoscopic cholecystectomy
What are jaundiced patients at higher risk of?
A jaundiced patient is at higher risk of infection, venous thrombosis, bleeding and hepatic/renal failure.
Management of ascending cholangitis
Sepsis six bundle, with IV antibiotics
Emergency ERCP
Malabsorption - Sx
Diarrhoea/ steatorrhoea
Weight loss / FTT
Lethargy
Malabsorption - signs of specific deficiencies
- Anaemia (Fe / B12 / Folate)
- Bleeding disorders (vitamin K)
- Oedema (protein)
- Osteomalacia (vitamin D)
- Neuropathy
Malabsorption - Ix
Bloods:
=> FBC, iron studies, B12 & folate, calcium, magnesium, phosphate, lipid profile, LFTs, TFTs, inflammatory markers, clotting & coeliac serology
Stool studies
=> MCS (plus ova, cysts & parasites if recent travel and C. diff toxin if recent ABX)
=> Faecal elastase (if ?chronic pancreatitis)
=> Calprotectin (r/o IBD)
Further studies are guided by clinical suspicion:
Endoscopy:
- OGD + duodenal biopsy – coeliac disease
- Colonoscopy + biopsy – Crohn’s disease
- ERCP – biliary obstruction/chronic pancreatitis
Breath hydrogen analysis
=> ?bacterial overgrowth
Coeliac disease - pathophysiology
= Inflammation of jejunal mucosa in response to gluten
Alpha-glandin is modified by tissue transglutaminase enzymes (TTG)
It then activates an autoimmune reaction against the mucosa
Biopsy of the duodenal mucosa will show flattened mucosa due to loss of villi
=> Hyperplasia of crypts to compensate
=> Also increased intraepithelial lymphocytes
Coeliac disease - presentation
1/3rd are asymptomatic
Non-specific features = IDA, weight loss/ fatigue or apthous ulcers
Dermatitis herpetiformis is a recognised skin manifestation
Coeliac disease - Investigations
FBC (anaemia), clotting (can be prolonged), bone profile (suggestive of osteomalacea)
Endomysial antibodies (EMA) and TTG antibodies present
Duodenal biopsy = gold-standard for diagnosis
Bone densitometry should be performed due to osteoporosis risk
What is the gold-standard for diagnosis of coeliac disease?
Duodenal biopsy
Coeliac disease - Management
Lifelong gluten free diet
=> Verify that gluten-free diet is working with EMA tests
Be aware there is a small increased risk of small bowel lymphoma/adenocarcinoma
Chronic pancreatitis - pathophysiology
Most commonly due to high alcohol intake, leading to inappropriate enzyme activity within the pancreas.
Leads to precipitation of proteins that plug the pancreatic ducts, providing a nidus for infection/calcification, and cause of ductal hypertension
The end result of the process is fibrosis of the parenchyma, and disturbed exocrine function (trypsins, amylases, and lipases).
Chronic pancreatitis - presentation
Epigastric pain, radiating to the back
=> Relieved by sitting forwards or hot water bottles on epigastrium/back
Weight loss, bloating & steatorrhoea
Brittle diabetes
Obstructive jaundice
Symptoms are relapsing, and progressively worsen
What is brittle diabetes?
= insulin dependent DM, characterised by sudden swings in glucose level for no apparent reason
Chronic pancreatitis - diagnosis
Serum amylase/lipase are rarely elevated, butFAECAL ELASTASE is elevated.
Trypsinogen levels >10 in steatorrhoea is diagnostic
There may be signs of alcohol abuse (macrocytic anaemia, GGT)
Transabdominal USS may show pseudocyst
Contrast CT/MRCP can confirm diagnosis with pancreatic calcifications
Chronic pancreatitis - Mx
Analgesia (pain management is a vital part of Mx)
Creon (lipase) and Multivite (fat soluble vitamins)
Monitoring of blood sugars
Treatment of alcohol abuse (complete abstinence)
Low fat diet
Partial pancreatectomy/pancreatojejunostomy may be required if there is unremitting pain, narcotic abuse or weight loss
Pancreatic cancer - aetiology
Typically presents in patients >60 years
Associated with smoking, alcohol, diabetes and chronic pancreatitis (also a genetic component)
- 60% in the head of pancreas
- 25% in the body
- 15% in the tail
Pancreatic cancer - Presentation
Presentation depends on the location of the tumour
HEAD
- Presents earlier
- Painless jaundice (obstructive); but pain may develop as disease progresses
- OE => signs related to obstructive jaundice, Courvoisier’s sign in some cases or palpable abdominal mass
BODY/TAIL
- More likely to present late
- Dull abdominal pain, radiating through to the back
Partially relieved on sitting forwards
- Non-specific B symptoms common
- Often no physical signs on examination
Either can also present as acute pancreatitis or diabetes
What cells form the majority of pancreatic cancers?
The majority of pancreatic malignancies are ductal adenocarcinomas.
Islet cell tumours make up <2% of pancreatic neoplasms
Trousseau’s Syndrome
= thrombosis of the superficial/deep leg veins (thrombophlebitis migrans) related to pancreatic carcinoma
Islet cell tumour - insulinoma
Symptomatic hypoglycaemia events (often in mornings/on exertion) as well as gross weight gain
90% are benign
Islet cell tumour - glucagonoma
Often asymptomatic;
Secondary diabetes may develop
Islet cell tumour - Gastrinoma
Zollinger-Ellison syndrome, with oesophagitis, GI ulcers and diarrhoea
Islet cell tumour - Somatostatinoma
Presents with:
diabetes (insulin release inhibited),
achlorrhydia (gastrin release inhibited)
gallstones (CCK release inhibited)
Pancreatic cancer - investigations
Bloods:
- FBC, U&Es, LFTs (obstructive jaundice)
- CA 19.9 or CEA (non-specific) are useful as a baseline
- Amylase is rarely elevated
USS:
=> Confirms obstruction & duct dilation
CT:
=> Pancreatic mass +/- dilated biliary tree +/- hepatic metastases
Endoscopic USS +/- biopsy
=> Detailed information about the location of the tumour, its local spread and involvement of local lymph nodes & allows biopsy
Staging laparoscopy may be required
Pancreatic cancer - Mx
Patients will be discussed at MDT
Only 10-15% of tumours are suitable for radical surgery (= Whipple’s procedure)
=> Tumour must be <3cm with no metastases in a fit patient
Non-curative surgery provides no survival benefit, if the tumour is non-operable, ERCP/PTC stent insertion may help jaundice/anorexia.
Whipple’s procedure
A portion of the pancreas is removed, along with a portion of the duodenum, the ball bladder and part of the bile duct
The remaining organs are reattached to restore digestive function
- Post-op mortality = ~5%; morbidity is high
- Post-op chemotherapy has been shown to improve survival
Pancreatic cancer - prognosis
Mean survival <6 months
5-year survival <2%; rising to 5-15% following Whipple’s procedure
Ampullary and islet cell tumours carry a better prognosis, as they often present relatively early.
At what level does the oesophageal hiatus lie?
What passes through it?
T10
Oesophagus, vagal nerve trunks, oesophageal branches of the left gastric vessels and lymphatics pass through the diaphragm here
What is a hiatus hernia?
= the protrusion of an organ (typically the stomach) through the oesophageal opening in the diaphragm, into the thoracic cavity.
Sliding Hiatus Hernia
80% of cases
G-O junction slides upwards through the hiatus to lie above the diaphragm.
Usually of no significance, but symptoms may occur due to associated reflux.
Rolling Hiatus Hernia
20% of cases
A small part of the fundus rolls up through the hernia alongside the oesophagus, but the sphincter remains competent below the diaphragm.
The proportion of the stomach that herniates is variable and may increase with time, eventually may evolve to have almost the entire stomach sitting in the thorax.
Very occasionally can present with severe pain, requiring surgical intervention for gastric volvulus/ strangulation.
What are the types of hiatus hernia?
Sliding
Rolling
Mixed
Hiatus Hernia - RFs
Age = biggest risk factor
Increased intra-abdominal pressure:
- Pregnancy
- Obesity
- Ascites
Hiatus hernia - symptoms
vast majority = completely asymptomatic
GORD Symptoms
Vomiting
Weight loss (a rare, but serious presentation)
Bleeding and / or anaemia (secondary to oesophageal ulceration),
Hiccups
Palpitations
Swallowing difficulties (either oesophageal stricture formation or rarely incarceration of the hernia).
Hiatus hernia - Ix
OGD = gold-standard
They can also be diagnosed incidentally, either on a CT or MRI scan.
If there are symptoms of gastric outflow obstruction or weight loss, whereby an upper GI malignancy may be suspected, an urgent CT thorax and abdomen is mandatory.
Hiatus hernia - Initial Mx
INITIAL Mx = CONSERVATIVE
1st line = PPI
=> Acting to reduce gastric acid secretion and aiding in symptom control.
Lifestyle modification:
=> Including weight loss, alteration of diet (earlier meals, smaller portions), and sleeping with the head of the bed raised.
=> Smoking cessation and reduction in alcohol intake should be advised
What is 1st line treatment for a symptomatic hiatus hernia?
PPI
Hiatus hernia - when is surgical Mx indicated?
- Remaining symptomatic, despite maximal medical therapy
- Increased risk of strangulation/volvulus*
=> rolling type or mixed type hernia, or containing other abdominal viscera) - Nutritional failure (due to gastric outlet obstruction)
Mx of suspected strangulated/obstructed/volvulus hiatus hernia
immediate stomach decompression via a NG tube prior to surgical intervention.
Gastric volvulus
the stomach twists on itself by 180 degrees, leading to obstruction of the gastric passage and tissue necrosis
Requires prompt surgical intervention.
Typically presents with Borchardt’s triad:
1. Severe epigastric pain
2. Retching without vomiting
3. Inability to pass an NG tube
What is Borchardt’s triad?
- Severe epigastric pain
- Retching without vomiting
- Inability to pass an NG tube
Indicates likely stomach volvulus
How is hiatus hernia repaired surgically?
The hernia is reduced from the thorax into the abdomen and the hiatus reapproximated to the appropriate size. Any large defects usually require mesh to strengthen the repair.
The gastric fundus is wrapped around the lower oesophagus and stitched in place (to strengthen LOS and keep GOJ in place)
Complications of hiatus hernia surgery
Recurrence
Inability to belch (due to reinforcement of LOS) => bloating
Dysphagia (if fundoplication is too tight)
Fundal necrosis (if blood supply disrupted)
What are the two functions of the pancreas?
