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Year 3 surgery > The acute abdomen > Flashcards

The acute abdomen Flashcards

1
Q

What is the pathophysiology of appendicitis?

A

Appendiceal obstruction: Faecolith, Colorectal neoplasia or lymphoid tissue hyperplasia
Inflammation of wall: Then get ischemia from distention of wall causing mural vessel thrombosis -> can lead to perforation, abscess or peritonitis.

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2
Q

What are the common symptoms of appendicitis?

A

Central abdo pain that migrates to RIF pain
Anorexia
GI upset
Dysuria

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3
Q

Why is there central/non-specific pain in appendicitis?

A

Because there is involvement of the visceral peritoneum - autonomic innervation

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4
Q

When does RIF pain occur in appendicitis?

A

When the parietal peritoneum is involved - somatic nervous system

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5
Q

What clinical signs can be felt in appendicitis?

A

Tenderness at McBurney’s point
Rovsing’s sign
Mass in RIF

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6
Q

Where is McBurney’s point?

A

2/3 of distance from umbilicus to ASIS

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7
Q

What is Rovsing’s sign?

A

Pain in RIF when pressure applied to LIF

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8
Q

What are the differential diagnoses for appendicitis?

A

Mesenteric adenitis
Meckle’s diverticulum
IBD (Crohn’s)
Diverticulitis

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9
Q

What is Meckel’s diverticulum?

A

Congenital diverticulum - Vestigial remnant of the vitelline duct.

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10
Q

Which condition does the ‘rule of 2’s’ refer to? What are the rule of 2’s?

A

Meckel’s diverticulum
2% prevalence
2 inches long
Located 2 feet proximal to the ileocaecal junction

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11
Q

What are the symptoms of Meckle’s diverticulum?

A

Most are asymptomatic.
PR bleeding
Can cause volvulus or obstruction
Can be inflamed and mimic appendicitis
Can be lined with gastric mucosa causing ulceration

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12
Q

Which investigations are done for suspected appendicitis?

A

Bloods - High WCC and CRP. High Bilirubin
USS
CTAP
MRI abdo

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13
Q

What might a raised bilirubin in appendicitis indicated?

A

Complicated appendicitis

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13
Q

How is an appendix mass managed?

A

Appendix mass = delayed presentation - walled off mass +/- collection
Give antibiotics and percutaneous drainage of collection.
Delayed appendicectomy after acute event settles

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13
Q

What is the recurrence rate of appendicitis if only treated with abx?

A

40% within 5 years

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14
Q

What is diverticular disease?

A

Protrusion of mucosal pouches through bowel wall musculature

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15
Q

In which part of the bowel is diverticular disease likely to be seen?

A

Sigmoid colon
Highest intra-luminal pressure
Linked to constipation

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15
Q

What causes acute diverticulitis?

A

Micro-perforation of a diverticulum.
Erosion of diverticular wall by increased intraluminal pressure or inspissated food particles, resulting in inflammation.
Progression of inflammation leads to focal necrosis resulting in perforation.

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16
Q

What is the typical presentation of sigmoid diverticulitis?

A

Abdominal pain - LIF, but can be in RIF as sigmoid mobile.
N+V
Infection signs/sepsis
Change in bowel habits
Rarely PR bleeding
Urinary urgency/frequency/dysuria
Peritonitis

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17
Q

What are the differential diagnoses for sigmoid diverticulitis?

A

IBS
Colorectal cancer
Acute appendicitis
Epiploic appendagitis
Infectious or Ischaemic colitis

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18
Q

Which investigations are done for suspected sigmoid diverticulitis?

A

Bloods - Raised WCC + CRP
CTAB to rule out complications (Abscess, obstruction)

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19
Q

Which classification is used to describe perforation of the colon due to diverticulitis?

A

Hinchey classification

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20
Q

What are the four Hinchey classification stages?

