Colorectal and general surgery Flashcards
1
Q
Laparoscopy complications
A
general anaesthetic risks
Vasovagal reaction in response to abdo distension
Extra-peritoneal gas insufflation (surgical emphysema)
Injury to GI tract
Injury to blood vessels
2
Q
Gastric MALT lymphoma
A
Associated with H pylori in 95% of cases
Good prognosis
Most respond to H pylori eradication
Paraproteinaemia may be present
3
Q
Complications of gastrectomy
A
Dumping syndrome:
- Early: food of high osmotic potential moves into small intestine causing fluid shift
- Late: rebound hypoglycaemia. Surge of insulin following food of high glucose value in small intestine - 2-3hrs later the insulin overshoots causing hypoglycaemia
Weight loss Early satiety Iron deficiency anaemia Osteoporosis Osteomalacia Vit B12 deficiency Increased risk of gallstones Increased risk of gastric cancer
4
Q
Abdominal stomas
A
Small bowel stomas should be spouted so that their irritant contents are no in contact with the skin
Types of stomas:
- Gastrostomy: in the epigastrium, used for feeding and gastric decompression or fixation
- Loop jejunostomy: any location, used following laparotomy with planned early closure
- Percutaneous jejunostomy: usually LUQ, usually performed for feeding
- Loop ileostomy: usually RIF, used following defunctioning of colon
- End ileostomy: usually RIF, usually following complete excision of colon or where ileocolic anatamosis is not planned
- End colostomy: either LIF or RIF, used when a colon diversion or resection is dont and anastamosis is not primarily achievable
- Loop colostomy: located anywhere, used to defunction a distal segment of colon
5
Q
Anal cancers
- type
- borders of the anus
- lymphatic drainage
- risk factors
- clinical features
A
- Majority are squamous cell carcinomas
- The anus ranges from the anorectal junction to the anal margin
- Lymphatic drainage/tumour spread at the anal margin goes to the inguinal lymph nodes, and tumours at the anorectal junction spread to pelvic lymph nodes
- Risk factors: HPV, anal intercourse, immunosuppression, HIV, women with a history of cervical cancer or CIN, smoking, 1:2 (m:f)
- Clinical features: perianal pain, perianal bleeding, palpable lesion, faecal incontinence, rectovaginal fistula
- Ix: T stage assessment (exam, DRE, anoscopic exam with biopsy, palpation of inguinal nodes), CT, MRI, endo-anal US, PET, HIV test
6
Q
Anal fissures
A
Longitudinal or elliptical tears of squamous lining of the distal anal canal
Acute if present for <6 weeks, chronic if present for ?6 weeks
Risk factors: constipation, IBD, STIs
Features: painful, bright red, rectal bleeding
90% occur on the posterior midline
Mx of acute fissure:
High fibre diet and high fluid intake, bulk-forming laxatives are first line, lubricants (petroleum jelly) before defaecation, topical anaesthetics, analgesia
Mx of chronic fissure:
All of the above, plus more. Topical GTN is first line, if topical GTN is not effective after 8 weeks then refer to secondary care (sphincterotomy or botox)
7
Q
Causes of anorectal abscess
Positions of anorectal abscesses
A
Causes: E coli, Staphylococcus aureus
Positions: perianal, ischiorectal, pelvirectal, intersphincteric
8
Q
Rectal prolapse
- risk factors
- two types
- presentation
- ix
- mx
A
RF: increasing age, female, multiparous, straining, anorexia, previous traumatic vaginal delivery
May be internal or external
External are at risk of ulceration and long term incontinence
Clinical features: rectal mucous discharge, faecal incontinence, PR bleed, visible ulceration
Full thickness: rectal fullness, tenesmus, repeated defaecation
Ix: colonoscopy, defaecating proctogram, anorectal manometry studies, examination under GA
Mx:
- acute: reduce the prolapse and cover with sugar to reduce swelling
- Delormes procedure (excise mucosa and plicate the rectum)
- Altmeirs procedure (resect the colon)
- Rectopexy (rectum is elevated and fixed at the level of the sacral promontory)
9
Q
Location of colorectal cancers in order of how common they are
A
Rectal (40%) Sigmoid (30%) Ascending colon and caecum (15%) Transverse colon (10%) Descending colon (5%)
10
Q
2 week wait referral criteria for colorectal cancer
A
Patients >=40 with unexplained weight loss and abdo pain
Patients >= 50 with unexplained rectal bleeding
Patients >= 60 with iron deficiency anaemia OR change in bowel habit
Or: anyone who shows occult blood in their faeces
11
Q
Faecal occult blood testing (FOBT) and faecal immunochemical testing (FIT) screening programme
A
FIT is a type of FOBT which is sent through the post to the patient
Used to detect and quantify the amount of human blood in a single stool sample
Screening programme offered every 2 years to all men and women aged 60-74
Patients >74 may request screening
Patients with abnormal results are offered a colonoscopy
50% will be normal, 40% will have polyps which are removed, 10% will have cancer
12
Q
Colorectal cancer management
A
- Following diagnosis, patients require a CT CAP for staging
- Their entire colon should also be evaluated with colonoscopy or CT colonography
- MDT discussion regarding treatment plan
- Treatment:
- Colonic cancer: resectional surgery is the only curative option. Stents, surgical bypass and diversion stomas as palliative adjuncts. The lymphatic chains are also removed. Once the affected colon is removed, there will either be an anastamosis formed or an end stoma. If at risk of disease recurrence, chemotherapy is offered afterwards.
-Rectal cancer: rectal tumours involving the sphincter complex or very low tumours on the anal verge require abdomino-perineal excision of the rectum. Upper and lower rectal tumours can have anterior resection. Rectal resections require a 2cm clearance margin, and meticulous dissection of mesorectal fat and lymph nodes (TME). Colo-rectal anastamosis can then occur.
Many patients are also offered neoadjuvant radiotherapy prior to resectional surgery. Patients with obstructing rectal cancers should have a defunctioning loop colostomy
13
Q
Site of colorectal cancer - type of resection - anastamosis
A
Caecal, ascending or proximal transverse colon: right hemicolectomy: ileo-colic anastamosis
Distal transverse, descending colon: left hemi-colectomy: colo-colon anasatmosis
Sigmoid colon: high anterior resection: colo-rectal anastamosis
Upper rectum: anterior resection and TME: colo-rectal anastamosis
Lower rectum: anterior resection and low TME: colo-rectal anastamosis or defunctioning stoma
Anal verge: abdomino-perineal excision of rectum: no anastamosis required
14
Q
Factors needed for an anastomosis to heal
In which situations would you construct an end stoma rather than attempting an anastomosis
A
Adequate blood supply
Mucosal apposition
No tissue tension
Sepsis, unstable patients, inexperienced surgeons -> end stoma rather than anastomosis
In an emergency setting where the bowel has perforated, the risk of an anastomosis is much greater (esp colon-colon) - an end colostomy is often safer and can be reversed later
15
Q
What is Hartmann’s procedure
A
Used in emergency bowel surgery, eg. bowel obstruction or perforation
Resection of the rectosigmoid colon with formation of an end colostomy and closure of the anorectal stump
16
Q
Dukes classification
A
Dukes A: tumour confined to mucosa (95% 5yr)
Dukes B: tumour invading bowel wall (80% 5yr)
Dukes C: lymph node metastases (65% 5yr)
Dukes D: distant mets (5% 5yr)
17
Q
Genetics of inherited colorectal cancer syndromes
A
Familial adenomatous polyposis: more than 100 adenomatous polyps affecting the colon and rectum. APC gene. Autosomal dominant.
