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Year 3 Surgery > 1 - The Acute Abdomen and Surgically Unwell Patient > Flashcards

1 - The Acute Abdomen and Surgically Unwell Patient Flashcards

1
Q

What does stridor indicate?

A

An upper airway obstruction

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2
Q

What is the epidemiology of appendicitis?

A

100 in 100k
M > F (1.4 : 1)

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3
Q

What is the pathophysiology of appendicitis?

A

Obstruction
Inflammation (appendix is blocked - continues to produce mucus - bacteria present then cause swelling)
Ischaemia
Perforation
Localised abscess
Generalised peritonitis

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4
Q

What are the S&S of appendicitis?

A

When the appendix is first inflamed - there is involvement of the visceral peritoneum over it - this is innervated by the ANS = vague pain in the midgut

As parietal peritoneum gets inflamed - this has somatic innervation - moves to the RLQ where it is sharper and more localised

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5
Q

What clinical signs can indicate appendicitis?

A
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6
Q

What are the DDs for appendicitis?

A

Mesenteric adenitis is the most common

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7
Q

What is mesenteric adenitis?

A

Inflammation of the lymph glands in the mesenteric tissues - when the layer of fat above is thin it can cause RLQ pain.

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8
Q

What is a meckel’s diverticulum?

A

Vestigial remnant of the vitelline duct - is a true diverticulum in that it involves all the layers of the bowel wall.

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9
Q

What is the rule of 2s regarding a meckel’s diverticulum?

A
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10
Q

What investigations can be done for appendicitis?

A
  • Clinical diagnosis
    Bloods - high WCC and CRP, raised bilirubin

USS
CT Scan
MRI

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11
Q

What is the management of appendicitis?

A

Surgery
ABx
If walled off mass - ABC and/- collect - treat with ABx and percutaneous drainage and appendicectomy when acute event has settled.

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12
Q

What are diverticulum of the intestines?

A

Protrusion of mucosal pouches through the bowel wall musculature.

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13
Q

Where in the body is the highest incidence of diverticulum found?

A

In the sigmoid colon - due the to high intra-luminal pressure here. Especially with a competent ileo-caecal valve.

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14
Q

What percentage of patients will have symptoms with diverticular disease.

A

10%
90% - have no symptoms

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15
Q

What is acute diverticulitis?

A

Inflammation of a diverticulum - thought to be due to a micro-perforation of a diverticulum.

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16
Q

How does diverticulitis present?

A
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17
Q

What are the differentials for diverticulitis?

A
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18
Q

What investigations can be done for diverticulitis?

A
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19
Q

How is diverticulitis classified?

A

The Hinchey classification - Stages I - IV

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20
Q

How is diverticulitis treated?

A

Contained abscesses will often resolve with ABx

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21
Q

What mechanisms can cause GI perforation?

A

Ischaemia (obstruction, vascular)
Infection
Erosion (malignancy or ulcerative disease)
Physical disruption

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22
Q

What is “a spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (eg, severe straining or vomiting)” called?

A

Boerhaave’s syndrome

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23
Q

What are the most common causes of oesophageal perforation?

A

Iatrogenic
15% Spontaneous - most due to Boerhaave’s
Foreign bodies
Caustic liquid ingestion (esp alkalis)

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24
Q

How does oesophageal perforation present?

A
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25
Q

Which triad is said to be classic of oesophageal perforation?

A

Mackler’s triad
- Vomiting
- Chest pain
- Subcutaneous emphysema

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26
Q

What investigations can be done for oesophageal perforation?

A

This pic - contrast has leaked out from lower oesophagus and into the chest.

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27
Q

How do we treat oesophageal perforation?

A

Small ones - may not need repair - sometimes just draining the leak and NBM will allow it to heal.

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28
Q

What is the most common cause of upper GI perforation?

A

Peptic ulceration

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29
Q

What are the RF for peptic ulceration?

A
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30
Q

What percentage of
- duodenal ulcers
- gastric ulcers
are caused by H pylori?