- ENDOCRINE
- Alpha and beta cells
- Secretes hormones like insulin and glucagon into the bloodstream for glucose homeostasis. - EXOCRINE
- Acinar cells
- Secrete amylases, lipases and proteases into the duodenum to aid digestion.
How does the pancreas protect itself from its digestive enzymes?
Keeping the enzymes away from sensitive tissues in vesicles (zymogen granules).
Storing the enzymes as proenzymes (Zymogens) which first need to be activated by the protease trypsin.
Causes of acute pancreatitis
I GET SMASHED:
Idiopathic (20%)
Gallstones (40%)
Ethanol (35%)
Trauma (15%)
Steroids
Mumps (+ CMV, EBV)
Autoimmune
Scorpion venom
Hyper/hypo (hyperlipidaemia, hypercalcaemia, hypothermia)
ERCP
Drugs (thiazides, sulphonamides, ACEIs, NSAIDs)
What are the most common causes of acute pancreatitis?
Gallstones
Ethanol
Acute Pancreatitis - Pathophysiology
An initial insult to the pancreas leads to leakage of activated pancreatic enzymes into the pancreatic and peripancreatic tissue, causing an acute inflammatory reaction.
The liberation of digestive enzymes results in extensive local tissue necrosis, particular fat necrosis.
Litres of extracellular fluid collect in the gut, peritoneum and retroperitoneum.
How does alcohol abuse cause acute pancreatitis?
Causes increased zymogen release from acinar cells; and also causes a decrease in fluids and bicarbonates in ducts.
This means pancreatic juices are thick and sludge-like (with many enzymes, but not much fluid) which can form a plug and block ducts.
Increase in pressure can cause distension of the ducts.
Distension can bring zymogen granules in contact with lysosomes which may contain digestive enzymes – can cause a cascade of pancreatic autodigestion.
In response to this, there is a release of cytokines, leading to an immune response.
How do gallstones cause acute pancreatitis?
gallstones => block Sphincter of Oddi
This then becomes a similar situation to alcohol-induced acute pancreatitis where there is backing up to pancreatic juices.
Acute Pancreatitis - Symptoms
Gradual/sudden onset severe epigastric pain
Classically radiates to the back
May be relieved by sitting forward
N&V is prominent
Acute Pancreatitis - Signs
Tachycardia (shock in severe disease)
Fever
Ileus
Jaundice
Rigid abdomen
Cullen’s sign
Grey-Turner’s sign
(In general, bruising signs occur after 48 hours and are an indicator of grave prognosis)
Cullen’s sign
= peri-umbilical bruising, due to peritoneal haemorrhage
Grey-Turner’s sign
= bruising of the flanks
Acute Pancreatitis - Glasgow Scoring System
Used to assess severity and prognosis
P – PaO2 <8 kPa A – Age >55 N – Neutrophils, WCC > 15x109/L C – Calcium <2mmol/L R – Renal, urea >16 mmol/L E – Enzymes, LDH >600 IU/L or AST >200 IU/L A – Albumin <32 g/L S – Sugar, glucose >10 mmol/L
A score of 3 or more is severe disease.
Acute Pancreatitis - APACHE II Scoring System
allocates points for assessment of clinical parameters (A), age (B) and co-morbid disease (C).
Scores >9 indicate severe pancreatitis
Mortality is high if this score increases after admission
Acute Pancreatitis - Ranson Criteria
includes age and lab scores on admission, then clinical findings at 48 hours to give a mortality risk figure.
Acute Pancreatitis - Bloods
Baseline FBC, CRP, U&E, LFT, glucose and calcium to assess progression
Raised serum amylase (>1000 U/mL)
=> Very sensitive if measured within 24h of onset and >3x normal
Raised serum lipase = more sensitive and specific
ABG to monitor oxidation and acid-base status
What can cause raised serum amylase?
Acute pancreatitis
Cholecystitis,
GI perforations
Mesenteric infarctions
Acute Pancreatitis - Imaging
AXR
Erect CXR - to assess for perforations
CT:
=> Can show enlarged pancreas with stranding, abscess, collections, necrosis, or pseudocyst
MRCP:
=> Better visualisation of collections and also the ductal system
Endoscopic USS:
=> Newest method of visualising the pancreas, but more rarely used.
Acute Pancreatitis - Initial Mx
ACBDE approach, then supportive treatment
Aggressive IV fluid resuscitation, catheterise and consider CVP monitoring
Regular Obs
Daily bloods (FBC, U&E, Calcium, glucose, ABG)
Analgesia
NBM until pain free – “rests” the pancreas
NG tube suction if ileus/emesis
PPI to prevent stress ulcer
Anticoagulation
Consider HDU/ITU
Acute Pancreatitis - Further Mx to consider
ABX in severe cases /infection/necrosis
Laparotomy and debridement if abscess/pancreatic necrosis on CT
Urgent ERCP (if due to gallstones)
Find & treat the causative agent
Acute Pancreatitis - early complications
Hypovolaemic Shock
ARDS
Renal failure
DIC
Hypocalcaemia
Hyperglycaemia
Acute Pancreatitis - late complications
Pancreatic pseudocyst
Abscesses
Bleeding from elastase eroding a minor vessel
Thrombosis of splenic/gastroduodenal aa. (causing bowel necrosis)
Fistulae
Necrosis of pancreas following pancreatitis
• The inflammatory process causes blood vessels to become leaky and then rupture, leading to pancreatic tissue swelling.
• This causes premature activation of lipases which then starts to destroy peripancreatic fat.
• The fat and tissues liquefy and can start necrosing (process called Liquefactive Haemorrhagic Necrosis)
What is a pancreatic pseudocyst?
= a localised fluid collection, rich in pancreatic enzymes, with a non-epithelialised wall containing fibrous/granulation tissue.
Commonly occur in pancreatitis, from day 10 onwards
Form due to disruptions of the pancreatic duct, leading to extravasation of enzymes.
How is a pancreatic pseudocyst managed?
Most resolve without intervention - only require supportive care and regular monitoring.
Indications for drainage include:
- Complications (bleeding / infection)
- Relief of symptoms
- Concern about malignancy (cytology and cystic fluid analysis)
Pancreatic psuedocyst - presentation
Deep, persistent abdominal pain
Abdominal mass
Anorexia (due to pressure on adjacent bowel)
Jaundice
Sepsis (if infected)
Pleural effusion
Pancreatic pseudocyst - Ix
Abdominal CT = gold-standard if pseudocyst is suspected
MRI may be better to differentiate pseudocyst from necrosis
ERCP/endoscopic USS can be useful to plan therapy if endoscopic drainage is being considered.
What is BPH?
benign prostatic hyperplasia
Benign nodular/ diffuse proliferation of glandular layers of the prostate, leading to enlargement of the inner transitional zone.
Affects 70% of those >70.
Presentation of BPH
FILLING Sx - Due to bladder overactivity
=> Frequency, nocturia, Urgency
VOIDING Sx - Due to bladder outlet obstruction
=> Hesitancy/ dribbling, Poor/ intermittent stream, Strangury, Retention with overflow incontinence/ acute retention
Sx DUE TO COMPLICATIONS
=> Occasionally haematuria (due to rupture of veins into the cyst but this is a red flag), Symptoms of associated UTI, Bladder stones, Chronic renal failure
Complications of BPH
UTI,
overflow incontinence,
bladder calculi,
bladder diverticulae,
bilateral hydronephrosis and renal failure.
BPH - Initial Investigations
Hx:
- Clarify symptoms and concerns
- QoL, international prostate symptom score (IPSS)
Abdo exam and DRE:
- ?signs of a distended bladder
- DRE - typically sulcus is still palpable, smooth & round (not craggy)
Urine dipstick, urinalysis and MCS
Bloods – FBC, U&Es, PSA* (<4ng/ml normal, can be adjusted for age and prostatic size)
Frequency/volume chart.
Uroflowmetry
15ml/sec usually normal.
<12ml/sec usually indicates obstruction or weak bladder contractility
Need to remember that it requires >150mL to be voided (not possible for some patients)!!!
Prostate-Specific Antigen
= a glycoprotein produced by normal and cancerous prostate cells.
Secreted by prostate epithelial cells into prostatic fluid, where its function is to liquefy semen and thus allow spermatozoa to move more freely.
Although PSA is secreted into prostatic fluid and semen, small amounts of PSA are present in blood.
Interpreting PSA results can be difficult because various things can increase/decrease serum PSA levels.
What can increase serum PSA levels?
Prostate enlargement.
Older age
Infection (e.g. prostatitis and urinary tract infection).
Physical causes, (including following vigorous exercise, digital rectal examination, catheterization, and prostate biopsy)
Prostate cancer
A normal prostate
What can decrease serum PSA levels?
Certain drugs (including 5-alpha reductase inhibitors, aspirin, statins, and thiazide diuretics)
Obesity.
What can cause normal PSA levels?
Prostate enlargement.
Prostate cancer.
Infection.
A normal prostate
BPH - Mx
Mild:
- Reassure not cancer, watchful waiting and follow-up.
- Lifestyle modification – avoid alcohol/caffeine, relax when voiding, void twice in a row to help emptying, bladder retraining therapy.
Moderate - Severe:
- Alpha blockers (e.g. doxazosin, tamsulosin)
- 5-alpha reductase inhibitors (e.g. finasteride, dutasteride)
Severe = Surgery
- Transurethral resection of the prostate (TURP) or open prostatectomy
- Laser, prostatic urethral lift, steam treatment
- Vascular: prostatic artery embolization
How should acute urinary retention in BPH be managed?
If acute retention – attempt urethral catheter drainage (suprapubic if urethral not possible).
Alpha blockers in BPH
Adrenoceptor antagonists, blocks receptors on prostatic SmM (stromal)
SEs: postural hypotension, drowsiness.
5-alpha reductase inhibitors in BPH
5-AR enzyme converts testosterone into dihydrotestosterone, reduces prostate volume
SEs – impotence, reduced libido, excreted in semen (condom use needed)
Transurethral resection of prostate - complications
Complications:
- TURP syndrome (dilutional hyponatraemia),
- UTI/Urethral stricture,
- Retrograde ejaculation,
- Prostate can regrow/perforate bleeding,
- incontinence,
- impotence,
- bladder neck stenosis.