Gardner syndrome: same as FAP but with desmoid tumours and mandibular osteomas. APC gene
Hereditary non-polyposis colon cancer (Lynch syndrome): colorectal cancer without extensive polyposis. Endometrial cancer, renal and CNS cancers.
18
Q
Diverticular disease
- what is it
- symptoms
- diagnosis
- complications
- treatment
A
Herniation of colonic mucosa through the muscular wall of the colon
Symptoms: altered bowel habit, bleeding, abdo pain
Diagnosis: colonoscopy, CT cologram or barium enema
In an acutely unwell surgical patient, they may also receive a plain AXR and CXR to exclude perforation, and an abdo CT with constrast to identify any acute inflammation and local complications
Complications: diverticulitis, haemorrhage, fistula, perforation and faecal peritonitis, perforation and development of abscess, development of diverticular phlegmon
Mx:
- Increase fibre
- Mild attacks may be managed with abx
- Peri colonic abscesses should be drained (surgically or radiologically)
- Recurrent episodes of acute diverticulitis requiring hospitalisation is an indication for a segmental resection
- Perforation with faecal peritonitis will require a resection and a stoma
- Less severe perforations may be managed with laparoscopic washout and drain insertion
19
Q
Diverticulitis
- what is it
- risk factors
- presentation
- signs
- investigations
- management
A
Infection of a diverticulum (out-pouching of intestinal mucosa)
RF: age, lack of fibre, obesity, sedentary lifestyle, smoking, NSAID use
Presentation: severe LIF pain, N+V, constipation (50%) or diarrhoea (25%), urinary frequency/ urgency/ dysuria, PR bleeding
Pneumaturia or faecaluria if colovesical fistula
Vaginal passage of faeces or flatus if colovaginal fistula
Signs: low grade pyrexia, tachycardia, tender LIF (may have a palpable mass due to inflam or abscess), possibly reduced bowel sounds
If perforation -> guarding, rigidity, rebound tenderness
Lack of improvement with treatment -> ?abscess
Ix:
- FBC (raised WCC)
- CRP (raised)
- Erect CXR (pneumoperitoneum if perforation)
- AXR (dilated bowel loops, obstruction, or abscess)
- CT (best modality in suspected abscesses)
- Colonoscopy (avoid initially due to increased risk of perforation)
Mx:
- oral abx, liquid diet and analgesia in mild cases
- if symptoms dont settle in 72 hours or patient initially presents with severe symptoms -> IV abx
20
Q
Haemorrhoids
- where are they found
- clinical features
- types
- grading of internal haemorrhoids
- management
A
Found in the left lateral, right posterior and right anterior portions of the anal canal (3 o clock, 7 o clock, 11 o clock)
Clinical features: painless rectal bleeding (bright red on the paper), pruritus, pain (usually not significant unless piles are thrombosed), soiling may occur with third or fourth degree piles
Types:
- external: originate below the dentate line, prone to thrombosis, may be painful
- internal: originate above the dentate line, do not generally cause pain
Grading of internal:
1: does not prolapse out of the anal canal
2: prolapse on defaecation but reduce spontaneously
3: manually reduced
4: cannot be reduced
Management:
- soften stools (increase fibre and fluid)
- topical local anaesthetics and steroids may relieve symptoms
- outpatient treatments: rubber band ligation is superior to injection sclerotherapy
- surgery is reserved for large symptomatic haemorrhoids which do not respond to outpatient treatments
21
Q
Acutely thrombosed external haemorrhoids
- typical presentation
- examination findings
- management
A
Typically presents with significant pain
O/E: purple, oedematous, tender subcutaneous perianal mass
If patient presents within 72 hours then referral should be considered for excision
Otherwise, patients can usually be managed with stool softeners, ice packs and analgesia.
Symptoms settle within 10 days usually.
22
Q
Perianal abscess
- what is it
- more common in who?
- features
- causes
- ix
- mx
A
Collection of pus within the subcut tissue of the anus that has tracked from the tissue surrounding the anal sphincter
More common in men, usually around 40 years
Features: anal pain worse on sitting, hardened tissue in the anal region, pus-like PR discharge, systemic infection if abscess is longstanding
Causes: usually E coli (gut flora). Those caused by Staph aureus are more likely to be a skin infection rather than originating from the GI tract
Ix:
- usually diagnosed through inspection and DRE
- if ?underlying cause -> colonoscopy and blood tests (cultures and inflam markers)
- transperineal ultrasound is the gold standard in imaging anorectal abscesses (rarely used, except for complicated abscesses)
Treatment:
- Surgical incision and drainage is first line, under local anaesthetic. Then pack the wound (or leave open -> heals in 3-4wks)
- Abx if systemic upset secondary to abscess
23
Q
Types of anorectal abscesses and where they are found
A
Ischiorectal: found between obturator internus muscles and external anal sphincter
Supralevator abscesses: forms when infection tracks superiorly from peri-sphincteric area to above the levator ani
Intersphincteric: between the internal and external anal sphincters
24
Q
Conditions associated with anorectal abscesses
A
- Underlying IBD (esp crohns)
- DM is a risk factor due to poor wound healing
- Underlying malignancy (due to risk of bowel perforation -> abscess formation)
25
Causes of rectal bleeding
```
Anal fissure
Haemorrhoids
Crohns disease
Ulcerative colitis
Rectal cancer
Diverticulosis and diverticulitis
```
26
```
Anal fissure
Haemorrhoids
Crohns disease
Ulcerative colitis
Rectal cancer
```
For all of the above: type of bleeding, features in history, examination findings
Anal fissure: bright red PR bleed. Painful bleeding that occurs post-defaecation in small volumes, usually due to constipation. Usually seen in the midline posteriorly.
Haemorrhoids: bright red PR bleed. Post defaecation bleeding on toilet paper and in toilet pan. May be alteration of bowel habit and history of straining. No blood mixed with stool. No local pain. Normal colon and rectum. Proctoscopy may show internal haemorrhoids. Internal haemorrhoids are usually palpable.
Crohns disease: bright red or mixed blood. Bleeding that is accompanied by other symptoms (altered bowel habit, malaise, fissures, abscesses). Perianal inspection may show fissures or fistulae. Proctoscopy may demonstrate indurated mucosa and possible strictures. Skip lesions on colonoscopy.
Ulcerative colitis: bright red bleed often mixed with stool. Diarrhoea, weight loss, nocturnal incontinence, passage of mucous PR. Proctitis is most marked finding. Colonoscopy will chow continuous mucosal lesions.
Rectal cancer: bright red blood mixed volumes. Alteration of bowel habit, tenesmus, symptoms of metastatic disease. Usually obvious mucosal abnormality, lesions may be fixed or mobile depending on extent of disease. Surrounding mucosa often normal, although polyps may be present.
