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.