A

Duodenal - 90-95%
Gastric - 70-85%

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31
Q

How does upper GI perforation present?

A
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32
Q

How is a perforated upper GI ulcer managed?

A

Rarely - very large holes may require a distal gastrectomy

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33
Q

What are the causes of small bowel perforation?

A

Ischaemia
Inflammatory
Erosion
Trauma

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34
Q

What is the most common cause of small bowel perforation?

A

Iatrogenic

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35
Q

How does a small bowel perforation present?

A
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36
Q

How is a small bowel perforation managed?

A
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37
Q

What are the Risk factors for large bowel perforation?

A

Diverticular disease
NSAID use (30% of cases)
Smoking

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38
Q

What are the causes of large bowel perforation?

A
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39
Q

How does large bowel peroration present?

A
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40
Q

What should you be considering if you have a large bowel obstruction and RIF pain?

A

Caecal perforation

Relief of pain can occur initially when perforation occurs.

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41
Q

How is colonic perforation diagnosed?

A

CT = gold standard

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42
Q

How is colonic perforation managed?

A
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43
Q

What is the most common cause of rectal perforation?

A

Trauma - foreign body, penetrating trauma or iatrogenic

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44
Q

What are the symptoms of rectal perforation?

A

Pelvic or back pain
May be systemically unwell (unless contained in the pelvis)
PR bleeding

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45
Q

How is rectal perforation treated?

A
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46
Q

What are the causes of bowel obstruction?

A

Extrinsic (external) compression
Bowel wall problem
Luminal

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47
Q

What is the problem of having an obstructed proximal bowel?

A

Bowels may still be functional despite obstruction - so be cautious. These Ps will have early vomiting as a symptom.

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48
Q

What are the causes of gastric outlet obstruction?

A

50-80% = gastric malignancy

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49
Q

What are the S&S of gastric outlet obstruction?

A
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50
Q

What investigations can you do for gastric outlet obstruction?

A
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51
Q

At which point of the duodenum does the common bile duct enter?

How can this be used to differentiate types of obstruction?

A

D2

If obstruction is before CBD - will not have bilious vomiting. If the obstruction is after D2 you will have bilious vomiting (green colour).

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52
Q

What electrolyte imbalance can you get from vomiting?

A

Hypokalaemia
Hypochloraemia

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53
Q

How is gastric outlet obstruction managed?

A
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54
Q

What is the main cause of small bowel obstruction?

A

Adhesions cause 80-90%

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55
Q

What are RF for small bowel obstruction?

A

Crohns
Previous abdominal surgery
Age

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56
Q

Which is the commonest site of obstruction in the GI tract?

A

Small bowel

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57
Q

How does adhesional small bowel obstruction present?

A
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58
Q

How is small bowel obstruction diagnosed?

A

CT = gold standard
Contrast can confirm obstruction

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59
Q

What is it called when a loop of intestine twists around itself and the mesentery that supplies it causing bowel obstruction?

A

Volvulus

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60
Q

What is a closed loop obstruction?

A

When a segment of bowel is incarcerated at two different points.

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61
Q

How is adhesional small bowel obstruction managed?

A
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62
Q

What is gallstone ileus?

A

A mechanical obstruction in which a large gallstone gets stuck onto nearby bowel - inflammation - over time, stone gradually erodes through the walls, goes into the bowel (fistula) and sometimes it can obstruct the bowel towards terminal ileum. .

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63
Q

Does gallstone ileus occur more commonly in M or F?

A

F

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64
Q

How does a P will gallstone ileus present?

A

Features of SBO
May have Hx of RUQ pain / cholecystitis

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65
Q

What will CT show for a gallstone ileus?

A

Small bowel obstruction - gallstone may be seen

Aerobilia (air in the biliary tree)

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66
Q

How is gallstone ileus treated?

A

Surgery usually needed - small bowel is opened and stone removed. Gallbladder fistula means they are unlikely to form more stones

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67
Q

What is the transient impairment of motor activity of the bowel called?