27
Investigations for PR bleeding
Bloods: FBC, U+E, LT, coag studies, G+S
(elevated serum urea:creatinine ratio suggests an upper GI bleed)
Stool cultures are useful to exclude infective causes
If haemodynamically stable: flexible sigmoidoscopy to exclude left-colonic pathology. If inconclusive -> full colonoscopy.
If haemodynamically unstable: emergency upper GI endoscopy, and colonoscopy
CT angiography can be used if colonoscopy non-diagnostic
If excessive pain or ?fissure -> exam under GA or LA
If malignancy: MRI of the rectum for local staging, and CT CAP for staging of distant disease
28
Indications for surgery in UC
- Disease that is requiring maximal therapy or prolonged courses of steroids (proctocolectomy)
- Dysplastic transformation fo the colonic epithelium with associated mass lesions (proctocolectomy)
- Emergency presentations of poorly controlled disease that fails to respond to medical therapy (sub-total colectomy with an end ileostomy)
- Emergency presentation of toxic megacolon or perforation
29
Types of surgeries for UC
Subtotal colectomy with end ileostomy: usually done as an emergency. colon is removed and ileum is brought out of the body and attached to stoma. Rectum may be left in situ, allowing a pouch to be created later on.
Pouch surgery: the rectum gets removed and the pouch is made from the ileum to connect to the anus (no need for a stoma bag)
Restorative proctocolectomy with ileo-anal pouch: requires two or three operations. usually done as an elective procedure. Removal of the whole colon, leaving rectum and anus in situ. Temporary ileostomy formed. Later on, the rectum is removed and a pouch is made using the ileum which is joined to the anus, and the ileostomy is removed.
Instead of having an ileo-anal pouch, some people choose to have a permanent end-ileostomy
30
Indications for surgery in crohns disease
complications such as fistulae, abscess formation and strictures
Surgery doesnt equate with cure in crohns but may produce substantial symptomatic improvement
31
Volvulus
Torsion of the colon around it's mesenteric axis resulting in compromised blood flow and closed loop obstruction
Occurs in the sigmoid (80%) or caecum (20%)
Features: constipation, abdominal bloating, abdominal pain, N+V
Diagnosis: plain AXR
- sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often with air-fluid levels) + coffee bean sign
- Caecum volvulus: small bowel obstruction
Management:
- Sigmoid: rigid sigmoidoscopy with rectal tube insertion
- Caecal: right hemicolectomy
32
Risk factors of sigmoid volvulus
Risk factors of caecal volvulus
Sigmoid: older patients, chronic constipation, Chagas disease, neuro conditions (parkinsons, duchenne), psychiatric conditions (schizophrenia)
Caecal: can occur in all ages, adhesions, pregnancy
33
Risk factors for colorectal cancer
```
Majority are sporadic
Increasing age
Family history
IBD
Low fibre diet
High processed meat intake
Smoking
High alcohol intake
```
34
Clinical features of bowel cancer
```
Change in bowel habit
Rectal bleeding
Weight loss
Abdo pain
Iron deficiency anaemia
```
Right-sided: abdo pain, occult bleeding, anaemia, mass in RIF, late presentation
Left-sided: rectal bleeding, change in bowel habit, tenesmus, LIF mass or mass on PR exam
35
Investigations for colorectal cancer
- Routine bloods: FBC (microcytic anaemia), LFTs, clotting
- Carcinoembryonic antigen tumour marker should not be used for diagnosis but can be used to monitor disease after diagnosis
-Imaging:
Gold standard is colonoscopy with biopsy
If colonoscopy not suitable, flexible sigmoidoscopy or CT colonography can be done
Following diagnosis -> staging:
- CT CAP for distant mets and local invasion
- MRI rectum for rectal cancer to assess local staging
- Endo-anal ultrasound for early rectal cancer
36
Causes of pseudo-obstruction
Electrolyte imbalance or endocrine disorders: hypercalcaemia, hypothyroidism, hypomagnesaemia
Medication: opioids, CCBs, antidepressants
Recent surgery, severe illness or trauma (inc cardiac ischaemia)
Neuro disease: parkinsons, MS, hirschsprungs disease
37
What is pseudo-obstruction?
Interruption of the autonomic nervous supply, resulting in the absence of smooth muscle action in the bowel wall
Untreated cases results in an increasing colonic diameter, leading to an increased risk of toxic megacolon, bowel ischaemia and perforation
38
Differential diagnoses for pseudo-obstruction
Mechanical bowel obstruction
Paralytic ileus
Toxic megacolon
Constipation
39
Investigations for pseudo-obstruction
Bloods:
- U+Es
- Calcium
- Magnesium
- TFTs
Imaging:
- AXR (bowel distension)
- CT abdo-pelvis with IV contrast (definitive diagnosis as it can exclude mechanical obstruction)
40
Management of pseudo-obstruction
Most cases can be managed conservatively
NBM
IV fluids and NG tube insertion (drip and suck)
If it doesnt resolve in 24-48hrs -> endoscopic decompression
If not responding -> segmental resection +/- anastomosis
41
Pilonidal sinus
- risk factors
- clinical features
RF: caucasian males with coarse dark body hair, associated with those who sit for prolonged periods, increased sweating, buttock friction, obesity, poor hygiene, local trauma
Clinical features: intermittent red, painful and swollen mass in the sacrococcygeal region.
Discharge from the sinus. May have systemic features of infection
Distinguishing features compared to a perianal fistula is that a pilonideal sinus opens up into the skin but does not communicate with the anal canal (perianal fistula can open up into the skin but does communicated with anal canal)
42
pathophysiology of pilonidal sinus
Starts from a hair follicle in the intergluteal cleft becoming infected or inflamed
The inflammation obstructs the opening of the follicle, which extends inwards, forming a pit
A foreign body type reaction may then lead to formation of a cavity, connected to the surface of the skin by an epithelialised sinus tract
43
Management of pilonideal management
-Conservative: shave the affected area, pluck embedded hairs, wash out any accessible sinuses, abx if septic
Surgical:
- Abscess: incision and drainage with washout
- Chronic disease: removal of the pilonidal sinus tract
44
Angiodysplasia
- what is it
- clinical features
- Ix
Most common vascular abnormality of the GI tract
Caused by formation of arteriovenous malformations
Common in the caecum and ascending colon
Clinical features: rectal bleeding and anaemia are most common features.