A

I - Pericolic abscess
II - Remote abscess (pelvic, retroperitoneum)
III - Purulent peritonitis
IV - Faecal peritonitis

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21
Q

How is Hinchey I and II generally treated?

A

Abx (with abscess <4cm)
Larger abscess may need drainage (Percutaneous or surgical)

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22
Q

How is Hinchey III treated?

A

Often with surgery - laparoscopy and washout, or laparotomy and resection +/- anastomosis

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23
Q

How is Hinchey IV treated?

A

Laparotomy and resection +/- anastomosis

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24
Q

What are the main categories of GI perforation?

A

Ischaemia - obstruction, vascular
Infection - Appendicitis, diverticulitis, colitis
Erosion - Malignancy, ulcerative disease
Physical disruption - Trauma, iatrogenic

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25
Q

What causes oesophageal perforation?

A

Iatrogenic most common - dilatation at OGD
15% spontaneous - intense vomiting or retching causing increase in intra-oesophageal pressure (Boerhaave’s syndrome)
Foreign bodies
Caustic liquid ingestion (Especially alkalis)

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26
Q

What are the symptoms of oesophageal perforation?

A

Chest pain
Non specific: back pain, shoulder tip pain, vomiting, SOB, unwell
Mackler’s triad: Vomiting, chest pain, subcutaneous emphysema

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27
Q

Which condition does Mackler’s triad refer to?

A

Oesophageal perforation

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28
Q

Which investigations are done for oesophageal perforation?

A

CXR - pleural effusion, air in mediastinum or subcutaneous emphysema
Oral contrast (GOLD STANDARD) - water soluble (as free barium causes high mortality) via XR or CT
Endoscopy

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29
Q

How is oesophageal perforation treated?

A

NBM, IVI, abx, ITU involvement
Non operative management (If iatrogenic) if small defect, no systemic upset, and able to drain pleural/mediastinal collection.
Surgical repair, drain infection and control further effluence. High risk of mortality.

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30
Q

What is the most common cause of upper GI perforation?

A

Peptic ulceration

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31
Q

Which infection is linked to peptic ulceration?

A

H. pylori
90-95% duodenal ulcers
70-85% gastric ulcers

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32
Q

What are the risk factors for peptic ulceration?

A

H. pylori and NSAIDS biggest factor
Smoking
Steroids
More common in women.

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33
Q

What is the typical presentation of upper GI perforation?

A

Abdo pain - initially upper then generalised
Sometimes back pain (If retroperitoneal perforation)
Upper GI bleeding
May have history of UGI reflux
Systemically unwell (If free perforation or significant contamination)

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34
Q

How is a perforated ulcer managed?

A

Occasionally posterior (Retroperitoneal) DU can be managed without surgery
Surgery to close ulcer, omental patch placed over hole, high dose PPI.
H. pylori testing/eradication
Gastric ulcer biopsy for cancer

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35
Q

What are the causes of small bowel perforation?

A

Ischaemia - strangulated hernia, SMA/SMV thrombosis, SBO
Inflammatory - Crohns
Erosion - Small bowel tumours rare. Lymphoma most common.
Trauma - blunt or penetrating, foreign body, iatrogenic

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36
Q

What is the typical presentation of small bowel perforation?

A

Abdo pain
Systemically unwell

May have apparent cause - recent surgery, strangulated hernia, Crohns, evidence of bowel obstruction

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37
Q

Which investigations are done in suspected small bowel obstruction?

A

CT best to confirm perforation and identify site
Erect CXR may show free gas and preferred in unstable patient

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38
Q

How is small bowel obstruction managed?

A

Surgery most likely
Find perforation, repair, resect, +/- anastomosis (depends on stability and contamination. Stoma may be preferable).
Correct underlying cause
Washout contamination

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39
Q

What is the most common cause of large bowel perforation?

A

Diverticular disease
More common in men
NSAID use in 30% of cases
smoking increases risk

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40
Q

How does large bowel obstruction present?