Tend to require catheter for few days post-op.
What is the most common histopathology of prostate cancer?
Most are adenocarcinomas:
generally, occurs in the posterior, outer, glandular portion of tissue (so biopsy must be transrectal).
Prostate cancer - RFs
Age
FHx
Raised testosterone levels.
Prostate cancer - spread
Can spread:
- locally (seminal vesicles, bladder, rectum);
- by lymphatics (iliac/ para-aortic nodes);
- by haematogenous spread (classically to the bone).
Prostate cancer - symptoms
Often asymptomatic (found on PR/ histology of BPH or suspected by raised PSA)
Symptoms can depend on extent of spread:
=> LOCAL disease = Weak stream, hesitancy, sensation of incomplete emptying, urinary frequency, urgency, urge incontinence.
=> LOCALLY INVASIVE Disease = Haematuria, dysuria, incontinence, haematospermia, Perineal and suprapubic pain, Obstruction of ureters, Impotence, Rectal symptoms (tenesmus)
=> METASTATIC DISEASE
Prostate cancer - O/E
PR Exam => hard, craggy, irregular prostate, possible nodule, immobile and palpable seminal vesicles
What is special about the metastasis of prostate cancer to the bone?
Most cancers cause lytic lesions, but prostate cancer causes sclerotic bony mets
Prostate cancer - Ix
DRE
PSA – >10ng/ml suggestive of tumour (better for monitoring than for diagnosis)
Multiparametric MRI
=> Vital for Gleason score which helps to decide management
Biopsy:
=> most common approach is transrectal ultrasound-guided (TRUS) biopsy
Bone XR/scan and CT for staging
Gleason score
two areas of prostate tissue are graded out of 5 and added together to give a combined score out of 10.
6 or less, considered low risk
8 or more, considered high risk
Prostate Cancer - Mx
Localised Prostate Cancer (T1/2):
- Active surveillance (regular PSA, DRE, re-biopsy monitoring)
- Radiotherapy or brachytherapy: lower risks of impotence and incontinence
- Radical prostatectomy (higher risk)
Advanced Prostate Cancer (T3/4):
- Active surveillance not recommended => choice of radiotherapy or surgery offered
Metastatic Disease:
- Hormonal therapy, GnRH agonists, e.g. Goserelin/ buserelin (reduce testosterone production)
- Used palliatively or as an adjunct to a curative therapy in high-risk disease
- An anti-androgen (e.g. cyproterone acetate) is co-prescribed initially to prevent the early rise in testosterone.
Causes of bladder outlet obstruction
LUMINAL
Bladder Tumour
MURAL
Urethral stricture
Congenital abnormalities
Neuropathic bladder
EXTRAMURAL
BPH / prostate cancer
Phimosis / paraphimosis
Bladder Outlet Obstruction - clinical presentation
SYMPTOMS
- Suprapubic pain
- Hesitancy and diminished force of the stream
- Terminal dribbling
- Overflow incontinence
- Signs of infection (due to stasis of urine)
SIGNS
- Palpable, full bladder
- Loin tenderness / palpable hypernephrotic kidney
- Enlarged prostate on PR (poor sensitivity for prostatic obstruction)
Bladder Outlet Obstruction - Ix
- Bloods – FBC, U&Es
- Urine – dip, MC&S
- USS – hydronephrosis
- CT/MRI
Bladder Outlet Obstruction - Mx
Catheterisation (suprapubic/urethral) – beware of large diuresis following relief of obstruction
Find and treat underlying cause
What is phimosis?
= narrowing of the preputial orifice, resulting in the inability to retract the foreskin.
Causes of phimosis?
When is phimosis normal?
Causes:
- Most often idiopathic
- Congenital
- Chronic balanitis
- Traumatic forcible retraction of the foreskin
Normal in children <2 years old.
Phimosis - presentation
In children, it may present as ballooning of the foreskin and poor stream during urination.
In adults, it presents as pain during intercourse and inability to retract the foreskin.
Phimosis - Mx
Good hygiene
Steroid cream (to help soften the foreskin)
Circumcision if troublesome symptoms.
Paraphimosis
Results from pulling a tight foreskin over the glans, obstructing venous return and leading to a swollen, painful glans.
As the gland swells, it becomes increasingly difficult to replace the foreskin.
Paraphimosis - causes
- After an erection/ vigorous sex,
- Chronic balanitis
- Following urethral catheterisation (remember to replace the foreskin).
Paraphimosis - Tx
Emergency Tx involves local anaesthesia and then applying pressure to the glans, or slitting the foreskin dorsally.
Circumcision is offered after paraphimosis to prevent recurrence.
Carcinoma of the penis - RFs
50% of cases associated with HPV 16/18
More common in smokers, and immunosuppression
Carcinoma of the penis - presentation
Presents as persistent itchy red patch on the penis, progressing to an infiltrating ulcer.
There is never any urethral involvement/symptoms
Carcinoma of the penis - Ix
Diagnosis is with punch biopsy => squamous cell carcinoma
Carcinoma of the penis - Mx
Early cancers – cured with radiotherapy or penis-preserving excision
Inguinal LN involvement – more radical Tx required (success rates lower)
What is priapism?
Persistent (hours to days) erection of the corpora cavernosa of the penis
Reduction in blood flow can lead to ischaemia.
Priapism - causes
Usually idiopathic
Trauma
Sickle-cell disease
Intra-cavernosal injections for impotence
Priapism - Mx
- Ice packs
- Alpha-agonists
- Selective embolisation
- Aspiration of corpus cavernosum
- Surgical intervention
Peyronie’s Disease
Upwards curvature of the penis when erect
Cause = unknown
=> Fibrous scarring following trauma is a possibility.
Peyronie’s Disease - Mx
Managing psychological effects
Surgical intervention may help penetration.
What causes penile erection?
Erection requires increased arterial inflow, and occlusion of venous outflow.
This is mediated by parasympathetic fibres from S2-4.
Causes of erectile dysfunction
Ageing (70% of 70 year olds have difficulty obtaining an erection)
Neurogenic – e.g. spinal cord lesion/stroke/nerve-damage
Vascular – HTN/arterial disease
Hormonal – DM/pituitary failure
Pharmacological – alcohol, anti-hypertensives, oestrogens, tranquilisers
Psychogenic
Erectile Dysfunction - Ix
Cause is usually determined using history and examination
+ Urine dipstick
+ Hormone screen
Erectile Dysfunction - Mx
Treat reversible medical cause / correcting hormonal disturbances
Smoking cessation, reduce alcohol
Sildenafil (Viagra) – causes vasodilation of corpus cavernosum
=> (CI in patients with hypotension)
Intracavernosal alprostadil (PGE-1) injection
Vacuum condoms or inflatable intrapenile prostheses if these treatments fail
Ectopic Testes
An uncommon form of undescended testes
The testicle has strayed from the normal line of descent
Most common site is superior inguinal pouch
Undescended testes
Common
The testis has followed the normal route of descent but stopped short of the scrotum
Most commonly due to a local defect in development, and the affected testis is small and accompanied by a persistent processus vaginalis.
Retractile testes
Normal testes, with an excessive cremasteric reflex.
They are often confused with maldescended testes, but on examination they can be found at the external inguinal ring, and can be coaxed down.
Maldescended testes - Mx
Retractile testes are normal and require no treatment
Ectopic/undescended testes must be surgically placed into the scrotum (orchidopexy) if they are to function as a reproductive organ (recommended age = 6 months).
Complications of maldescended tests
Defective spermatogenesis
Increased risk of torsion, malignancy and indirect inguinal hernia.
Approach to a scrotal lump/swelling
- Can I get above it?
Yes => primary scrotal swelling
No => ?inguinal hernia
If primary:
2. is it cystic or solid?
- Is it separate to the testes?
ALWAYS suspect torsion and order doppler USS to exclude if any suspicion.
=> Cremasteric reflex – absent ipsilaterally in torsion
What is an Epididymal Cyst ?
A common cause of scrotal lump
Occurs due to cystic degeneration of epididymal structures.
Previously known as spermatocoele
Epididymal Cyst - Presentation
- Lump should be cystic (transilluminates) and separate from the testes (almost always at the upper pole)
- Contained fluid can be clear/contain sperm/be milky (previously termed spermatocoele)
- Can sometimes be painful or the bulkiness can be troublesome
Epididymal Cyst - recurrence
If they cause significant symptoms they may be excised (rather than just aspirated, as this can lead to recurrence).
What is a hydrocoele?
Most common cause of scrotal enlargement
Due to an excessive collection of serous fluid in the processus vaginalis
Hydrocoele - presentation and causes
A fluctuant swelling that transilluminates
PRIMARY (idiopathic): also “vaginal hydrocoele”, separate from the peritoneal cavity
SECONDARY: fluid collects due to underlying inflammation in the epididymis/testes or an underlying cancer.
Hydrocoele - Ix
O/E - soft, fluctuant lump; will transilluminate
May need USS to r/o more severe underlying pathology
Hydrocoele - Mx
Most often, reassurance of benign nature is suitable treatment
If swelling is causing problems, then excision of sac is possible (aspiration can lead to recurrence).
What is Varicocoele?
= varicosities of the pampiniform plexus
Varicocoele - features
Most commonly on the left (90%)
Patients complain of a dragging sensation and ache
Feels like a “bag of worms” on palpation, and may only be palpable in a standing position
Associated with reduced spermatogenesis and subfertility
Why is varcocoele more common on the left?
The left testicular vein drains into the left renal vein at a right angle, rather than the right testicular vein that drains into the IVC obliquely.
Valvular incompetence at the junction of the left renal vein is the pathological process that leads to varicocoele.
Rarely, it can be caused by a left renal tumour or other pathology compressing the left renal vein.
Varicocoele - Mx
Usually, reassurance of benign nature is enough.
Treatment options are radical embolisation of the left renal vein, or surgical ligation and division of the testicular veins.
Testicular Torsion
= a urological/ surgical emergency.
The testicle twists on itself, obstructing venous return => ischaemia
Testicular torsion - causes
Usually due to a congenital abnormality – e.g. maldescent/ bell-clapper testes.
Testicular Torsion - Presentation
In adolescents, often with a history of mild trauma or previous attacks of pain due to partial torsion and spontaneous resolution.
Sudden onset severe pain in the groin/ lower abdomen (T10)
Often accompanied by N&V.
Can be intermittent and brought on by physical activity.