- asymptomatic
- painless occult PR bleeding
- acute haemorrhage (upper GI -> haematemesis or malaena, whereas lower GI -> passage of fresh blood from anus)
Ix:
- Bloods (FBC, U+E, LFTs, clotting, ?G+S, ?crossmatch)
- Imaging: upper GI endoscopy and/or colonoscopy if occult angiodyspasia. Small bowel bleeds are harder to identify and requires wireless capsule andoscopy. Mesenteric angiography in overt angiodysplasia
45
Management of angiodysplasia
10% present with major GI bleed -> treat accordingly
If minimal bleeding and haemodynamically stable -> treat conservatively
Conservative treatment: bed-rest, IV fluids, tranexamic acid
If persistent or severe:
- Endoscopy: usually first line. Most widely used technique is argon plasma coagulation
- Mesenteric angiography: used for small bowel lesions that cannot be treated endoscopically (super selective catheterisation and embolisation of the vessel)
Surgical management: resection and anastamosis of affected bowel. Associated with high mortality so only dont if absolutely necessary
46
Indications for bowel resection in angiodysplasia
Continuation of severe bleeding despite treatment
Severe acute life-threatening GI bleeding
Multiple angiodysplastic lesions
47
Complications of angiodysplasia
Complications are mainly related to the treatment
Re-bleeding post-therapy is common
Endoscopic techniques has a small risk of bowel perforation
Mesenteric angiography carries risks of haematoma formation, arterial dissection, thrombosis and bowel ischaemia
48
Gastroenteritis
- risk factors
- infective causes
- non infective causes
- clinical features
- investigations
- management
RF: poor food prep, immunocompromised, poor personal hygiene
Infective causes:
- Viruses: norovirus, rotavirus, adenovirus
- Bacteria: campylobacter, E coli, Salmonella, Shigella
- Bacterial toxins: Staph aureus, Bacillus cereus, Clostridium perfringes
- Parasites: cryptosporidium, Entamoeba histolytica, giardia intestinalis, Schistoma
- Hospital acquired: Clostridium difficile
Non-infective causes:
- radiation colitis
- IBD
- Microscopic colitis
- Chronic ischaemic colitis
Clinical features:
- Cramping abdo pain
- Diarrhoea (+/- blood or mucus)
- Vomiting
- Pyrexia
- Dehydration
Ask about bowel movements, any affected friends or family, recent travel, recent use of antibiotics
Ix: not necessary as self limiting
-Stool culture often done, especially if blood or mucus in stool, if patient is immunocompromised or if severe/persistent
Mx:
- Rehydration (encourage oral fluid intake where possible, consider admitting for IV fluids)
- Education to prevent future episodes
- Exclusion from work for 48 hours form last episode of D+V
- Food poisoning and infectious bloody diarrhoea are notifiable diseases
- Campylobacter and salmonella are notifiable organisms
49
Epigastric hernia
- where does it occur
- why does it occur
- who does it occur in
- what are the symptoms
- what is a differential to exclude
Occurs in the upper midline through the fibres of the linea alba
Secondary to chronically raised intra-abdominal pressure (obesity, pregnancy, ascites)
Most common in middle-aged men
Typically asymptomatic, may present as a midline mass that disappears when lying down
Differential: divarication of the recti
50
Paraumbilical hernia
- where does it occur
- why does it occur
- how does it present
Herniation through the linea alba around the umbilical region (not through the umbilicus itself)
Typically secondary to chronic raised IAP
Presents as a lump around the umbilical region
Generally contain pre-peritoneal fat, although sometimes contain bowelO
51
Obturator hernia
- where does it occur
- who does it occur in
- how does it present
- sign elicited if obturator nerve is compressed
Hernia of the pelvic floor, through the obturator foramen into the obturator canal
More common in women (wider pelvis), typically in elderly patients
Present: mass in upper medial thigh, often patients will have features of small bowel obstruction
About 50% of causes causes compression of the obturator nerve -> positive Howship-Romberg sign (hip and knee pain exacerbated by thigh extension, medial rotation and abduction)
52
Richters hernia
- what is it
- how does it present
- complication
Can occur at any site
It is a partial herniation of the bowel. The mesenteric border of the colon is unaffected, and the anti-mesenteric border herniates and gets strangulated
Presents as a tender irreducible mass
Causes obstruction -> surgical emergency
53
Femoral hernia
- what is it
- risk factors
- clinical features
- investigations
- management
Abdominal viscera or omentum passes through the femoral ring and into the potential space of the femoral canal
RF:
- Women (wider pelvis)
- Pregnancy (multiparity)
- Raised IAP
- Increasing age
Clinical features:
- Small lump in the groin (infero-lateral to the pubic tubercle and medial to the femoral pulse)
- Usually asymptomatic at presentation but can present as an emergency due to obstruction or strangulation
- Unlikely to be reducible due to the tightness of the femoral ring
Investigations:
- Clinical diagnosis but imaging often required
- USS (but user-dependent)
- CT abdo-pelvis
- Surgical exploration if still in doubt
Management:
- All femoral hernias require surgical intervention within 2 weeks due to strangulation risk
- Low/high approach surgical reduction of the hernia and narrowing of the femoral ring with sutures or a mesh plus (high approach done in an emergency)
54
Anatomy of the femoral canal
Located in the anterior thigh
```
Superior border = femoral ring
Anterior border = inguinal ligament
Posterior border = pectineus muscle
Lateral border = femoral vein
Medial border = lacunar ligament
```
Due to the rigidity of the femoral ring and the concave margin of the lacunar ligament, femoral hernias are prone to strangulation and ischaemia
55
Locations of femoral hernia and inguinal hernia
Femoral: infero-lateral to the pubic tubercle and medial to the femoral pulse. May roll up superiorly and in front of the inguinal ligament and may therefore be misdiagnosed as inguinal
Inguinal: supero-medial to the pubic tubercle
56
'lump in groin' differential diagnoses
```
Femoral hernia
Inguinal hernia
Femoral canal lipoma
Femoral canal lymph node
Saphena varix
Femoral artery aneurysm
Athletic Pubalgia
```
57
Emergency presentation of a hernia
Complications that require urgent intervention:
- Irreducible or incarcerated
- Obstruction (bowel obstruction)
- Strangulation (compression of the hernia has compromised blood supply, leading to ischaemia)
Strangulation presents as an irreducible and tender tense lump, with the pain being out of proportion to the clinical signs. Accompanied with clinical features of obstruction
Surgical emergency due to risk of bowel infarction
58
Inguinal hernia
- what is it
- risk factors
- clinical features
- examination findings
Abdo cavity enters into the inguinal canal.
RF: male, increasing age, raised IAP, obesity
Clinical features: lump in groin, which initially disappears with minimal pressure or when the patient lies down. There may be mild to moderate discomfort which can worsen with activity or standing.
Incarceration -> painful, tender, erythematous
Strangulation -> irreducible and tender tense lump with the pain often being out of proportion to clinical signs
May present with features of bowel obstruction
OE:
- Cough impulse
- Location (inguinal hernias are supermedial to the pubic tubercle)
- Reducible on lying down +/- minimal pressure
- If it enters the scrotum, can you get above it/ is it separate from the testis
59
Direct vs indirect inguinal hernia
Direct (20%): bowel enters directly into the inguinal canal through a weakness in the posterior wall of the canal (Hesselbach's triangle)
-more common in older patients, often secondary to abdo wall laxity or a significant increase in IAP
Indirect (80%): bowel enters the inguinal canal via the deep inguinal ring. They arise from incomplete closure of the processus vaginalis, an outpouching of peritoneum allowing for embryonic testicular descent, therefore are usually deemed congenital in origin.
Indirect hernias are lateral to the inferior epigastric vessels.
Direct hernias are medial to the inferior epigastric vessels.