A

History of causative event (recent colonoscopy)
Localised abdo pain (low left or low right)
Systemically unwell
Progressing to generalised peritonitis
Abdo distension (If cause is obstruction)
Closed loop large bowel obstruction and RIF pain 0 suggests impending caecal perforation. Relief of pain can occur initially when perforation occurs.

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41
Q

What does a closed loop large bowel obstruction and RIF pain suggest?

A

Impending caecal perforation.
Relief of pain can occur initially when perforation occurs.

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42
Q

How is colonic perforation diagnosed?

A

CT gold standard - establish anatomical site of perforation, identify additional pathology and assist pre-op planning.

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43
Q

How is colonic perforation managed?

A

Usually surgery - occasionally managed conservatively with percutaneous drainage.
Diseased bowel (cancer or Crohns) will never heal spontaneously
Segmental resection for localised problem
Subtotal colectomy may be needed if: Proctocolitis, Distal obstruction with proximal perforation, Rectal preservation usual in acute setting
Decide on anastomosis or stoma (depends on contamination and patient condition)

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44
Q

What are the symptoms of a rectal perforation?

A

Pelvic or back pain
PR bleeding
May not be systemically unwell due to containment in pelvis

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45
Q

How are rectal perforations diagnosed?

A

CT or XR with rectal contrast
MRI - high sensitivity and specificity for rectal pathology

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46
Q

How are rectal perforations managed?

A

Often conservatively
Complications need intervention - defunction with upstream colostomy, may heal spontaneously them stoma can be reversed

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47
Q

What are some extrinsic compression causes of bowel obstruction?

A

Abdominal masses
Adhesions/scar tissue (small bowel)
Hernias (mostly small bowel)
Volvulus

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48
Q

What are some bowel wall problems that can cause bowel obstruction?

A

Neoplasia
Inflammatory or fibrotic stricture/narrowing
Ischaemia
Paralytic ileus

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49
Q

What are some luminal causes of bowel obstruction?

A

Gallstones
Bezoar (Partially digested material that collects in body)/foreign body

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50
Q

Can bowels still be functional if they are obstructed?

A

Yes

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51
Q

What does absolute constipation often indicate?

A

Distal mechanical obstruction of colon

52
Q

Which type of bowel obstruction will usually settle without surgery on >90% of cases?

A

Adhesional SBO

53
Q

What is Gastric Outlet Obstruction?

A

Results from a disease process that causes mechanical impediment to gastric emptying

54
Q

What causes gastric outlet obstruction?

A

Malignancy 50-80% (Gastric, pancreatic or duodenal)
Peptic ulcer disease 5%

55
Q

What are the rarer causes of gastric outlet obstruction?

A

Foreign body obstruction
Crohn’s stricture
Gastric volvulus
Pancreatitis
Motility disorders (gastroparesis)

56
Q

What are the signs and symptoms or gastric outlet obstruction?

A

Vomiting (If non bilious, suggests obstruction proximal to D2)
Early satiety
Bloating
Weight loss and malnutrition
Succession splash (retained gastric material) - if noted >4 hours after meal, 50% will have GOO

57
Q

Which investigations are done for gastric outlet obstruction?

A

Bloods - may have low K+ or Cl- = metabolic acidosis from vomiting
CT usually diagnostic
Endoscopy
Contrast studies

58
Q

How is GOO managed?

A

Rehydrate
Correct electrolyte abnormality
NG tube
If benign -> High dose PPI, avoid NSAIDS, H. pylori eradication. Attempt endoscopic balloon dilatation. Surgery if above fails - resection or bypass
If malignant - resection if curative, bypass if palliative. Stenting.

59
Q

What are the causes of small bowel obstruction?

A

Adhesions
Hernias
Rarer: Paralytic ileus, Gallstone ileus, Tumours most commonly caecal cancer invading ICJ), Small bowel strictures (Crohn’s disease)

60
Q

How does adhesional SBO present?