Testicular Torsion - O/E
Unilateral hot, swollen, tender testis, sometimes lying high and transverse within the scrotum
Absent cremasteric reflex.
Raising testis worsens pain.
Testicular Torsion - Ix
Torsion is a CLINICAL DIAGNOSIS so this wouldn’t be done, but: doppler USS shows a lack of blood supply to the testes.
Urine dip to exclude infective cause.
If in doubt, surgical exploration
Testicular Torsion - Mx
URGENT SURGERY – manual distortion can be attempted under analgesia for temporary relief of pain
=> Viable testis = surgically untwisted and sutured to the tunica vaginalis with fixation of the contralateral testicle also.
=> Non-viable testis = orchidectomy an fixation of the contralateral testicle also.
How successful is testicular torsion surgery?
Salvage rate of 80% for patients operated on within 6 hours of initial torsion.
Torsion of testicular Appendage
Similar to testicular torsion, but it is an embryological remnant that twists
Less painful, causes a small blue nodule to be visible under the scrotum.
Classically occurs at the start of puberty
Testicular Tumour - RFs
Undescended/ectopic testes (greater risk if not in the anatomical position by 13 years)
Infertility
Hypospadia
FHx / PMHx
What are the two main forms of testicular tumours ?
Seminomas
Non-seminomatous germ cell tumours (NSGCTs) – include teratomas, yolk sac tumours and choriocarcinomas
Testicular Tumour - Seminoma
Arises from the cells of the seminiferous tubules, in 30-40 year olds
It has a solid appearance macroscopically
Microscopically, can range from well-differentiated spermatocyte cells to undifferentiated round cells.
Testicular Tumour - teratoma
Arises from totipotent germ cells, in 20-30 year olds
Cystic appearance macroscopically, and variable cell types microscopically
Testicular Tumour - Spread
Local spread of testicular tumours through the capsule is rare
Lymph node spread is to the para-aortic nodes
Bloodborne spread is early to the lungs and liver
Testicular Tumour - Presentation
PAINLESS LUMP in the testes
Hydrocoele
Haematospermia
Symptoms of metastases (e.g. abdominal swelling, breathing difficulties)
Drain to para-aortic nodes, so first palpable node is likely to be supraclavicular
Rarely – as a painful, rapidly enlarging swelling; or gynaecomastia due to paraneoplastic syndrome
Testicular Tumour - Ix
Scrotal USS
Tumour markers
=> NSGCTs – usually produce AFP, some produce bHCG
=> Seminomas – never produce AFP, 10% produce bHCG
(^^Useful for diagnosis and also follow-up)
CT CAP – for staging
Testicular Tumour - Mx
If suspected, early surgical exploration through an inguinal incision is indicated.
Orchidectomy for obvious/previously diagnosed tumours
Biopsy and frozen section if diagnosis unclear (then orchidectomy if confirmed)
Retroperitoneal LN dissection may also be undertaken
Post-surgical radiotherapy (for seminomas) or combination chemotherapy (NSCGTs)
Sperm banking is used due to the risk of infertility.
Epididymo-Orchitis - causes
Acute infections usually arise due to an ascending infection via the vas deferens.
=> After gonococcal/non-gonoccocal urethritis
=> After UTI due to E. coli
Can spread haematogenously – e.g. TB, mumps
Epididymo-Orchitis - Presentation
Painful swelling of the epididymis
Often with secondary hydrocoele
History of discharge (STI) /dysuria (UTI)
Examination of the prostate may reveal co-existent prostatitis
Positive Phren’s test
Epididymo-Orchitis - Investigation
First catch urine MCS + STI screen
USS
Epididymo-Orchitis - Mx
6 weeks ciprofloxacin (add doxycycline if suspecting chlamydia)
Analgesia and scrotal support may provide pain relief
Acute Bacterial Prostatitis - Presentation
Fever/rigors,
Perineal pain,
Difficulty voiding,
UTI symptoms
Pain on ejaculation / haematospermia
PR – prostate exquisitely tender and enlarged
Often presents alongside epididymo-orchitis
Acute Bacterial Prostatitis - Mx
Mx = 6 weeks ciprofloxacin
What is urethritis?
= discharge and discomfort within the penis in men.
Generally split into gonococcal urethritis and non-gonococcal urethritis (of which the most common cause is chlamydia).
Gonococcal urethritis - symptoms
Gonorrhoea = gram -ve intracellular diplococcus spread by sexual contact.
SYMPTOMS:
• 50% of women and 10% of men are asymptomatic
• Men present with dysuria and urethral discharge, and can ascend to cause epididymitis or prostatitis
• Women present with vaginal discharge, pelvic pain, dysuria, and IMB
Gonococcal urethritis - Ix
• Gram stain (for gram negative diplococci) and culture of the discharge
• NAAT from urine as an alternative
• Blood culture if suspecting disseminated gonococcus
• Test for co-existing pathogens (chlamydia/syphilis)
Gonococcal Urethritis - Mx
Stat IM ceftriaxone
Follow-up and repeat cultures 72 hours after treatment.
Trace and treat all sexual contacts
Non-gonococcal urethritis (chlamydia) - Sx
Asymptomatic in 50% of men, and 80% of women
Men – dysuria, discharge, can ascend (epididymitis)
Women – discharge, bleeding, and lower abdo pain
Non-gonococcal urethritis (chlamydia) - Ix
First void urine in men, endocervical swab in women
Cell culture is gold standard but takes time, so immunofluorescence/PCR are used.
Assess for co-existing gonnorhoea.
Non-gonococcal urethritis (chlamydia) - Mx
1g azithromycin as a single dose,
OR 7 day course of doxycycline/ erythromycin
What is urethral syndrome?
= frequency/dysuria without infection (abacteriuric)
Can be caused by post-coital bladder trauma, atrophic vaginitis, interstitial nephritis.
Urethral Trauma
Urethral tears require special urological action.
=> Need contrast urethrography to determine if partially or fully torn
If partially intact, it can be treated conservatively by prolonged catheterisation.
Complete tears require suprapubic catheterisation and then formal repair.
What is a urethral stricture?
= a scar of the urethral epithelium, which commonly extends into the underlying corpus spongiosum.
The fibroblastic activity leads to a shortening of urethral length, and narrowing of luminal size.
Causes of urethral strictures
- Blunt perineal trauma (straddle injury, pelvic fracture)
- Iatrogenic – catheter insertion/long-term catheterisation
- Gonoccocal/non-gonococcal urethritis
- Balanitis xerotica obliterans (white atrophic plaques leading to phimosis)
Urethral stricture - presentation
Obstructive voiding symptoms that worsen gradually
Initial frequency/dysuria
Hesitancy/straining
Urinary retention
Splayed stream (if meatal stricture present)
O/E:
- firm areas consistent with periurethral scarring
- The patient is often <50, and there will be no prostate abnormalities
Urethral Stricture - Ix
Uroflowmetry
Urethrogram – determine stricture length, location, calibre, significance.
Urethroscopy may also be of use
Urethral Stricture - Mx
1st line – optical urethrotomy
Urethroplasty for those that recur (50%)
Transitional Cell Carcinoma
= a tumour of the transitional cell epithelium (lines the calyces, renal pelvis, ureter, bladder and urethra)
=> Bladder tumours are 50x more common than tumours of the ureter/renal pelvis.
Transitional Cell Carcinoma - RFs
Smoking
Aromatic amines – rubber/plastic/dye industry workers
Chronic cystitis
Pelvic irradiation
Transitional Cell Carcinoma - Presentation
Painless haematuria +/- clots (= most common presentation)
Recurrent UTI
Voiding symptoms
Pain from invasion of local structures
Bladder Transitional Cell Carcinoma - Investigations
Urine MCS / cytology (cancers can cause sterile pyuria)
Cystoscopy and biopsy (gold standard)
CT/MRI or lymphangiography to assess spread
Transitional Cell Carcinoma - Mx
Carcinoma in situ / T1 bladder carcinomas
=> Transurethral resection on bladder tumour (TURBT) at cystoscopy with intravesical chemotherapy
T2-T3 tumours, or high grade tumours:
=> Radical cystectomy is gold-standard, with pre-operative chemo
=> An ileal conduit is used to leave a urostomy
T4 (invasion beyond the bladder)
=> Treated palliatively
Long-term follow-up with cystoscopy is required
Squamous Cell Carcinoma of Bladder
Rarer than TCC
Presents similarly to TCC
RFs = anything that irritates the lining of the bladder, leading to squamous metaplasia
=> E.g. schistosomiasis or bladder calculi
Bladder trauma
Intraperitoneal bladder rupture
=> Treated with laparotomy and suturing of the bladder
Extraperitoneal bladder rupture
=> Treated conservatively with prolonged urethral/suprapubic catheterisation.
Renal Cell Carcinoma
vascular tumours, arising from the proximal tubular epithelium
Account for 90% of renal tumours
Main risk factor is prolonged haemodialysis (15% develop this)
Renal Cell Carcinoma - presentation
50% are incidental findings
10% present as classic triad – haematuria, loin pain & abdominal mass – plus vague B symptoms
Rarely, invasion of left renal vein leads to varicocoele
There may be signs of polycythaemia / HTN (if renin/EPO secretion)
Renal Cell Carcinoma - Ix
Urine cytology
USS to differentiate solid from cystic mass
CT/MRI to assess tumour
CXR (“cannonball” mets)
Renal angiography (if considering partial nephrectomy)
Renal Cell Carcinoma - Mx
Radical nephrectomy
Partial nephrectomy
• If peripheral tumour smaller than 5cm
• If bilateral tumours or poor kidney function
Post-op chemotherapy
Wilm’s Tumour
An undifferentiated mesodermal tumour (nephroblastoma)
Generally presents at 3.5 years with:
- Flank pain
- Abdominal mass
Should NOT be biopsied (risk of spread due to tumour fragility!)
Treatment:
- Pre-operative chemotherapy
- Nephrectomy
Renal Cysts - causes and presentation
Solitary/multiple cysts
Commonly occur in the elderly (50% will have a renal cyst by age 50%)
Presentation:
- Often asymptomatic
- Can cause haematuria/pain
Polycystic kidney disease is a common cause, with other causes being medullary cystic disease, or medullary sponge kidney
Acute ureteric obstruction
= blockage of ureter, leads to enlargement of the urinary tract superior to the obstruction
Causes can be luminal, mural, or extra-mural
What is hydronephrosis?