60
How to elicit a cough reflex to distinguish between direct and indirect inguinal hernias
Reduce the hernia
Place pressure over the deep inguinal ring (mid-point of the inguinal ligament)
Ask the patient to cough
If the hernia protrudes despite occlusion of the deep inguinal ring, this indicates a direct hernia
If the hernia does not protrude, this indicates an indirect hernia
Unreliable assessment, the only definitive method to differentiate them is at the time of surgery
61
Investigations for inguinal hernia
Typically a clinical diagnosis
Explorative surgery for further definitive diagnosis
Ultrasound (first line imaging) should only be considered if there is diagnostic uncertainty or to exclude other pathology
62
Management of inguinal hernia
Symptomatic inguinal hernias should be offered surgical intervention
If strangulation -> urgent surgical exploration
A third of patients with an inguinal hernia will never experience any symptoms and can be managed conservatively
Surgical intervention:
- Open repair: open mesh repair are preferred for those with primary inguinal hernias
- Laparoscopic repair: preferred for those with bilateral or recurrent inguinal hernias, or those with unilateral hernia and chronic pain, or if female
63
Hiatus hernia
- what is it
- risk factors
- clinical features
- investigations
Protrusion of the stomach (or small bowel/colon/mesentery) through the oesophageal hiatus into the thorax
RF: increasing age, increased IAP (pregnancy, obesity, ascites), increase size of diaphragmatic hiatus
Clinical features:
- Majority are completely asymptomatic
- May experience gastroesophageal reflux symptoms (burning epigastric pain, worse on lying flat) which are treatment resistant
- Vomiting and weight loss
- Bleeding and/or anaemia
- Hiccups or palpitations
- Dysphagia
Examination is typically normal
Investigations:
- OGD is gold standard investigation showing upward displacement of the GOD (Z-line)
- May be diagnosed incidentally on a CT or MRI scan
64
Different types of hiatus hernias
- Sliding (80%): gastro-oesophageal junction and the cardia of the stomach slides upwards through the diaphragmatic hiatus into the thorax
- Rolling (20%): upward movement of the gastric fundus occurs to lie alongside a normal positioned gastro-oesophageal junction which creates a bubble of stomach in the thorax
65
Differential diagnoses for hiatus hernia
Cardiac chest pain
Gastric cancer
Pancreatic cancer
GORD
66
Management of hiatus hernia
- conservative
- indications for surgery
- surgical options
Conservative:
-First line: PPI (take in the morning before food), weight loss, low fat diet, earlier meals, smaller portions, smoking cessation, reduced alcohol intake
Surgical indications: remaining symptomatic despite maximal medical therapy, increased risk of strangulation/volvulus, nutritional failure
Surgery:
-Nissen's fundoplication (gastric fundus is wrapped around the lower oesophagus to strengthen the LOS and keep the GOD below the diaphragm)
67
Complications of hiatus hernias
Incarceration
Strangulation
Gastric volvulus (stomach twists on itself leading to obstruction of the gastric passage and tissue necrosis): presents with Borchardt's triad (severe epigastric pain, retching without vomiting, inability to pass an NG)
68
Peptic ulcer disease
- what is it
- risk factors
- clinical features
Peptic ulcer = break in the lining of the GI tract, extending through to the muscular layer of the bowel wall. Occurs in the lining of the stomach or the first part of the duodenum.
Duodenal ulcers are more common than gastric ulcers
RF: H pylori, NSAIDs, corticosteroids, previous gastric bypass surgery, physiological stress, zollinger-ellison syndrome
Clinical features:
- Majority are asymptomatic
- Epigastric or retrosternal pain
- Nausea
- Bloating
- Duodenal: epigastric pain when hungry, relieved by eating
- Gastric: epigastric pain worsened by eating
- Complications of PUD (bleeding, perforation, gastric outlet obstruction)
69
Referral criteria for urgent upper oesophago-gastro-duodenoscopy (OGD) for ?oesophageal cancer
New onset dysphagia
Age >55 with weight loss and either upper abdo pain, reflux or dyspepsia
New onset dyspepsia not responding to PPIs
70
Differential diagnoses for PUD
```
Acute coronary syndrome
Gastroesophageal reflux disease
Gallstone disease
Gastric malignancy
Pancreatitis
```
71
Investigations for PUD
Many patients may be treated empirically before requiring an OGD
Most patients, especially younger patients, should undergo non-invasive H-pylori testing: stool antigen test or carbon-13 urea breath tests are first line
Older patients, or those with red flags, or those with ongoing symptoms despite treatment require an OGD
At OGD, any peptic ulceration can be biopsied, which will be sent for histology and for a rapid urease test (tests for H pylori)
72
Management of peptic ulcer disease
Conservative:
- Lifestyle advice: stop smoking, weight loss, reduction in alcohol consumption, avoid NSAIDs
- Start on a 4-8 week course of PPIs. Reassess after this period for resolution of symptoms.
- Those with positive H pylori test should be started on triple therapy (7 days PPI + oral amoxicillin + clarithromycin/ metronidazole)
- If symptoms have not resolved post PPI +/- eradication therapy -> OGD required to exclude malignancy
Surgery:
- Surgery for PUD is rare, except for in emergencies (eg. perforation), or in the management of Zollinger-Ellison syndrome
- A partial gastrectomy or selective vagotomy may be considered in severe or relapsing disease
PUD perforation -> A-E, blood transfusion if necessary, urgent OGD.
During OGD: injections of adrenaline and cauterisation of the bleed, with administration of high dose IV PPI therapy
73
Complications of PUD
Perforation
Haemorrhage
Pyloric stenosis (rare)
74
Helicobacter pylori
- what is it
- where is it found
- how does it cause ulcers
- investigations
- management
Gram neg spiral-shaped bacillus
Found in the mucous layer of those with duodenal ulcers (90%) or gastric ulcers (70%)
It survives in the stomach by producing an alkaline micro-environment and induces an inflammatory response in the mucosa, leading to ulceration
It produces urease which breaks down urea into CO2 and ammonia, creating an alkaline microenvironment
Ix: Carbon-13 urea breath test or stool antigen test
Mx: triple therapy eradication
-7 day course of PPI + amoxcillin + clarithromycin or metronidazole
75
Gastric cancer
- what type are the majority of gastric cancers
- risk factors
- clinical features
Majority are adenocarcinomas
RF: japan/ korea, male, H pylori, increasing age, smoking, alcohol consumption, family history, pernicious anaemia, salt in diet
Clinical features:
- often vague and non-specific so presents late
- Dyspepsia
- Dysphagia
- Early satiety
- Vomiting
- Malaena
- Markers of late stage disease: anorexia, weight loss, anaemia
O/E: epigastric mass
76
Differential diagnoses for gastric cancer
Peptic ulcer disease, GORD< gallstone disease, pancreatic malignancy
77
Investigations for gastric cancer
Urgent routine bloods (inc FBC and LFTs)
Imaging:
Urgent upper GI endoscopy with biopsies
Biopsies should be sent for: histology (classification and grading of cancer), CLO test (for H pylori), HER2/neu protein expression (allows for targeted monoclonal therapies)
Staging: CT CAP and a staging laparoscopy
78
Management of gastric cancer
MDT management
- Adequate nutrition (nutritional status assessment required)
- Many patients need NG or RIG (radiologically inserted gastrostomy) tube
Curative:
- Surgical resection with 3 cycles of neo-adjuvant chemotherapy and 3 cycles of adjuvant chemotherapy
- Proximal gastric cancers need total gastrectomy
- Distal gastric cancers need subtotal gastrectomy
- Remove lymph nodes with the tumour
Roux-en-Y reconstruction: post-gastrectomy, the distal oesophagus is end-to-end anastamosed directly to the small bowel, and the proximal small bowel is end-to-side anastomosed to another part of the small bowel
Palliative: this is most patients due to the late presentation. May include: chemotherapy, best supportive care, stenting, or rarely palliative surgery (usually distal gastrectomy or bypass surgery)
79
Complications of gastrectomy
```
Death
Anastomotic leak
Re-operation
Dumbing syndrome
Vitamin B12 deficiency (patients require 3-monthly vit B12 injections)
```
80
Barrett's oesophagus risk factors
Caucasian, male, >50, smoking, obesity, presence of hiatus hernia, positive family history of barretts oesophagus
81
Management of Barrett's oesophagus
All patients should be started on high dose PPI
Stop any drugs which impact stomach protective barrier (eg. NSAIDs)
Risk of progression into adenocarinoma. Therefore all patients must undergo regular endoscopy (frequency depends on degree of dysplasia)
82
Oesophageal cancer
- main types and their risk factors
- clinical features
- investigations
Squamous cell carcinoma: more common in developing world, typically in middle and upper third. Associated with smoking, alcohol, chronic achalasia, low vit A and iron deficiency.