A

Paralytic ileus

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68
Q

What is the major cause of paralytic ileus?

A

Surgery (10-30% of Ps after colorectal surgery)

Can also occur from
- Critical illness
- Uraemia or renal failure
- Peritonitis
- Abdominal trauma

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69
Q

How long does paralytic ileus last?

A

1-14 days after surgery

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70
Q

How is paralytic ileus diagnosed?

A

Often can be done clinically due to Hx of previous surgery.

If doubt - CT = gold standard

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71
Q

How is paralytic ileus managed?

A

Supportive Tx
- IV fluids
NG tube
Reduced oral intake
IV nutrition if prolonged (v rare)

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72
Q

Within 20 years of diagnosis - 25-30% of Crohn’s patients will have at least 1 SB stricture and 10% will have a LB stricture.

What are the risk factors for this?

A

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

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73
Q

How is SBO in Crohn’s Ps diagnosed?

A

CT & MRI

Absence of inflammation = surgery is more likely to be needed.

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74
Q

How is acute SBO managed in Crohn’s Ps?

A

If fibrotic stricture = surgery

If inflammation = medical therapy can be tried

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75
Q

What percentage of bowel obstruction cases involve the large bowel?

A

75%

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76
Q

What percentage of large bowel obstructions occur distal to the splenic flexure?

Why?

A

> 75%

Wider and thinner bowel more distally and more solid luminal contents.

Also - cancer and diverticular disease are more common in the distal colon

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77
Q

What are the most common causes of large bowel obstruction?

A

Cancer (60%)
Diverticular disease (20%)
Volvulus
Intussusception
Acute colonic pseudo-obstruction

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78
Q

What is Ogilvie’s syndrome?

A

Ogilvie syndrome, also known as acute colonic pseudo-obstruction (ACPO), is a sudden and unexplained paralysis of your colon. Your colon acts like it’s blocked or obstructed by something (pseudo-obstruction) but nothing is physically obstructing it. The problem is in your colon’s motor system.

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79
Q

How is Ogilvie’s syndrome managed?

A
80
Q

How does large bowel obstruction present?

A
81
Q

How is large bowel obstruction diagnosed?

A

AXR - may show dilated bowel
CT = gold standard

82
Q

How is closed loop large bowel obstruction treated?

A

Surgical emergency

Urgent decompression of obstruction needed to prevent upstream caecal perforation

83
Q

The caecum has the widest diameter and thinnest wall of the colon - which means the wall tension is the highest here when distended. What is this called?

A

Laplace’s law

84
Q

How is large bowel obstruction due to cancer managed?

A
85
Q

How is large bowel obstruction due to diverticular disease managed?

A

Acute obstruction - surgery - resection +/- anastomosis or +/- stoma.

If resection not possible - defunction upstream.

86
Q

What is telescoping of a proximal segment of the GI tract within the lumen of the adjacent tract called?

A

Intussusception

87
Q

What percentage of all intussusceptions occur in adults?

A

5-10%

88
Q

What is most intussusception in adults caused by?

A

Cancer (2/3rds)

Also - IBD, Meckel’s diverticulum, large colonic polyps

89
Q

What are the RF for intestinal ischaemia?

A

AF
HF
Kidney failure
Prothrombotic conditions
Older Ps
Smoking

90
Q

What can cause acute ischaemia of the bowel?

A

Embolus
Thrombus
Volvulus

91
Q

How does acute ischaemia of the bowel present?

A

Abdo pain - out of proportion with clinical findings

Nausea, vomiting, diarrhoea

PR bleeding if colonic

Academia

92
Q

What investigations are done for small bowel ischaemia?

A

Can also get raised IRP

93
Q

Why may the lactate be normal in a P who has small bowel ischaemia?

A

If it is due to a venous occlusion = the lactate can’t return into the bloodstream - so serum lactate appears normal.

94
Q

How is small bowel ischaemia treated?

A
95
Q

What are the causes of acute ischaemic colitis?