Dilation of the renal pelvis
Luminal causes of ureteric obstruction
Calculus
Sloughed renal papilla
Blood clot
TCC of renal pelvis/ureter
Bladder tumour
Mural causes of ureteric obstruction
Ureteric stricture (TB, post-calculus, post-surgery)
Congenital pelviureteric neuromuscular dysfunction
Congenital megaureter
Extra-luminal causes of ureteric obstruction
Pelviureteric compression (due to external tumours, diverticulitis, AAA, retroperitoneal fibrosis)
Acute ureteric obstruction - presentation
Varying loin pain, greater when urine volume increases
Anuria (if complete bilateral obstruction) or polyuria (if partial blockage causes renal impairment)
Loin tenderness
Palpable hydronephrotic kidney
Acute ureteric obstruction - Ix
ALWAYS exclude acute scrotum and AAA in men and pregnancy in women.
- Urine dip (positive blood) + MCS
- USS to confirm upper tract dilation
- Abdominal plain film
- CT to outline detailed cause of obstruction
- Retrograde pyelogram may be used at cystoscopy to further outline ureteric abnormalities (e.g. TCC)
Acute ureteric obstruction - Mx
Nephrostomy may be required to decompress the pelvicalyceal system,
=> preserving kidney function
=> preventing infection from developing
Surgical management (e.g. stenting) may be required depending on the cause
Location of renal calculi
Calculi can form in the collecting ducts and may be deposited anywhere from the renal pelvis to the urethra.
Classic sites are the:
1. Pelviureteric junction,
2. Pelvic brim
3. Vesicoureteric junction
Composition of renal calculi
Calcium oxalate (75%)
Magnesium ammonium phosphate
Urate-based
RFs for renal calculi
- Obesity
- Dehydration
- FHx/PMHx of stone disease
- Anatomical abnormalities
Renal/ureteric Calculi - Presentation
can present in many ways:
- Renal colic – excruciating “loin to groin” spasms, with N&V ; occurs if stone is impacted in the ureter.
- Dull loin pain – if the stone is in the major/minor calyx
- UTI – secondary to partial/complete obstruction
O/E => There are few clinical signs on examination
Renal/ureteric Calculi - Ix
Bloods – include calcium, phosphate, glucose, bicarbonate, and urate levels
Urine dip – 95% positive for blood; r/o infection; beta-HCG is vital
Urine MCS
Imaging:
• AXR (80% visible)
• Non-contrast CT KUB (99% visible, can also also exclude abdominal DDx)
Renal/ureteric Calculi - Mx
A-E Assessment (IV fluids if no oral intake)
75mg diclofenac IM unless contraindicated
=> Beware of post-renal AKI
IM metoclopramide if severe nausea/vomiting
IV ABX according to guidelines if signs of infection
Assess whether admission is required, if there is…
- Still severe pain at 1 hour
- A risk of AKI
- Signs of shock/infection
- Uncertainty over diagnosis
Consider Active (surgical) Treatment
Conservative (medical) Treatment
Indications for active (surgical) Tx of ureteric calculus
- Low chance of spontaneous passage (>10mm)
- Persistent pain
- Ongoing obstruction
- Signs of infection
- Renal insufficiency
Active (surgical) Treatment of obstructing ureteric/renal calculus
Extracorporeal shockwave lithotripsy (ESWL)
If hydronephrosis present, may need a percutaneous nephrostomy to decompress the pelvicalyceal system prior to outpatient ESWL
Uretoscopy
=> Various energy sources (e.g. laser) can be used to break up the stone
Percutaneous nephrolithotomy
=> Used for renal (not ureteric) calculi that do not respond to ESWL
Extracorporeal shockwave lithotripsy (ESWL) Procedure
Outpatient procedure for ureteric calculus
Shockwave is focused on the stone to break it up, so it can be passed spontaneously
If hydronephrosis present, may need a percutaneous nephrostomy to decompress the pelvicalyceal system prior to outpatient ESWL
Conservative (medical) Treatment for renal/ureteric calculi
Tamsulosin (1st line; alpha-blocker) or nifedipine – increase the rate of spontaneous expulsion
Patient Education, if sending them home
Refer the patient to urology within one week for r/v
If conservatively managing a ureteric calculi, what advice should be given to the patient?
Many stones (80%) will pass naturally
Advise to maintain a high fluid intake
Advise to return if there is any increase in pain or signs of infection
First-time stone formers should also be advised to pass urine through a sieve to collect the stone for analysis
Bladder Calculi - causes
Bladder outflow obstruction
Presence of a foreign body (prolonged catheterisation)
Upper urinary tract stone passing down
Bladder calculi - presentation
Symptoms of UTI (there is often significant bacteriuria)
Can be distinguished from UTI as haematuria and pain generally occur at the end of micturition as the bladder contracts
In males, the pain can be felt at the tip of the penis rather than a general burning
May be perineal pain if there is trigonitis
Anuria/bladder distension if the stone is obstructing
Bladder calculi - Ix
Same as for upper tract stone
Bladder calculi - Mx
Medical expulsive therapy
ESWL if the stone is large
What are the complications of bladder calculi
Can predispose to SCC
What is the definition of an aneurysm?
= a focal dilation of an artery >150% of its normal diameter
How can an aneurysm present?
Asymptomatic (found incidentally)
Mass effects – pressure on adjacent structures
Embolic events – due to development of mural thrombi
Haemorrhage – due to rupture
What is an AAA?
= dilations of the abdominal aorta to >3cm
RFs for AAA
Male gender (5x more common in males)
Increasing age
Smoking
HTN
FHx
Hyperlipidaemia
AAA - complications
Main complication = AAA rupture
Retroperitoneal leak
Embolisation
Aortoduodenal fistula
AAA - Presentation
NORMALLY ASYMPTOMATIC => mostly detected as an incidental finding or during screening.
PRESENTATION OF AAA RUPTURE:
- Severe continuous/intermittent epigastric pain, radiating to the back/groin
- Pulsatile, expansile abdominal mass
- Signs of shock / haemodynamic compromise
“Classic” Triad = flank or back pain, hypotension, and a pulsatile abdominal mass
What should be considered in any male <50 presenting with renal colic?
consider and r/o AAA
What is the classic triad of symptoms for ruptured AAA?
- flank or back pain,
- hypotension
- pulsatile abdominal mass
Where do AAAs rupture into?
~20% of AAA ruptures will rupture anteriorly into the peritoneal cavity (which are associated with a very poor prognosis)
~80% rupture posteriorly into the retroperitoneal space
suspected non-ruptured AAA - Ix
In the routine outpatient setting, any suspected AAA should be initially investigated by USS.
(AXR is not indicated!!)
a follow-up CT scan with contrast is warranted when at threshold diameter of 5.5cm.
=> This provides more anatomical details in order to determine suitability for endovascular procedures.
Ruptured AAA - Mx
Emergency A-E resuscitation
=> Including 2 large bore cannulae, urgeny bloods (incl. XM)
=> Any shock should be treated very carefully – “permissive hypotension”
Transfer to local vascular unit
Patient taken to theatre
=> Open repair if unstable
=> If stable, CT angiogram to consider EVAR
Prognosis of a ruptured AAA
Only 50% of ruptured AAAs make it to hospital, and of these patients only 50% will survive the operation.
permissive hypotension in AAA
Raising the BP will dislodge any clot and may precipitate further bleeding, therefore aim to keep the BP ≤100mmHg
Mx of small, unruptured AAA
AAAs that measure <5.5cm:
- Monitored by regular USS/CT
- Modification of risk factors – e.g. control of HTN
- 75% will eventually require surgery
Indications for surgery in unruptured AAA
In a patient who is otherwise fit:
- AAAs >5.5 cm
- AAAs expanding >1cm/year
- Symptomatic
In a patient who is unfit:
- AAA may be left until 6cm or more prior to repair, due to the significant risk of mortality from an elective repair compared to the risk of mortality if not repaired.
What RFs increase the risk of AAA rupture?
HTN,
FHx of rupture,
Smokers
Females
=> these patients may have surgery performed at an earlier stage.
Options for surgical repair of AAA
Endovascular Aneurysm Repair (EVAR):
= Most common surgery, uses femoral arteries to access and stent the aorta under fluoroscopic guidance
=> Lower mortality rate, Lower post-op morbidity and shorter hospital stay, ITU not required.
=> Lifelong monitoring is required and re-intervention is not uncommon
Open Surgery:
- Involves a midline laparotomy or long transverse incision, exposing the aorta, and clamping the aorta proximally and the iliac arteries distally
- The aneurysm segment is then removed and replaced with a prosthetic graft
These have similar long-term outcomes, but EVAR has better short-term outcomes
Complications of EVAR
ENDOVASCULAR LEAK
=> an incomplete seal forms around the aneurysm resulting in blood leaking around the graft.
often asymptomatic hence regular surveillance (usually USS) is needed.
If left untreated, the aneurysm can expand and subsequently rupture. As such, any aneurysm expansion following EVAR warrants investigation for endoleak.
What can popliteal aneurysms be associated with?
Frequently associated with other aneurysms elsewhere in the body
Popliteal aneurysm - Presentation
Usually asymptomatic
may present with complications:
- Acute limb ischaemia – due to rupture/thrombosis of the aneurysm or due to distal emboli
- Chronic limb ischaemia – gradual occlusion of the aneurysm
- DVT – if occluding popliteal veins
Popliteal aneurysm - Ix
- USS – to determine the size of the aneurysm
- Angiography – prior to surgery to assess distal arterial tree
Popliteal Aneurysm - Mx
- Femoral to distal popliteal bypass grafts
- Intra-vascular thrombolysis or embolectomy may occur at time of surgery for distal emboli.
What is a TRUE aneurysm?
= all layers of the arterial wall are involved.
Can be Symmetrical/fusiform vs. asymmetrical/saccular
What is a TRUE aneurysm?
= all layers of the arterial wall are involved.
Can be Symmetrical/fusiform vs. asymmetrical/saccular
What is a FALSE or PSEUDO aneurysm?
= the surrounding soft tissues lined by thrombus form the wall of the aneurysm, mainly following trauma.
=> E.g. femoral artery puncture with inadequate compression.
Layers of an artery
tunica intima (innermost layer),
tunica media (middle layer)
tunica adventitia (outermost layer).
What is an arterial dissection?