A

Colicky central (midgut) abdo pain +/- distension
Visible peristalsis in slim patients
History of previous surgery
Vomiting or constipation (depends on level of obstruction)

61
Q

How is adhesional SBO diagnosed?

A

AXR - helpful but not specific
CT - gold standard
- Confirm diagnosis, identify level of
obstruction, identify adverse features such as
bowel ischaemia, volvulus or ‘closed loop’
Water soluble contrast follow through
- to confirm obstruction
- Some evidence osmotic action of contrast may
help resolve obstruction

62
Q

How is adhesional SBO managed?

A

Conservatively (>90%)
IVI,
NG (to decompress stomach and reduce aspiration risk)
Fluid balance monitoring (cathater)
NBM
If fails >72 hours, need surgery

Mechanical causes mostly need surgery - virgin abdomen (never had surgical procedure on abdo) and SBO usually necessitates urgent surgery.

63
Q

What is a gallstone ileus?

A

Mechanical obstruction due to gallstone impaction within GI tract
>70% female

64
Q

What is the pathophysiology of gallstone ileus?

A

Large gallstone (>2cm) forms and causes chronic cholecystitis
Gallbladder adheres to adjacent GI tract (most commonly duodenum)
Fistula from gallbladder to adherent bowel
Stone erodes into bowel and impacts in small bowel (up to 90% in distal ileum)

65
Q

What is the presentation of gallstone ileus?

A

Presents with features of SBO
May have hx of RUQ pain/cholecystitis (30-80%)

66
Q

Which findings on a CT are there for gallstone ileus?

A

SBO - gallstones may be seen
Aerobilia - air in biliary tree

67
Q

How is gallstone ileus usually managed?

A

Surgery but gallbladder NOT removed

68
Q

What is a paralytic ileus?

A

Transient impairment of motor activity of the bowel
Functional rather than mechanical obstruction

69
Q

Common cause of paralytic ileus?

A

Following major colorectal surgery - lasts 1-24 days post surgery
Thought to be due to adrenergic stimulation

Can also occur due to:
Critical illness
Uraemia or renal failure
Peritonitis
Abdominal trauma

70
Q

Incidence of paralytic ileus post surgery?

A

10-30%

71
Q

What is the gold standard investigation for paralytic ileus?

A

CT

72
Q

How is a paralytic ileus treated?

A

IVI
NG tube
Reduce oral intake
Iv nutrition if prolonged

73
Q

In Crohn’s disease, what % of patients within 20 years, will have a small bowel and large bowel stricture?

A

SB - 25-30%
LB - 10%

74
Q

Why do strictures occur in Crohn’s disease?

A

Likely prolonged inflammation leading to fibrosis and stricturing

75
Q

What are the risk factors for developing a SB/LB stricture in Crohn’s disease?

A

Ileal Crohn’s
Age <40 at diagnoses
Smoking
Perianal disease

76
Q

Is surgery more likely to be needed if there is inflammation or no inflammation at a SB/LB stricture in Crohn’s?

A

No inflammation
Inflammatory element may improve with medical treatment

77
Q

How is acute SBO managed in Crohn’s?

A

If fibrotic stricture - surgery
If inflammatory element - medical therapy, support nutrition
Surgery - Preserve bowel length, relieve obstruction, resection vs stricturoplasty, laparoscopic vs open surgery, +/- stoma

78
Q

What is the difference between a resection and a stricturoplasty?

A

Resection - removing bowel sections that stricture has affected
Stricturoplasty - Preserves bowel by widening strictures

79
Q

What % of cases of bowel obstruction are large bowel?

A

25%

80
Q

In LBO, >75% occur distal to which flexure?

A

Splenic

81
Q

Why are LBO more common distal to the splenic flexure?

A

Smaller calibre bowel compared to proximal, and more solid luminal contents.
Cancer + diverticular disease more common in distal colon

82
Q

What are the common causes of LBO?