A

HF
Atherosclerotic disease
AF
Acute thrombosis
Medications - chemo, NSAIDs, vasopressors
Previous AAA repair (causing interruption of IMA)

96
Q

How does acute ischaemic collitis present?

A
97
Q

Which two main areas of the colon are prone to ischaemia?

A

Splenic flexure
Rectosigmoid junction

These are watershed areas

98
Q

What is the main diagnostic method for AIC?

A

CT

Endoscopy can differentiate between causes of colitis

99
Q

How is ischaemic collitis treated?

A
100
Q

What is chronic mesenteric ischaemia also known as?

What causes it?

A

Mesenteric angina

Usually caused by chronic arterial stenosis / occlusion due to atherosclerosis.

101
Q

How does chronic mesenteric ischaemia present?

A

Abdominal pain 15-30 mins after eating a meal - leading to chronic weight loss and a fear of eating.

Caused by arterial stenosis - not enough blood can enter into the bowel to deal with increased demands.

102
Q

How is chronic mesenteric ischaemia diagnosed and treated?

A
103
Q

What is shock?

A

An acute circulatory failure that compromises tissue perfusion

104
Q

What are the following signs of?

A

Carcinoid syndrome - sign of neuroendocrine tumour

105
Q

What are gynaecomastia and spider naevi caused by?

A

Increased oestrogen levels due to chronic liver disease

106
Q

What are the 5Fs of abdominal distension?

A

Fat
Fluid
Faeces
Foetus
Flatus

107
Q

Which side of the abdominal wall is an ileostomy sited?

A

Always the RHS

108
Q

What can swelling of the parotid lymph nodes be caused by?

A

Alcohol Excess

109
Q
A
110
Q

Name the 9 areas of the abdomen

A
111
Q

Can you normally palpate the kidney?

A

No

112
Q

Which structures in the abdomen are resonant and which are dull?

A

Resonant = gas - bowel / lungs

Dull = solid organs

113
Q

How do you percuss for the liver?

A

Start at 5th IC space and percuss downwards. An abnormal liver will extend > 2 finger breaths below the costal margin

114
Q

An enlarged spleen is?

A

Always pathological

115
Q

Which screening tool is used to identify adults at risk of malnourishment?

A

MUST Screening Tool

116
Q

What is the name of the folds of small bowel seen on Xray?

A

Valvulae conniventes

117
Q

What is the name of folds of large bowel?

A

Haustra

118
Q

Where does the embryological foregut extend to?

What is the blood supply of these structures?

What is the autonomic nerve supply of these structures?

A

Extends from oesophagus to D2

Supplied by coeliac artery

Nerve = vagus nerve

119
Q

What prevents reflux in the oesophagus?

A
120
Q

What produces acid in the stomach?

A

Parietal cells produce H+ via H+/K+ ATPase

These can be stimulated by
- PSS vagus nerve directly
- by Histamine release (from ECL cells)
- by gastrin release (from G cells) - produced in response to peptides in bowel lumen

121
Q

What is the commonest disorder of the GIT?

A

GORD

122
Q

What causes GORD?

A
123
Q

What are the RF of GORD?

A
124
Q

What are the symptoms of GORD?

A
125
Q

How is GORD diagnosed?

A
126
Q

Why is H pylori harmful?

A
127
Q

Which conditions are associated with H Pylori?

A

Gastritis
Dyspepsia
Peptic ulceration
Gastric cancer

128
Q

What is the medical treatment of GORD?

A
129
Q

How do
- PPIs work?
- Ranitidine work?

A
130
Q

What are the side effects of PPIs?

A

Diarrhoea
Inc risk of GI infection (e.g. C Diff)

131
Q

What is a hernia?

A
132
Q

What are the two types of hiatal hernia?

A

Sliding & Rolling

133
Q

What causes a sliding hiatal hernia?

What are the symptoms of this?

A
134
Q

What causes a rolling hiatus hernia?

What are the symptoms of this?

A
135
Q

What is the cause of gastritis?