= A tear in the intima leads to blood tracking into the arterial media.
The arterial media splits, forming a false channel.
Most commonly occurs in the aorta
Anterograde aortic dissection
propagates towards the iliac arteries
Retrograde aortic dissection
propagate towards the aortic valve (at the root of the aorta)
=> Can result in prolapse of the aortic valve, bleeding into the pericardium, and cardiac tamponade
Causes of aortic dissection
HTN
Atherosclerotic disease
Connective tissue disorders (Marfan’s / Ehler’s-Danlos)
Male gender
Aortic dissection - possible outcomes
External rupture – massive fatal haemorrhage
Internal rupture – (rare) blood tracks back into the lumen to produce a double channelled aorta.
Blockage of distal main artery branches:
- Coronary arteries => MI
- Brachiocephalic trunk => unequal arm pulses + central neurological Sx
- Renal arteries => anuria/AKI
- SMA/IMA => acute mesenteric ischaemia
- Iliac arteries => acute lower limb ischaemia
Cardiac tamponade
Aortic Dissection - STANFORD CLASSIFICATION
A. TYPE A – involves the ascending aorta and can propagate to the aortic arch and descending aorta; the tear can originate anywhere along this path
- i.e. DeBakey Types I and II
- ~70% of cases
B. TYPE B - does not involve the ascending aorta, occurring in any other part of the aortic arch and descending aorta
- i.e. DeBakey Type III
- ~30% of cases
Aortic Dissection - DEBAKEY CLASSIFICATION
I. Type I – originates in the ascending aorta and propagates at least to the aortic arch
=> Carry the highest mortality
II. Type II – confined to the ascending aorta
III. Type III – originates distal to the subclavian artery in the descending aorta
- IIIa = extends distally to the diaphragm
- IIIb = extends beyond the diaphragm into the abdominal aorta
Aortic Dissection - Presentation
Severe, very sudden onset central chest pain, described as “tearing”
=> It may radiate down the arm/to the back (mimicking MI)
Shock (hypovolaemic / cardiogenic)
=> Tachycardia, Hypotension
Signs of end-organ hypoperfusion
=> such as reduced urine output, paraplegia, lower limb ischaemia, abdominal pain secondary to ischaemia, or deteriorating conscious level
Aortic Dissection - Ix
Bloods:
- FBC, U&Es, LFTs, troponin, coagulation;
- XM of at least 4 units,
- ABG to aid initial assessment.
ECG – to exclude any cardiac pathology.
CT angiogram confirms diagnosis
(Transoesophageal ECHO)
Aortic Dissection - Ix
Bloods:
- FBC, U&Es, LFTs, troponin, coagulation;
- XM of at least 4 units,
- ABG to aid initial assessment.
ECG – to exclude any cardiac pathology.
CT angiogram confirms diagnosis (double lumen seen)
(Transoesophageal ECHO)
Type A Aortic Dissection - Initial Mx
A-E resuscitation with urgent cardiothoracic advice
=> Cautious fluid resuscitation – target pressure should be sufficient for cerebral perfusion only
Patients managed on ITU
Type A:
- Patients are considered for surgery if fit enough, due to the risk of tamponade
- Surgery is removal of ascending aorta (with or without the arch) and replacement with synthetic graft.
- Carries high operative mortality.
Type B Aortic Dissection - Initial Mx
A-E resuscitation with urgent cardiothoracic advice
=> Cautious fluid resuscitation – target pressure should be sufficient for cerebral perfusion only
Patients managed on ITU
Patients are managed medically unless there are certain complications (rupture, renal, visceral or limb ischaemia, refectory pain, or uncontrollable hypertension)
First line Tx = management of HTN with intravenous beta blockers (labetalol) (or calcium channel blockers as second line therapy).
Long-term management of aortic dissection
Following initial management, all patients need:
- lifelong antihypertensive therapy
- surveillance imaging
What is the thoracic outlet?
= the space between the first rib and clavicle, through which the subclavian artery, subclavian vein and brachial plexus pass.
What is thoracic outlet syndrome?
= narrowing of the thoracic outlet causing compression of the neurovascular bundle.
Symptoms can be neurological (most common), venous, or arterial.
Causes of thoracic outlet syndrome
- Cervical rib
- Healed clavicular fracture
- Excess scalene muscle development
- Hyperextension/repetitive stress injuries
Thoracic Outlet Syndrome - Presentation
The specific clinical features present will be dependent on neurological, arterial, or venous involvement.
Symptoms may also worsen with certain movements – e.g. shoulder abduction or extension.
BRACHIAL PLEXUS Sx:
- Paraesthesia and/or motor weakness (most often in the C8-T1 distribution)
- Wasting of the small muscles of the hand
ARTERIAL Sx:
- Upper limb claudication if working their hands above their head
- Acute limb ischaemia – due to occlusion, distal embolisation or aneurysm.
VENOUS Sx:
- Swelling of extremities
- Can lead to DVT
- Can be prominent veins over the shoulder due to collateralisation
Thoracic Outlet Syndrome - Ix
Blood Pressure:
- Arm BP will be lower in the affected arm, and will vary with posture.
Bloods
- including FBC and clotting screen
Plain CXR for potential bony abnormalities
- can show cervical rib or healed clavicular fracture
For suspected venous/arterial TOS
- Venous/arterial duplex USS
- Arteriography can confirm obstruction
- Any patient presenting with acute limb ischaemia needs CT angiogram
For suspected neurogenic TOS:
- Nerve conduction studies
Thoracic Outlet Obstruction - Mx
The treatment approach depends upon the cause of TOS and what is being compressed.
For nTOS:
- Physiotherapy for 6 months
=> Aiming to improve mobility in the neck and shoulder, strengthen the surrounding muscles, and relax the scalene muscles.
- Botox injections can be used to relax the scalene muscles
For vTOS:
- May need thrombolysis and anti-coagulation, under guidance form the haematology teams
- Most cases will need surgical management
For aTOS:
- Acute limb ischaemia – urgent vascular input
- Otherwise, most cases are caused by anatomical abnormalities that can be managed in the elective surgical setting.
What is mesenteric ischaemia?
= vascular compromise of the bowel.
most commonly occurs due to arterial occlusion of the SMA, supplying the small bowel and some of the colon.
Common causes of Acute vs Chronic mesenteric ischaemia
Acute = most commonly caused by a blood clot in the main mesenteric artery.
Chronic = most commonly caused by thrombosis superimposed on atherosclerosis.
Common causes of Acute vs Chronic mesenteric ischaemia
Acute = most commonly caused by a blood clot in the main mesenteric artery.
Chronic = most commonly caused by thrombosis superimposed on atherosclerosis.
Mesenteric Ischaemia - Sx
- Severe post-prandial colic (“gut claudication”) – about 30 min after eating
- PR bleeding
- Weight loss (eating is painful)
- Malabsorption
Mesenteric Ischaemia - Ix and Mx
It is difficult to diagnose, but can be visualised on angiography and treated with angioplasty.
What is Large Bowel Ischaemia ?
Typically a disease of the elderly (age >60 years).
Diminished / absent blood flow leads to bowel wall ischaemia and secondary inflammation.
Bacterial contamination may produce superimposed pseudomembranous inflammation.
If necrosis develops then ulcerations or perforation can occur
Large Bowel Ischaemia - Presentation
“Ischaemic colitis”
- Left sided abdominal pain
- Bloody diarrhoea
Pyrexia, tachycardia, leucocytosis
Can progress to gangrenous colitis, with peritonitis and shock.
Large Bowel Ischaemia - Ix
Barium enema / AXR => “thumb printing” due to mucosal oedema/haemorrhage
Contrast enhanced CT
MR angiography = diagnostic
Large Bowel Ischaemia - Mx
Conservative – most recover with fluids and ABX
Percutaneous transluminal angioplasty and stenting for severe cases.
What is renal artery stenosis?
What causes it?
= the narrowing of one or more renal arteries.
Causes:
- ~90% due to atherosclerosis
- 10% due to fibromuscular dysplasia
Renal Artery Stenosis - Presentation
Resistant HTN
Worsening renal function after ACEIs (if bilateral)
Oedema (usually legs/feet/ankles; sometimes hands/face)
Other signs of reduced renal function
Renal bruits on examination
Renal Artery Stenosis - Ix
- Renal USS – small affected kidney, doppler showing disturbance in renal flow.
- CT/MR angiography can then confirm diagnosis
- Renal angiography = gold-standard
Renal Artery Stenosis - Mx
Lifestyle changes if due to atherosclerosis:
- Exercise, weight loss if necessary, healthy diet.
- Smoking cessation
Medical regimens:
- ACEis with statins & antiplatelets (contraindicated in bilateral disease)
Surgical management:
- Angioplasty and stenting (thought to be equally as effective as medical Mx)
- Endarterectomy – cleaning out plaque from the vessel
- Bypass surgery – vein or plastic tube used to connect the kidney to the aorta
Vascular trauma
A blunt injury = when a blood vessel is crushed or stretched.
A penetrating injury = when a blood vessel is punctured, torn or severed.
Either type of vascular trauma can cause the blood vessel to clot (=> ischaemia), or cause bleeding which can lead to life-threatening haemorrhage
Vascular Trauma - presentation of haemorrhage
If there is pulsatile external haemorrhage => diagnosis of arterial injury is obvious
When blood accumulates in deep tissues the only manifestation may be shock
Presence of pulses distal to injury DOES NOT EXCLUDE ARTERIAL INJURY
Vascular Trauma - presentation of ischaemia
Must be suspected when patient has 1 or more of the “6 Ps”:
=> Pain, pallor, paralysis, perishingly cold, paraesthesia, pulselessness
Transected Artery - presentation and Mx
A cleanly transected artery will often constrict and retract, limiting blood loss.
A longitudinal / badly lacerated vessel cannot limit blood loss and may produce greater blood loss.
Mx:
- Haemorrhage can normally be arrested by applying pressure to gauze swabs.
- If there is significant ischaemia, vascular grafting/repair may be needed.
- If the main artery and vein have been severed, the vein will always be repaired first to allow venous drainage before repairing the artery.
Causes of arterio-venous fistula
- Penetrating trauma = most common
- Erosion of aneurysm into a neighbouring vein
- Iatrogenic – patients on haemodialysis
What is an arterio-venous fistula?
= an acquired communication between an artery and vein.
There is shunting from the high-pressure arterial side to the low-pressure venous side.