Adenocarcinoma: more common in developed world, typically in the lower third of oesophagus. Due to Barrett's oesophagus. (long-standing GORD, obesity, high dietary fat intake)
Clinical features:
- late presentation
- progressive dysphagia (initially solids then liquids)
- significant weight loss
- odynophagia, hoarseness
- supraclavicular lymphadenopathy
Investigations:
- OGD within 2 weeks
- Any malignancy on OGD will be biopsied and sent for histology
- CT CAP and PET-CT for staging distant mets
- Endoscopic USS to measure penetration into oesophageal wall and biopsy suspicious mediastinal lymph nodes
- Staging laparoscopy (for junctional tumours with an intra-abdominal component to look for intra-peritoneal mets)
- Any palpable cervical lymph nodes may be investigated via fine needle aspiration biopsy
- Any hoarseness may warrant bronchoscopy
83
Complications of oesophageal resection
Mortality
Anastomotic leak
Re-operation
Pneumonia
84
Management of oesophageal cancer
Prognosis
Curative management:
- SCC of the upper oesophagus require definitive chemoradiotherapy.
- SCC of the middle/lower oesophagus require either definitive chemo-radiotherapy or neoadjuvant CRT followed by surgery.
- Adenocarcinomas require neoadjuvant chemo/CRT followed by oesophageal resection.
- Following surgery, patients require post-op nutrition help. Feeding jejunostomy inserted usually.
Palliative management:
- Majority of patients
- Dysphagia -> oesophageal stent
- CRT can be used to reduce tumour size and bleeding
- Photodynamic therapy can reduce tumour size
- Nutritional support is essential (thickened fluid, nutritional supplements)
- If dysphagia is too severe, a RIG tube may be inserted to bypass the obstruction (radiologically inserted gastrostomy)
Prognosis: overall 5yr survival is 5-10%
85
Oesophageal perforation
- what is it
- cases
- most common site
- why is it dangerous?
- clinical features
- ix
- mx
Surgical emergency
Full thickness rupture of the oesophageal wall
Causes:
- Severe forceful vomiting (Boerhaave's syndrome)
- Iatrogenic (eg. endoscopy)
Most common site of perforation: just above the diaphragm in the left postero-lateral position
Perforation -> leakage of stomach contents into the mediastinum and pleural cavity -> severe overwhelming inflamm response -> physiological collapse, multi-organ failure and death
Clinical features: severe sudden onset retrosternal chest pain, resp distress, subcut emphysema following severe vomiting or retching
Ix:
- Routine bloods inc G+S
- CXR (pneumomediastinum) although do not delay definitive imaging inorder to obtain CXR
- IMaging of choice: CT CAP with IV and oral contrast
Mx:
- Urgent aggressive resuscitation (high flow O2, IV access, fluid resus, broad spec abx)
- Definitive managements involves controlling the oesophageal leak, washout mediastinum and pleural cavity, decompression of the oesophagus and nutritional support (TPN or feeding jejunostomy)
86
Mallory Weiss tears
- what are they
- where do they usually occur
- why do they usually happen?
- what are typical features
- management
Lacerations in the oesophageal mucosa, usually at the gastroesophageal junction
Tends to occurs after a period of profuse vomiting
Causes a short period of haematemesis. Generally small and self-limiting, in the absence of clotting abnormalities
Most cases are benign and resolve spontaneously, therefore providing patient reassurance and monitoring is usually all that is required
Prolonged or worsening haematemesis warrants OGD
87
Achalasia
- what is it
- clinical features
- ix
- mx
Primary motility disorder of the oesophagus, characterised by failure of relaxation of the LOS and progressive failure of contraction of the oesophageal smooth muscle
A common histiological feature is progressive destruction of the ganglion cells in the myenteric plexus
Clinical features:
- progressive dysphagia with both solids and liquids from the start
- eventually leads to vomiting and chest discomfort
- regurgitation of food
- coughing
- chest pain
- weight loss
Ix:
- urgent endoscopy to exclude oesophageal malignancy
- Gold standard for diagnosis is oesophageal manometry (absence of oesophageal peristalsis, failure of relaxation of LOS, high resting lower oesophgeal sphincter tone)
- Barium swallow rarely done but shows 'birds beak' appearance at the LOS
Mx:
-Conservative: sleep with multiple pillows to minimise regurgitation, eat slowly and chew food thoroughly, drink plenty of fluids with meals.
CCBs or nitrates can cause temporary relief.
Botox into the LOS can provide temporary relief.
-Surgical: endoscopic balloon dilatation or laparoscopic Heller myotomy
88
Differential diagnoses for achalasia
Other oesophageal motility disorders
GORD
oesophageal malignancy
Angina pectoris
89
Diffuse oesophageal spasm
Multi-focal high amplitude contractions of the oesophagus
Caused by dysfunction of oesophageal inhibitory nerves
Can progress to achalasia
Clinical features:
- Severe dysphagia to both solids and fluids
- Central chest pain usually exacerbated by food
- Pain relieved by nitrates (difficult to distinguish from angina pectoris)
- Examination normal
Ix:
-definitive diagnosis made via oesophageal manometry (repetitive, simultaneous and ineffective contractions)
Mx:
- Nitrates and CCBs are first line as they relax the oesophageal smooth muscle
- Pneumatic dilatation
- Myotomy if severe
90
Management of rectal bleeding
Careful resuscitation using A-E
Most settle spontaneously
Patients who are stable and, in whom the bleeding has stopped and who have normal Hb, can be discharged and investigated as outpatient
Those who are haemodynamically unstable or have ongoing bleeding ->
- If undergoing endoscopy: injection of diluted adrenaline), contact and non-contact thermal devices (electrocoagulation), or mechanical therapies (endoscopic clips and band ligation)
- If undergoing angiography: arterial embolisation
91
Differential diagnoses for melena
Due to upper GI bleed..