A
136
Q

Why do NSAIDs cause gastritis?

A

Are reversible inhibitors of COX enzymes

COX1 = produces prostaglandins which are protective in the GI tract

COX2 = produces PGs which mediate pain and inflammation

Lose these PGs - get reduced gastric mucous and bicarb production, reduced gastric BF –> reduced protection of gastric mucosa and a reduced ability to repair.

137
Q

What are the causes of peptic ulceration?

A

H Pylori
NSAIDs

Rarer:
- Stress
- Malignancy
- Zollinger-Ellinson syndrome
- Medications

138
Q

What is Zollinger-Ellinson syndrome?

A

Rare neuroendocrine tumour of G cells - most often of the pancreas –> uncontrolled and excessive gastrin = multiple GI ulcers due to excessive acid production.

139
Q

Name 2 types of peptic ulcer. Which is the most common?

A

Duodenal ulcers
Gastric ulcers

Duodenal x 4 more likely than gastric

140
Q

Where are gastric ulcers most commonly found?

A

Lesser curve of the stomach

141
Q

How do peptic ulcers present?

A
142
Q

How are peptic ulcers diagnosed?

A

Hx and Ex
OGD

143
Q

How are peptic ulcers treated?

A
144
Q

What is acute upper GI bleeding split into?

A

Variceal (11%) and non-variceal bleeds (89%)

145
Q

What causes variceal bleeding?

A

Increased portal venous pressure (e.g. cirrhotic liver disease)

146
Q

How do we treat variceal bleeding?

A

Stop the bleeding
Reduce portal pressure
Medication (β blockers reduce portal pressure)
Radiological intervention
Endoscopic tx

147
Q

How do we non-variceal UGI bleeding?

A
148
Q

Where does the gastric duodenal artery travel?

What is the risk of this?

A

Behind D1

Can be eroded into by a posterior ulcer

149
Q

What is the difference between metaplasia and dysplasia?

A

Metaplasia = change from one cell type to another

Dysplasia = disordered cell development

150
Q

What is Barrett’s oesophagus?

A

Replacement of squamous epithelium with columnar epithelium in the oesophagus

151
Q

What are the RF for Barrett’s oesophagus?

A
152
Q

How is Barrett’s oesophagus categorised?

A

Based on level of dysplasia

High grade - needs Tx inc ablation, endoscopic removal or surgery
Low grade - mostly surveillance
Metaplasia without dysplasia - surveillance only

153
Q

What may reduce the progression of Barrett’s?

A

PPI

154
Q
A
155
Q

What are the causes of shock?

A

Hypovolaemic
Cardiogenic
Distributive (severe peripheral dilation - sceptic or anaphylactic)
Obstructive

156
Q

What are the S&S of shock?

A

Hypotension
Hyperventilation
Rapid weak pulse
Cold, clammy, cyanotic skin
Oliguria
Poss confusion, combativeness or anxiety

Clinically - metabolic acidosis, low O2, low central venous pressure.

157
Q

What are the 3 stages of shock?

A

Stage 1 - attempt at compensation = vasoconstriction

Stage 2 - decompensation - body mechanisms are unable to sustain perfusion

Stage 3 - irreversible changes - major damage to organs

158
Q

Which is the most common cause of shock?

A

Hypovolaemic

159
Q

How does hypovolaemia cause shock?

What causes this?

A

Preload insufficiency = reduces diastolic filling = low cardiac output.

Causes = haemorrhagic or non-hemorrhagic (e.g. volume loss from burns, V&D)

160
Q

What causes distributive shock?

A

Inappropriate expansion of circulatory capacity compared to volume.

Caused by failure of peripheral resistance or vasodilation of large veins

161
Q

What does peripheral resistance do?

A

Maintains cardiac after load - is controlled by the tone of arteriolar and capillary sphincters.

162
Q

Which is the most common distributive shock?

A

Septic shock

163
Q

What is anaphylactic shock caused by?

A

IgE Type 1 hypersensitivity - mast cells release histamine -> dilation of venous compartment and rapid movement of fluid into tissues.