=> Peripheral venous pressures are increased
=> Peripheral arterial resistance decreases
AVF - Symptoms/signs
Patient’s with non-iatrogenic AVFs may complain of limb heaviness, aggravated with dependency and relieved by elevation.
Pain
OE – oedema, prominent veins, audible murmur/palpable thrill (can be pulsatile)
=> Rarely, can be signs of CCF if the communication is very large.
AVF - Ix
VBG will show higher O2 sats distal to the AVF.
Can be consumptive coagulopathies due to changes in blood flow activating the clotting cascade
Duplex USS or contrast CT can confirm diagnosis
AVF - Mx
Most symptomatic AVFs are amenable to surgical or interventional treatment.
- Surgical Repair (often surgical bypass)
- Endovascular Treatment (balloon +/- stenting)
Superficial venous system of LL
Medial long (great) saphenous vein – drains to the saphenofemoral junction
Lateral short saphenous vein – drains into the popliteal vein
=> Drains the skin and superficial tissues
Deep venous system of LL
- Veins accompanying the major arteries of the lower limb
- Drain the muscular compartment
What are varicose veins?
= abnormally dilated and lengthened superficial veins.
They can be primary (most common) or secondary.
- Primary:
- Likely to be due to a primary superficial valve defect, with familial elements
- There is NO deep venous incompetence. - Secondary:
- Occur secondary to deep venous incompetence
=> Previous DVT (although veins recanalize, their valves remain incompetent)
=> Raised systemic venous pressure (due to compression, A-V fistula, or severe tricuspid valve incompetence
RFs for varicose veins
prolonged standing,
obesity,
pregnancy,
FHx
Varicose Veins - symptoms
- Most patients are most affected by the unsightly appearance
- Can cause tiredness, aching or throbbing of the legs.
- Oedema of the ankles (particularly on standing for long periods)
- Itching and nocturnal cramps
- Signs of deep venous insufficiency (haemosiderosis, venous eczema, lipodermatosclerosis)
What is Saphena varix?
What are the investigations and management?
= a dilatation of the saphenous vein at the saphenofemoral junction in the groin.
As it displays a cough impulse, it is commonly mistaken for a femoral hernia;
=> Suspicion should be raised in any suspected femoral hernia if the patient has concurrent varicosities present in the rest of the limb.
[Ix] These can be best identified via duplex ultrasound
[Mx] is via high saphenous ligation.
Deep Venous Insufficiency
Occurs when the valves of the deep venous system are incompetent.
=>The calf pump can no longer efficiently return blood to the thoracic cavity.
Primary cause = congenital absence of valves
Secondary cause = DVT causing vascular damage or AVF raising venous pressure
Deep Venous Insufficiency - Sx
Lower limb aching pain / discomfort
Oedema of lower leg
Superficial varicose veins (raised central pressure causes perforator vein incompetence)
Haemosiderin deposition in gaiter area
Venous eczema (particularly over pigmented area), causing pruritis
Atrophie blanche
Lipodermatosclerosis (s.c. tissue replaced by thick fibrous tissue, giving an inverted champagne bottle appearance)
Ulceration
Deep Venous Insufficiency - Ix
Hand-held Doppler:
- Can identify reflux at saphenofemoral/ saphenopopliteal junctions.
Duplex USS = gold-standard
- Can diagnose valve at the great/short saphenous veins and any perforators, as well as large vein occlusion.
Venography:
- Can detect deep vein occlusion and perforating vein reflux
How is a venography done?
- Tourniquet placed around the ankle to occlude superficial veins, and contrast is injected into the foot.
- Fluoroscopy then used to see the progress through the deep system
Indications for referral to vascular service for Surgical Tx of varicose veins
- Symptomatic primary or recurrent varicose veins
- Lower‑limb skin changes, such as pigmentation or eczema, thought to be caused by chronic venous insufficiency
- Superficial vein thrombosis (characterised by the appearance of hard, painful veins) with suspected venous incompetence
- A venous leg ulcer (a break in the skin below the knee that has not healed within 2 weeks)
Varicose Veins - Conservative Tx
Lifestyle advice:
- Avoid prolonged standing
- Exercise regularly (promotes calf muscle function)
- Weight loss
Graded compression stockings:
- For minor varicosities, the elderly/unfit and for pregnancy
- Check ABPI before use
- Any venous ulceration from deep venous incompetence generally requires four-layer bandaging
Options for Surgical Tx of varicose veins
Endothermal Ablation:
- Involves heating the vein from inside (via radiofrequency or laser catheters), causing irreversible damage to the vein which closes it off.
Sclerotherapy:
- For cosmetically undesirable superficial varicosities
- Chemical sclerosing agent (foam) is injected into the varicose vein, causing an inflammatory response that closes off the vein. and the vein is kept compressed with bandaging for two weeks to allow fibrosis to take place.
Surgical Ligation
- Remains the gold-standard treatment
- Making an incision in the groin (or popliteal fossa) and identifying the responsible, refluxing vein, before tying it off and stripping it away.
Complications of untreated varicose veins
Worsen over time:
- Even many patients who have treated varicose veins often require re-intervention surgery.
Haemorrhage – caused by minor trauma to a dilated vein
Phlebitis – can occur spontaneously, or following foam sclerotherapy
=> Veins become hard (thrombosis) and tender, with overlying erythema
What is chronic peripheral arterial disease?
What are the causes?
Progressive occlusion of the arteries
Causes:
1. Atherosclerosis (= most common)
2. Fibromuscular dysplasia (non-inflammatory artery wall thickening)
3. Vasculitis (inflammation)
4. Buerger’s Disease (acute inflammation and thrombosis of lower limb veins, common in young heavy smoker)
ABPI - Normal
0.9 – 1.0
ABPI - Intermittent Claudication
0.6 – 0.9
ABPI - Ischaemic Rest Pain
0.3 – 0.6
ABPI - ulceration / gangrene
< 0.3
ABPI >1.2
indicates calcified blood vessels or an incorrect calculation
Intermittent Claudication
= leg pain (aching/ cramping/ tired feeling) upon exertion due to narrowing of the arteries not allowing enough blood flow to support the oxygen demand of the tissues (“angina of the legs”).
At rest, the collateral system is able to meet the oxygen requirement of the muscles.
DDx of intermittent claudication
Spinal stenosis – symptoms are similar, but pain is relieved by sitting down or flexing spine rather than standing still.
Venous claudication – pain comes on gradually from the moment walking starts, relieved by leg elevation.
Arthritis
Peripheral neuropathy
Popliteal artery entrapment
Intermittent Claudication - signs
Absent pulses
Cold, pale legs
Atrophic, hairless & shiny skin
Buerger’s angle <20 degrees
Arterial ulcers
Intermittent claudication - symptoms
Ischaemic “cramping” pain on walking, relieved by rest
Pain reproducible at a similar level – claudication distance
Most commonly in the calf (femoral disease)
Pain in thigh/buttock suggests ileal disease, which is often bilateral.
=> Ask about penile function (Leriche Syndrome)
Chronic Ischaemic Rest Pain
Indicative of critical lower limb ischaemia.
Classically occurs at night, in the forefoot
=> Due to decreased effects of gravity and decreased BP
Pain wakes patient from sleep
Often gain relief by swinging leg over the side of the bed, or walking on a cold floor.
There will be a history of intermittent claudication and signs of arterial insufficiency in the leg.
At this stage, ulcers are likely to form from minor injuries (as healing is impaired).
Chronic Limb Ischaemia - Ix
Bloods – FBC (r/o anaemia), HbA1c, lipids
Vascular examination
BP
ABPI = most important initial investigation
CT/MR angiography
What does the Mx of chronic limb ischaemia depend on?
depends on ABPI results and level of symptoms
Mx - chronic limb ischaemia ABPI >0.6
Progression from intermittent claudication to critical ischaemia is unlikely
=> conservative measures are used (progression more likely in diabetics and those with claudication distance <50m, so more aggressive treatment may be considered in these patients).
Conservative measures:
1. Lifestyle measures – stop smoking, exercise to the point of claudication to improve collaterals, weight loss
2. Raising the heel of shoes (decrease calf work)
3. Foot care to prevent minor trauma and ulceration
4. Optimisation of BP (but avoid beta-blockers) and diabetes
5. Start on antiplatelet and statin
Mx - chronic limb ischaemia ABPI <0.6 / Highly symptomatic / Conservative measures ineffective
Referral to vascular surgery
Revascularisation:
1. Percutaneous Transluminal Angioplasty +/- stenting
2. Surgical reconstruction
Amputation
- Relieve pain and prevent death from sepsis
- Level of amputation must be high enough to ensure healing (but above knee amputation has worse outcome than below knee)
How might peripheral neuropathy pain differ to arterial disease pain?
Unlike arterial disease, the pain is unlikely to be relieved by swinging the foot over the bed
the foot will be red and warm, with strong pulses.
What an Peripheral neuropathy combined with arterial disease
can lead to the foot being severely ischaemic but PAINLESS.
Diabetics more likely to present with ulceration of critically ischaemic limb, which can rapidly progress to gangrene.
Dry vs Wet gangrene
DRY – just dead tissue, no infection (no ABX required), can self-amputate
WET – dead tissue infected with bacteria (ABX required), gangrenous part needs to be removed.
It presents in the toes first, progressing proximally to line where there is adequate oxygenation.
Characteristically, it is initially blue-purple in colour, with progressive blacking of tissues and numbness.
Acute/critical limb ischaemia - causes
Embolus
Thrombus
Trauma (including during angioplasty)
Virchow’s Triad for predisposition to thrombosis
- Endothelial Dysfunction – trauma, inflammation, atheroma
- Changes in blood flow – stasis or slow flow
- Changes in blood coagulability
Acute/Critical Limb Ischaemia - embolus vs thrombus
EMBOLUS
Sudden onset
Very severe Sx due to lack of collaterals
Normally identifiable cause (e.g. AF, AAA)
Previously normal pulses
No history of arterial disease
THROMBUS
Insidious onset
Less severe Sx as advanced collaterals
No obvious source
Long-standing decreased pulses bilaterally
Previous history of intermittent claudication, stroke, MI, etc.
The 6 P’s of limb ischaemia
- Pain
- Pallor
- Pulselessness
- Perishingly cold
- Paraesthesia
- Paralysis
5&6 in late-stage disease only, indicate a threatened limb
What are signs of a threatened limb in critical limb ischaemia?