A

Cancer (60%)
Diverticular disease (20%)
Volvulus
Intussusception
Acute colonic pseudo-obstruction (Ogilvie’s syndrome)

83
Q

What is intussusecption?

A

Bowel ‘telescopes’ in on itself, causing obstruction
Common cause in babies

84
Q

What is Acute colonic pseudo-obstruction (Ogilvie’s syndrome)?

A

Acute dilatation of the colon in absence of an anatomic lesion.
Problem with peristalsis.

85
Q

How does LBO present?

A

Absolute constipation - mechanical problem. May not be present initially with more proximal obstruction.
Abdo pain + bloating.

86
Q

What should you be aware of with RIF pain + obstruction?

A

Can imply impending caecal perforation

87
Q

Is vomiting always present in LBO?

A

No - can be absent, especially if ileocaecal junction patent

88
Q

How is LBO diagnosed?

A

AXR may show, but CT gold standard.
CT also shows latency of ICJ

89
Q

How do you determine on imaging if there is a closed loop bowel obstruction?

A

If small bowel distended - ICJ is incompetent (50%)
If SB if collapses - ICJ is competent = closed loop obstruction

90
Q

How is closed loop LBO managed?

A

Surgical emergency
Urgent decompression to prevent upstream (caecal) perforation
Laplace’s law

91
Q

What is Laplace’s law?

A

Caecum has widest diameter + thinnest wall of colon, therefore wall tension is highest when distended.

92
Q

How is LBO managed in cancer?

A

If operable + patient fit - Resection +/- anastomosis or stoma
Advanced cancer/patient not fit - Stoma or stent. Palliation.

93
Q

How is LBO managed in diverticular disease?

A

Acute obstruction - likely surgery. Resection +/- anastomosis, +/- stoma
If resection not possible - defunction upstream
Stents are not long-term option

94
Q

Why may a resection not be possible in LBO with diverticular disease?

A

Dense fibrosis with pelvic side adhesion

95
Q

What is intussusception?

A

Telescoping of a proximal segment of the GI tract within the lumen of the adjacent segment

96
Q

What are most cases of adult intussusceptions caused by?

A

Intraluminal pathology
2/3 causes by colorectal cancer
Other causes - IBD, Meckel’s diverticulum, large colonic polyp

97
Q

How is an intussusception treated?

A

Resection of whole intussusception +/- anastomosis

98
Q

What is Ogilvie’s syndrome?

A

Pseudo-obstruction
Severe impairment of gut peristalsis without mechanical obstruction

99
Q

What is the differential for Ogilvie’s syndrome?

A

Mechanical obstruction

100
Q

What are the risk factors for Ogilvie’s syndrome?

A

Critical illness
Recent major surgery
Postpartum (10% of cases, more common after C-section)
Medications - Clozapine

101
Q

What is the pathophysiology of Ogilvie’s syndrome?

A

Likely impaired regulation of colonic motor activity by the ANS

102
Q

In Ogilvie’s syndrome, there is significant risk of what when the caecum is >10cm?

A

Perforation

103
Q

How is Ogilvie’s syndrome managed?

A

Conservative - NG tube, reduce oral intake. Serial AXR to monitor caecal size.
Colonoscopic decompression
Neostigmine - rapid decompression. Needs cardiac monitoring - can cause bradycardia
Surgery if medical management failed or evidence or perforation

104
Q

What is intestinal ischaemia?

A

Any process that reduced intestinal blood flow
e.g. arterial occlusion, venous occlusion, arterial vasospasm

105
Q

What are the risk factors for intestinal ischaemia?

A

AF
HF
Renal failure
Prothrombotic condition
Older patient
Smoking

106
Q

What is acute ischaemia?

A

Sudden reduction in GI blood pressure
e.g. Embolic or thrombotic event, volvulus of vessel.

107
Q

Are younger patients without cardiac disease more likely to have venous of arterial acute ischaemia?