164
Q

What are common culprits of anaphylactic shock?

A

Abx
Radiological contrast

165
Q

What is cardiogenic shock?

A

Failure of the pump = drastic reduction in cardiac output.

166
Q

What is obstructive shock?

A

Caused by extracardiac causes - e.g. pulmonary problems (causing RHF) or mechanical disruption = reduced preload.

E.g. PE, pul HT, valvular stenosis, tension pneumo etc.W

167
Q

What happens in shock?

A

Is a fall in arterial BP
SS activated. HR inc and tries to inc CO. Intense vasoconstriction (except sepsis) to restore vol by inc peripheral resistance.

Hypoxic tissues use anaerobic respiration - causes metabolic acidosis - then tachypnoea tries to compensate.

P = cold, pale, clammy, hypotensive, thready pulse and increased RR.

Septic shock - peripheries are vasodilator - unresponsive to SS. Skin is flushed, hot and CO is increased to fill dilated periphery. Pulse = bounding.

168
Q

How is hypovolaemic shock treated?

A

Identify cause of fluid loss - stop loss and give fluid replacement.

169
Q

How is cardiogenic shock treated?

A

Respiratory support
Correct electrolyte and acid-base
Drugs to maintain BP and CO
Treat underlying cause.

170
Q

What is a major problem in sepsis?

A

DIC (disseminated intravascular coagulation)

Sepsis - activation of clotting cascade exhausts supply of platelets and clotting factors and fibrinogen. Get high D-Dimer (as this is a fibrin degradation product).

DIC - causes spontaneous bruising or bleeding and uncontrollable haemorrhage

171
Q

How can you treat DIC?

A

Manage initial cause
IV heparin
Transfusion of clotting factors (FFP and cryoprecipitate)

172
Q

How do you treat anaphylactic shock?

A

Remove cause
Secure airway and give O2
Lie flat and raise feet
Start IV fluids
500mcgs IM adrenaline - 5m intervals if necessary.
Antihistamine by IV
Hydrocortisone by IV - blocks histamine receptors (takes several hours)

173
Q

What is the biphasic response of anaphylaxis?

A

Ps stabilise but relapse later on

174
Q

How does small bowel and large bowel obstruction differ?

A

Small bowel obstruction - get symptoms within hours

Large bowel obstruction - more insidious onset - presentation can be delayed by up to a week

175
Q

How much fluid is secreted into the GI tract each day?

A

10L

176
Q

What do the following types of vomiting suggest?
- Semi-digested food eaten a day or two earlier
- Bile-stained fluid
- Faeculent fluid

A

(1). Gastric outlet obstruction
(2). Small bowel obstruction
(3) Large bowel obstruction - distal.

177
Q

What percentage of ileocaecal valves are competent?

A

About 50%

178
Q

How does bowel strangulation occur?

A

Bowel can become trapped and the lumen obstructed. Venous return is occluded - causes bowel wall oedema and further obstruction. Closed loop of bowl dilates with gas fermentation - this and venous back pressure inhibits arterial inflow - this causing ischaemia and infarction.

179
Q

What types of hernia are there?

A

Inguinal
Femoral
Umbilical
Incisional

180
Q

How does a peritonitic abdomen present?

A

Rigid and tender abdomen
Bowel sounds are absent (no peristalsis)

181
Q

How does blood affect the peritoneum?

A

Causes irritation and peritonitis like symptoms, but more muted.

182
Q

What are the S&S of an intraabdominal abscess?

A

Worsening continuous abdominal pain
Diarrhoea
High swinging temperature

183
Q

AT which point is the cut off for blood passing via haematemesis or malena?

A

Blood lost beyond the duodenum should pass rectally.

184
Q

What bloods should you order for suspected GI haemorrhage?

A

FBCs
U&Es
Prothrombin ratio
LFTs
Blood group & antibody test
Order blood for transfusion

185
Q

What is a group and save blood test?