6 Ps (particularly paraesthesia and paralysis)
Pain on passive movement or squeezing the calf are also signs of a threatened limb
What are signs of a non-viable limb in critical limb ischaemia?
Fixed staining (colour changes that are non-blanching) of the leg
Rigid muscles
How long is there to re-establish blood flow of a critically ischaemic limb?
maximum of 6 hours
Critical Limb Ischaemia - Mx
- A-E Resuscitation
- IV heparin as soon as the diagnosis is made.
- Prevent propagation of the clot - Assessment of the limb
- ?thrombolysis if blockage appears to be resolving
- ?urgent surgery if no apparent blood supply
- Amputation if leg not thought to be viable - Urgent CT angiogram
- Can help differentiate between thrombotic/embolic causes and direct management - Mx of embolus:
- Open embolectomy or intra-arterial thrombolysis; investigate underlying cause. - Mx of thrombus:
- thrombolysis and angioplasty or bypass surgery or intra-arterial thrombolysis to treat underlying cause
What is a re-perfusion injury?
= inflammation and oxidative damage when blood flow is restored after long period of anoxia, can lead to oedema and compartment syndrome.
Indications for amputation in limb ischaemia
To relieve ischaemic rest pain, consider for end of life care
Dangerous leg => e.g. full of pus, full of dead muscle
Oncological => e.g. sarcoma
Useless => e.g. severely mangled following trauma, congenital defects
Common Intra-abdominal Abscess Locations
Alongside the organ of origin – e.g. paracolic, parapancreatic
Pelvic – e.g. post-pelvic sepsis (appendicitis)
Subphrenic – e.g. post-GI perforation
Intra-abdominal Abscess - Clinical Features
malaise,
anorexia,
SWINGING PYREXIA,
tachycardia,
possibly a mass.
Intra-abdominal Abscess - Ix
Diagnosis is generally with CT abdo/pelvis
Intra-abdominal Abscess - Mx
IV empirical ABX
Radiologically-guided (CT/USS) drainage where possible.
Surgical drainage is a last-line measure.
Mx of superficial subcutaneous abscess
Drainage:
- Often performed under GA, and strong analgesia is required.
- The point of maximum fluctuance is incised, and then blunt probing ensures that all loculi are drained.
Small abscesses need only a dry dressing.
Deeper abscesses required frequent packing with antiseptic gauze/use of a corrugated drain to keep them open until they have filled with granulation tissue.
Factors contributing to Surgical Site Infection
GENERAL
Age, malnutrition, immunosuppression, malignancy, obesity, hypoxia, anaemia
LOCAL FACTORS
Type of surgery (clean vs. contaminated), length of procedure, residual local malignancy, foreign body insertion, ischaemia
MICROBIOLOGICAL FACTORS
Lack of ABX prophylaxis, virulence of organism
Prophylactic ABX in surgery
Used for:
- Contaminated/dirty surgeries,
- Placement of foreign materials
- Immunosuppression,
- Previous foreign body implants,
- Heart valve disease,
- peripheral vascular disease
Dose and timing factors are important, with the highest tissue concentration required at the moment of tissue contamination.
=> This normally means IV administration at the moment of incision.
Often 2 further doses are given at appropriate times to complete a 24-hour course.
Anaerobic Gangrene
Caused by clostridium perfringens found in soil/faeces
Can arise from trivial injury, often in immunosuppressed patients
There is initially gas in the tissues and skeletal muscles (crepitus), with oedema and spreading gangrene plus systemic upset.
Patients may need resuscitation
Tx = aggressive debridement and IV penicillin + metronidazole.
Synergistic Gangrene
(necrotising fasciitis):
Aerobes and synergistic anaerobes infect an initial wound/surgical site.
Leads to severe wound pain and gas in the tissues.
There may be excessive subdermal gangrene
Tx = debridement, ABX and systemic support.
Post-op Pyrexia
when and what should be reviewed?
MILD pyrexia is common post-operatively as a response to tissue injury and stress.
When called to review the patient for infection vs. post-op fever:
1. Cut – inspect wound for superficial infection/haematoma
2. Collection
3. Cannula – any thrombophlebitis/infection
4. Chest – exclude infection, infarction, acute heart failure.
5. Central line - ?infection
6. Catheter – urine output, ?infection
7. Calves - ?DVT
Triad of signs of shock
- Signs of reduced perfusion
• Prolonged capillary refill time
• Reduced urine output
• Altered mental state. - Low BP
• Usually by at least 40mmHg - Raised lactate
• Anaerobic respiration produces lactate, which accumulates in the blood, causing a hyperlactataemia.
What are the types of thyroid malignancy?
Papillary Carcinoma
Follicular Carcinoma
Medullary Carcinoma
Anaplastic Carcinoma
Thyroid - papillary carcinoma
~70% of malignant carcinomas
Presents most commonly age 40-50
RFs – previous neck radiation
Spreads locally and metastasises to local nodes
=> Can go to bone/lung, but this is rare
Tx:
- Cured by surgical resection, including metastases
- +/- Neck LN dissection if nodal involvement
- +/- Radio-iodine therapy as an adjunct
Prognosis is good
Thyroid - Follicular Carcinoma
20% of cases of malignant carcinoma
Metastasises via the bloodstream, classically to the bone
Tx:
- As per papillary ca.
Prognosis is good
Thyroid - Medullary Carcinoma
- how common is it and who does it affect?
- what cells does it arise from?
- What is the treatment and prognosis?
5% of cases of malignant carcinoma
Generally affects older adults
Can affect children/young adults as part of MEN syndromes (MEN IIa/IIb)
Arise from parafollicular / “C” cells
=> Secrete calcitonin, so plasma calcitonin levels are raised.
=> Calcitonin levels can be measured following treatment for monitoring
Tx:
- Total thyroidectomy +/- lymph nodes if involved +/- radiotherapy if haven’t been able to get it out.
Prognosis is poor
Thyroid - Anaplastic Carcinoma
<5% of cases of malignant carcinoma
Occurs in elderly populations
Extremely locally aggressive , with rapid and extensive local invasion
Complications of tracheal/ SVC obstruction
Total thyroidectomy often not possible
External radiotherapy may give palliation
Prognosis is poor
Thyroid Malignancy - Presentation
Most present as asymptomatic thyroid nodules or lymph nodes
There may be hoarseness/ dysphagia / weight loss
Thyroid dysfunction is rare
Thyroid Malignancy - Ix
History & examination
USS
Technetium scans:
- “Hot” suggests adenoma
- “Cold” may suggest malignancy
Fine needle aspiration and cytology
What are typical cardiac surgery incisions and their uses?
Median Sternotomy – most common approach for heart / aortic arch operations
Anterolateral Thoracotomy – access to the right side of the heart.
Posterolateral Thoracotomy – access to distal aortic arch and descending thoracic aorta.
Bilateral transverse thoracotomy (clam shell) – popular for double lung transplants or heart-lung transplants
What is the difference between open and closed heart surgery?
Open heart surgery – any surgery requiring cardio-pulmonary bypass
Closed heart surgery – does not require a bypass
Cardiopulmonary Bypass
Takes over the function of the heart and lungs, allowing a motionless blood-free field for operation.
The ascending aorta is clamped and cannulated, and a venous line inserted into the right atrium to drain venous blood.
The system involves a heat exchanger to regulate temperature, an oxygenator, an arterial pump and a filter.
There is no coronary blood supply, so the potential for ischaemic damage is minimised by arresting the heart in a high potassium (cardioplegic) solution, and also cooling the myocardium to between 4 and 12 degrees.
What are the main complications of cardiopulmonary bypass?
How is this prevented?
Main complications are due to activation of the clotting cascade within the bypass machine, which consumes clotting factors and platelets.
This is prevented with high-dose systemic heparin before cannulation,
This is reversed after the operation with protamine sulfate (blood products may also be needed to reverse this).
Coronary Artery Bypass Graft (CABG)
Performed through median sternotomy incision and cardio-pulmonary bypass.
The left internal mammary artery is most commonly used as a conduit, harvested from the chest wall.
=> Enlarges in response to demand, resistant to atheroma formation.
Saphenous vein harvest was previously used and continues to be used for secondary targets, however results are less good than IMA grafts.
CABG vs PCI in coronary artery disease
CABG provides better symptomatic relief and requires fewer late re-interventions than PCI in managing coronary artery disease
CABG - complications
• MI
• Bleeding
• Stroke
• Arrythmias
• Tamponade
• Aortic dissection
• Respiratory / systemic complications
Man-made Heart Valves
e.g. ball-in-cage or bileaflet valves
Durable, but thrombogenic (this require anticoagulation with warfarin)
Will be able to hear the valve “click” from the end of the bed
Tissue Prosthetic Heart Valves
Homographs (human) or Xenographs (generally from pigs
Anticoagulation is not required, but more prone to degenerative failure.
Homographs are more resistant to degeneration, so are preferred in younger patients to avoid long-term anticoagulation.
Prosthetic Heart valves - infection risk
Infection of a prosthetic valve is rare but devastating
risk is lowest with homograft valves.
Indications for splenectomy
Splenic trauma
Hypersplenism
Autoimmune haemolysis (ITP, congenital haemolytic anaemias).
Splenectomy - complications
Main issue = increased risk of infection
mainly by encapsulated organisms (e.g. strep pneumoniae), as the spleen usually contains a large number of macrophages.
Splenectomy - Mx
Mobilise soon after operation due to transient increase in platelets.
=> LMWH whilst in hospital
=> Aspirin advised in the short-term
Immunise according to local regimens
=> Pneumococcal 2 weeks prior to surgery, or ASAP following emergency surgery
=> Hib, Men C and annual flu vaccinations
Lifelong penicillin V (erythromycin if allergic)
=> Penicillin V does not protect against haemophilus infections, however.
Advice to carry alert card and seek immediate medical advice if signs of infection.
If travelling abroad, warn of severe malaria risks.
((This advice also applies to hyposplenic patients – e.g. sickle cell ))
Boerhaave’s syndrome - presentation
= Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.
PRESENTATION:
- sudden onset of severe chest pain that may complicate severe vomiting.
- Subcutaneous emphysema may be observed on the chest wall.
Boerhaave’s syndrome - diagnosis and management
Diagnosis is CT contrast swallow.
Treatment is with thoracotomy and lavage
If less than 12 hours after onset then primary repair is usually feasible