A

Venous

108
Q

How does acute ischaemia present?

A

Clinically vague
Abdo pain, out of proportion with clinical findings
If patient has AF - must suspect ischaemia
Nausea, vomiting, diarrhoea
PR bleeding if colonic
Acidaemia

109
Q

How is small bowel ischaemia investigated?

A

Bloods - high WBC and lactate
Imaging - XR may show SB distension or obstruction
CT - High specificity for SB ischaemia

110
Q

What CT findings in SB ischaemia would suggest gangrene?

A

Intramural gas
Portal venous gas
Free abdominal air/perforation evident

111
Q

How is small bowel ischaemia treated?

A

High mortality
IVI
NG tube for decompression
If gangrene
- Sugery for resection. Palliation of extensive.
- Stoma or anastomosis depending on case and patient condition. - Mechanical occlusion (volvulus) less likely to propagate. Vascular occlusion may get worse.
No gangrene - conservative in limited cases
- Severe mesenteric vasospasm or unfit for surgery
-Heparinisation
-?Thrombolysis

112
Q

What is acute ischaemia colitis?

A

Acute, transient compromise in blood flow below the metabolic needs of the colon
Resulting in mucosal ulceration, inflammation and haemorrhage.
Bleeding may be absent if ischaemia severe.

113
Q

What is the outcome of acute ischaemic colitis determined by?

A

Duration of hypoperfusion episode

114
Q

What are the causes of acute ischaemia colitis?

A

Heart failure, atherosclerotic disease (chronic reduction in flow)
AF (Embolic event)
Acute thrombosis
Medications - Chemo, NSAIDS, vasopressors
Previous AAA repair (Interrupton of IMA)

115
Q

How does acute ischaemic colitis present?

A

Colicky abdo pain
Diarrhoea and PR bleeding
Peritonitis unusual but suggests full thickness ischaemia or perforation

116
Q

What are the differentials for acute ischaemic colitis?

A

Other causes of colitis e.g. IBD, infective colitis

117
Q

How is acute ischaemic colitis diagnosed?

A

CT

118
Q

What findings would you see on a CT scan in acute ischaemic colitis?

A

Usual distribution around splenic flexure with normal bowel proximal and distal
Watershed area of usually poor perfusion at the splenic flexure

119
Q

What investigation can differentiate between causes of colitis?

A

Endoscopy

120
Q

How is ischaemic colitis treated?

A

> 90% conservatively
Resuscitation and monitoring
Anticoagulation - prophylactic dose may be adequate. Only long term if AF. No anti platelets.
Abx may or may not help
Smoking cessation

121
Q

When would surgery be considered in ischaemic colitis?

A

If severe, ongoing or concerns about gangrene

122
Q

What is the recurrence rate of ischaemic colitis?

A

<15%

123
Q

Is chronic mesenteric ischaemia more common in males or females?

A

Females 3:1

124
Q

What causes chronic mesenteric ischaemia/mesenteric angina?

A

Chronic arterial stenosis or occlusion
Mostly atherosclerotic (CV risk factors), can progress to acute event e.g. thrombosis

125
Q

20% of >65 year olds will have some stenosis of coeliac trunk or SMA in which condition?

A

Chronic mesenteric ischaemia/mesenteric angina

126
Q

What is chronic mesenteric ischaemia also known as?

A

Mesenteric angina

127
Q

What are the common symptoms of chronic mesenteric ischaemia?

A

Abo pain 15-30 minutes post meal
Chronic weight loss due to pain

128
Q

Why is there Abdo pain post mean in chronic mesenteric ischaemia?

A

After eating, mesenteric blood flow increases significantly. If arterial stenosis, limited increase is possible, therefore causing pain

129
Q

How is chronic mesenteric ischaemia treated?

A

Reduce risk factors
Revascularisation - surgical, end-vascular, post procedure anti platelet therapy

130
Q
A

Year 3 surgery (3 decks)

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