A

Determining the patient’s ABO and Rh D group. Performing an antibody screen, and identifying any atypical antibodies which may be present. Checking the results against any historical data that might be available for the patient.

The process takes around 40 minutes and no blood is issued.
If patient blood have atypical red cell antibodies, the laboratory will do additional tests to identify them.

If they have been pregnant or transfused in the last 3 months the sample is valid for 72 hours. If not, sample is valid for 7 days.

186
Q

What is a crossmatch?

A

A crossmatch is the final step of pretransfusion compatibility testing, to request blood from the laboratory.
Crossmatching involves physically mixing of patient’s blood with the donor’s blood, in order to see if any immune reaction occurs
After ensuring that donnor blood is compatible, the donor blood is issued and can be transfused to the patient.
This process takes around 40 minutes, in addition to the 40 minutes required to G&S the blood.
It is not possible for the laboratory to provide crossmatched blood without having processed a G&S sample first.
When is Crossmatch required?
Crossmatch is performed if blood loss is anticipated – the surgeon will usually inform about this.

187
Q

When should you order U&Es?

A

Vomiting and diarrhoea, dehydration, reduced urine output, diuretic therapy, urinary tract disease, renal failure, pancreatitis and sepsis

188
Q

When should you order clotting studies?

A

Acute pancreatitis and septicaemia (DIC), severe bleeding (consumption coagulopathy) or those with Hx of bleeding disorders

189
Q

How does pancreatitis affect clotting?

A

Can affect the clotting of the blood and make it hypercoaguable

190
Q

A 78 year old patient presents acutely unwell with generalised peritonitis. He has a background of COPD which causes him to get short of breath when he walks at speed but generally he is not symptomatic from this. He is talking coherently in full sentences in the Emergency Department but he is clearly unwell with the following observations:

HR 130
BP 90/50
SaO2 92%
RR 22

What is the first priority in managing him using the ABCDE approach?

(1). Activate the sepsis 6 protocols

(2) Give high flow oxygen (15L via non re-breathe mask)

(3) Administer 1L IV fluids over 4 hours

(4) Give 28% oxygen via Venturi mask in view of his COPD

(5) Organise a CT abdomen and alert emergency theatres

A

(2) Give high flow oxygen (15L via non re-breathe mask)

This question is about understanding the ABCDE priorities as discussed in the lecture for this week. As the patient is talking coherently, one can assume that his airway is patent which means that breathing should be the next priority. There are 2 oxygen options here – high flow or 28%. In the lecture, we discuss that an acutely unwell surgical patient is by default given high flow oxygen. The COPD here actually is clearly not too significant as he is generally fairly asymptomatic. In reality there are actually very few COPD patients who are genuinely dependent on their hypoxic drive to breathe, and therefore giving high flow oxygen is the correct answer for a clearly unwell surgical patient as he is more likely to die from hypoperfusion and hypoxia of the tissues than from hypoventilation from retention of CO2. Regardless, the latter will take time to develop (if at all), and clearly if concerned about the risk then you should monitor for signs of hypoventilation which can then be corrected/managed should the need arise, but the priority is to get the patient high flow O2 as he is clearly critically unwell. Sepsis 6 comes later after initial resuscitation (or during for some of the elements), fluids come as part of circulation (the next priority) and a CT and emergency theatre are clearly likely going to be needed at some point but are not the next priority.

191
Q

Which of the following are part of the classic triad of symptoms suggesting the presence of appendicitis (select 3 answers)?

-Right iliac fossa mass

-Pain migrating from right iliac fossa to central abdomen

-Vomiting and/or diarrhoea

-Right iliac fossa pain

-Positive Rovsing’s sign

-Dysuria

-Anorexia

-Pain migrating from central abdomen to right iliac fossa

-Raised temperature

A

The classic triad for appendicitis is migratory abdominal pain moving from the central area to the right iliac fossa (McBurney’s point), GI upset (vomiting and/or diarrhoea) and anorexia (>70% of cases). Despite this, appendicitis remains a challenge to diagnose clinically as many patients do not have some or even all of these. Three of the options are signs not symptoms, although they are strong indicators of appendicitis when present with the symptoms (RIF mass, raised temperature Rovsing’s sign). Dysuria is sometimes seen with appendicitis due to irritation of the bladder, but is not a classic feature and non-migratory RIF pain alone is not a classic symptom, although clearly some patients do present in this way. Answer b has the migratory pain moving in the wrong direction.