```
Peptic ulcer disease
Variceal bleeds
Upper GI malignancy
Gastritis
Oesophagitis
Mallory-weiss tear
Meckel's diveritculum
Vascular malformations
```
92
Clinical features of melena
Colour and texture of stool: jet black, tar-like, sticky, offensive smell
Associated symptoms: haematemesis, abdo pain, dyspepsis, dysphasia, odynophagia
PMHx: smoking, alcohol, IBD
DHx: steroids, NSAIDs, anticoagulants, iron tablets
PR exam is essential
93
Investigations for melena
-Routine bloods: FBC, U+E, LFTs, clotting, G+S and 4 units cross-matched
A drop in Hb and a rise in urea: creatinine ratio is very indicative of an upper GI bleed
- ABG
- OGD (definitive)
- CT abdomen with IV contrast
94
Management of melena
A-E
Give blood transfusion to those with low Hb or ongoing significant blood loss
Correct any deranged coagulation (reversal agents for anticoagulants, or FFP for impaired liver function)
Once stable -> arrange OGD
During OGD a range of therapeutic options are available depending on underlying cause
- PUD: injections of adrenaline and cauterisation of the bleed, with administration of high dose IV PPI therapy
- Oesophageal varices: endoscopic banding is most definitive but is difficult, prophylactic abx therapy, somatostatin analogues (terlipressin) to reduce splanchnic blood flow, Sengstaken-Blakemore tube if severe
- Upper GI malignancies: biopsy
95
GI perforation causes
Most common causes are peptic ulcers and sigmoid diverticulum
Other causes:
- foreign body
- diverticulitis
- cholecystitis
- meckels diverticulum
- mesenteric ischaemia
- obstructing lesions (eg. cancer) resulting in bowel distension and subsequent ischaemia and necrosis
- toxic megacolon
- recent surgery
- endoscopy or overzealous NG insertion
- trauma
- excessive vomiting
96
Clinical features of GI perforation
Rapid onset, sharp pain
Systemically unwell (malaise, vomiting, lethargy)
O/E: looks unwell, features of sepsis, peritonism (localised or generalised)
Perforation in the thorax -> pain in the chest or neck, or pain radiating to the back, typically worse on inspiration, associated vomiting and resp symptoms
O/E: auscultation and percussion reveals signs of pleural effusion with the potential for palpable crepitus
97
Important differential diagnoses to consider for GI perforation
Acute pancreatitis
MI
Tubo-ovarian pathology
Ruptured AAA
98
Investigations for GI perforation
Baseline blood tests including G+S (raised WCC and CRP, amylase is often mildly elevated)
Urinalysis (excludes renal and tubulo-ovarian pathology)
Imaging:
- Erect CXR shows pneumoperitoneum. If thoracic origin -> pneumomediastinum or widened mediastinum
- Gold standard is CT scan (confirms free air passage)
Although AXR is rarely done, the features include:
- Riglers sign (both sides of the bowel wall can be seen due to free intra-abdominal air acting as an additional contrast
- Psoas sign (loss of sharp delineation of the psoas muscle border secondary to fluid in the retroperitoneum)
99
Management of GI perforation
A-E assessment and resuscitation
Rapid diagnosis
Early definitive treatment
Broad spec abx
NBM and NG tube insertion
IV fluids and analgesia
Most require surgical intervention (depends on specific type of perforation)
100
What is a closed loop obstruction?
Bowel obstruction where there are two sites of obstruction (eg. volvulus)
Surgical emergency as the bowel will continue to distend until it becomes ischaemic and/or perforates
101
Causes of bowel obstruction
SBO: adhesions and herniae
LBO: malignancy, diverticular disease, volvulus
LBO is GI cancer until proven otherwise
Intraluminal causes of bowel obstruction: gallstone ileus, ingested foreign body, faecal impaction
Mural causes: carcinoma, inflammatory strictures, intussusception, diverticular strictures, Meckels diverticulum, lymphoma
Extramural: hernias, adhesions, peritoneal mets, volvulus
102
Clinical features of bowel obstruction
Abdo pain (colicky or cramping secondary to bowel peristalsis)
Vomiting (initially of gastric content before becoming bilious and then eventually faeculent)
-Vomiting is a late feature in LBO and an early feature in SBO
Abdominal distension
Absolute constipation
-late feature in SBO, early feature in LBO
O/E: may show evidence of underlying cause, shows abdo distension, focal tenderness (+/- guarding and rebound tenderness), tympanic sound on percussion and tinkling bowel sounds on aucultation
103
Investigations for bowel obstruction
Urgent bloods:
- FBC, CRP, U+E, LFTs, G+S
- VBG (high lactate, metabolic derangement due to dehydration or vomiting)
Imaging:
-CT abdo-pelvis with IV contrast is the imaging modality of choice
AXRs are still done in some settings as an initial investigation, even though it is not definitive
SBO AXR findings: dilated bowel >3cm, central abdo location, valvulae conniventes visible (lines completely crossing the bowel)
LBO AXR findings: dilated bowels (>6cm, or 9cm if caecum), peripheral location, haustral lines visible (lines not completely crossing the bowel)
If an erect CXR is performed -> may see pneumoperitoneum if bowel perforation has occured
104
Management of bowel obstruction
Patients with closed loop bowel obstruction or evidence of ischaemia require urgent surgery
Conservative ('drip + suck'):
- NBM
- NG tume to decompress bowel (suck)
- Start IV fluids and correct electrolyte disturbances (drip)
- Urinary catheters and fluid balance
- Analgesia and anti-emetics
A water-soluble contrast study should be performed in cases that do not resolve in 24 hours of conservative management. If contrast does not reach the colon by 6 hours then it is unlikely that it will resolve and patients needs to be taken to theatre
LBO and SBO in a patient who has not had previous surgery rarely settles without surgery
Surgical:
- laparotomy
- if bowel resection is required, anastamosis is often not possible and a stoma may be necessary
105
Indications for surgical intervention in bowel obstruction
?intestinal ischaemia or closed loop bowel obstruction
Small bowel obstruction in a patient with a virgin abdomen (never had surgery before)
A cause that requires surgical correction (eg. strangulated hernia)
If patient fails to improve with conservative management (typically >48 hours)
106
Causes of haematemesis
Emergencies:
- Oesophageal varices
- Gastric ulceration
Non-emergencies:
- Mallory Weiss tear
- Oesophagitis
- Gastritis
- Gastric malignancy
- Meckel's diverticulum
- Vascular malformations
107
Oesophageal varices
- what are they
- why do they cause haematemesis
- common cause
Dilations of the porto-systemic venous anastomoses in the oesophagus
The dilated veins are swollen and thin-walled so prone to rupture (catastrophic haemorrhage)
Most common underlying cause is portal hypertension resulting from alcoholic liver disease
Any haematemesis in a patient with known history of alcohol abuse should be investigated with an urgent OGD
108
Causes of oesophagitis
```
GORD
Infections (candida albicans,)
Medicaiton (bisphosphonates)
Radiotherapy
Ingestions of toxic substances
Crohns disease
```
109
Key features to ascertain from a history of haematemesis
Timing, frequency and vol of bleeding
History of dyspepsia, dysphagia or odynophagia
PMHx and smoking and alcohol status
Use of steorids, NSAIDs, anticoag, bisphosphonates
110
Investigations for haematemesis
-Routine bloods: FBC, U+Es, LFTs, clotting, VBG, G+S, 4 units cross match if severe bleed
Acute bleeding may not initially show an anaemia in the FBC, whereas LFTs may reveal underlying liver damage as a potential cause
A drop in Hb and a rise in urea:creatinine ratio is highly indicative of upper GI bleed
Definitive Ix: OGD within 12 hours
CT abdo with IV contrast can be useful if OGD is unremarkable and patient is too unwell to undergo invasive investigation
Erect CXR may be required if a perforated peptic ulcer is suspected -> pneumoperitoneum
111
Scoring system for upper GI bleed
Glasgow-Blatchord bleeding score
Based purely on clinical and biochemical parameters
Calculated prior to an OGD
Assesses: urea, Hb, systolic BP, pulse, melena, syncope, known hepatic failure, cardiac failure
A score of >=6 is associated with a >50% risk of needing intervention
112
Severity scoring system for GI bleeding post-OGD
Rockall Score
| Glasgow-Blatchford bleeding score is used pre-endoscopy
113
Management of haematemesis
A-E, two large bore canulae, IV fluid resuscitation, G+S and 4 units cross match
Most cases warrant an urgent OGD from which a range of therapeutic options are available depending on the underlying cause:
- PUD: injections of adrenaline and cauterisation of the bleeding. High dose IV PPI therapy +/- H pylori eradication therapy (7 days PPI + amoxicillin + clarithromycin or metronidazole)
- Oesophageal varices: terlipressin (vasopressor) or octreotide (somatostain analogue) should be started to reduce splanchnic blood flow, endoscopic banding is the most definitive method of management but is difficult, prophylactic abx therapy should be started. Long term management warrants repeat banding of the varices and long-term beta blocker therapy
- An actively bleeding patient can be treated with angio-embolisation in which the bleeding vessel is embolised (usually gastro-duodenal artery which is eroded by an ulcer in the first part of the duodenum)
114
Oesophageal varices management
A-E, two large bore canulae, IV fluid resuscitation, G+S and 4 units cross match
Urgent OGD ->
- Terlipressin (vasopressor) or Octreotide (somatostatin analogue) to reduce splanchnic blood flow
- Prophylactic abx therapy
- Endoscopic banding (Sengstaken-Blakemore tube can be used in severe cases)
-Long term management warrants repeated banding of the varices and long term beta blocker therapy
115
The key principles of making surgical incisions
Follow Langer's lines where possible for maximal wound strength with minimal scarring
Muscles should be split not cut where possible
116
Incisions used to access the appendix
Gridiron incision: oblique (superolateral to inferomedial) incision at McBurney's point
Lanz incision: transverse incision made at McBurney's point (two-thirds from the umbilicus to the anterior superior iliac spine). Because it follows langers lines, Lanz produces more aesthetically pleasing results with reduces scarring
117
Location of incisions:
- Midline incision
- Kocher incision
- Chevron/ Rooftop incision
- Mercedes Benz incision
- Midline incision: runs anywhere from the xiphoid process to the pubic symphysis, passing around the umbilicus. used in emergencies or to access multiple viscera.
- Kocher incision: subcostal incision used to access the gallbladder and biliary tree. Incision made to run parallel to the costal margin, starting below the xiphoid process and extending laterally.
- Chevron/ Rooftop incision: extension of the Kocher incision to the other side of the abdomen.
- Mercedes Benz incision: Chevron incision + a vertical incision and break through the xiphisternum
118
Causes of intra-abdominal bleeding requiring urgent surgery?
Most severe causes is ruptured AAA
| Other common causes: rupture ectopic pregnancy, bleeding gastric ulcer, trauma
119
Causes of GI perforation
Peptic ulceration, small or large bowel obstruction, diverticular disease, IBD
120
Characteristic features of generalised peritonitis
Patients lie completely still, not to move their abdomen, and look unwell
Tachycardia
Hypotension
Completely rigid abdomen with percussion tenderness
Involuntary guarding
reduced or absent bowel sounds
121
Acute abdomen conditions which require urgent surgery
Bleeding: rupture AAA, ruptured ectopic, perforated gastric ulcer, trauma
Perforation: peptic ulcer, SBO, LBO, diverticular disease, IBD
Ischaemic bowel
122
What is colic?
Abdominal pain that crescendos to become very severe and then goes away completely. typically seen in ureteric obstruction or bowel obstruction
Biliary colic is not a true colic because the pain does not completely go away
123
What is peritonism? (not peritonitis)
Localised inflammation of the peritoneum, pain starts in one place before localising to another area (appendicitis)
124
Differential diagnoses for the acute abdomen
RUQ: cholecystitis, pyelonephritis, hepatitis, pneumonia, Fitz-hugh curtis syndrome
LUQ: gastric uler, pyelonephritis, ureteric colic, pneumonia
RLQ: appendicitis, ureteric colic, inguinal hernia, IBD, UTI, gynae (ovarian torsion, ruptured ectopic pregnancy, testicular torsion, PID, Mittelschmerz), Meckels diverticulum
LLQ: diverticulitis, ureteric colic, inguinal hernia, IBD, UTI, gynae (ovarian torsion, ruptured ectopic pregnancy, testicular torsion, PID, Mittelschmerz)
Epigastric: peptic ulcer disease, cholecystitis, pancreatitis, MI
Peri-umbilical: SBO, LBO, appendicitis, AAA
Generalised: mesenteric ischaemia
DKA and MI are important non-surgical causes that must not be missed
125
Investigations of acute abdomen
Urine dipstick and MC+S (infection, haematuria, proteinuria)
Pregnancy test
ABG (lactate, rapid result for Hb levels, pH, pO2, pCO2)
Routine bloods (FBC, U+E, LFTs, CRP, amylase), serum calcium if ?pancreatitis, G+S
Blood cultures
Imaging:
- ECG to exclude MI
- USS (KUB, biliary tree and liver, ovaries, fallopian tubes and uterus)
- Erect CXR for ? bowel perforation
- CT imaging
126
Eponymous abdominal signs on examination
Rovsings sign = appendicitis
Boas sign = cholecystitis
Murphy's sign = cholecystitis
Cullens sign = pancreatitis (and other intraabdominal haemorrhage). umbilical area
Grey-Turners = pancreatitis (and other retroperitoneal haemorrahges). flank areas
127
Causes of abdominal swelling
```
Pregnancy
Intestinal obstruction
Ascites
Urinary retention
Ovarian cancer
IBD(?)
```
128
Causes of surgical chest pain
```
Dissection of the thoracic aorta
Diffuse oesophageal spasm
GORD
Boerhaaves syndrome
Achalasia
```