192
Q

Which of the following is true of diverticular disease?

(1). Diverticulitis occurs in up to 50% patients with known diverticula

(2). Diverticular disease is most commonly found in the rectum

(3). The Hinchey classification helps to guide treatment for diverticular perforation

(4). Laparotomy is always required for diverticular perforation

(5). >60% patients with diverticulitis will get a further episode within 10 years

A

The correct answer here is c) the Hinchey classification helps to guide treatment for diverticular perforation. Complications of diverticular disease only occur in around 10% of patient with diverticula in the bowel with diverticulitis being the most common. The diverticula protrude between the teniae coli muscles which run along the length of the colon but which fuse together in the rectum so therefore diverticula are not seen there. Many diverticular perforations can be managed without surgery if localised, often with antibiotics and sometimes requiring interventional radiology drainage of an abscess. Most cases of diverticulitis are isolated with <1/3 patients experiencing a further episode so hence elective surgery is not indicated for those with a first episode. Even a second episode is unlikely to be repeated further.

193
Q

A patient undergoes a laparotomy for a bowel perforation. Which of the following information does the surgeon need to consider when deciding whether to give the patient a stoma or perform an anastomosis (tick all that apply)?

a) Length of resected bowel

b) Age of the patient

c) Physiological stability

d) Contamination in the abdomen

e) Bowel obstruction

f) Current steroid treatment

g) Length of surgery

h) Perforation from Crohn’s disease

A

he correct answers here are c), d), f) and h). There are so many factors that can impact this decision and the list below is not exhaustive. This is simply to identify some of the considerations as has been eluded to in the lecture to say why patients may or may not be suitable for an anastomosis. The age of the patient per se is not a factor in deciding on an anastomosis but comorbidities are more likely in this group. Bowel obstruction can lead to relative size discrepancy between the proximal and distal bowel making an end to end join impossible, however a side to side or end to side join are alternatives and bowel obstruction per se does not mean an anastomosis is not possible – clearly this is a factor in the decision making that will need to be considered.

Disease factors
Malignant v non malignant (and if malignant then evidence of residual or metastatic disease?)
Crohns disease – possibly more likely to fail
Degree of contamination (faecal peritonitis v local contamination)
Abnormality of bowel ends (inflammation, ischaemia, diverticular disease)
Cause of perforation (gangrene from vascular problem high risk of worsening; isolated pathology less likely to propagate (e.g. strangulated hernia, iatrogenic injury))

Patient factors
Comorbidity (diabetes, heart/vascular disease)
Medications (steroids, immunosuppressants)
Cardiovascular instability in surgery (need for inotropic support)
Anatomical variants (narrow pelvis for male, short bowel segments or mesentery, hostile splenic flexure etc)
Previous surgery (adhesions, vascular compromise from previous bowel resection)
Body habitus (stoma complications higher from obese patients)

Surgeon factors
Senior v junior surgeon
Specialty experience (colorectal surgeon more likely to join a diverticular resection than a non specialist)
Personality (degree of risk acceptance/aversion)
Outcomes (surgeon level morbidity and mortality data in public domain)
Recent experience (similar cases with complications or not)

Environmental factors
Time available
Assistance available (colorectal anastomosis often requires an additional assistant)
Equipment availability (staplers etc)

194
Q

The majority of cases of adhesional small bowel obstruction will settle with conservative management. Which one of the following features suggest the patient is more likely to need surgical correction?

Vomiting and constipation at presentation

Obstruction of the more proximal small bowel

Developing peritonitis and rising blood lactate levels

Persistently high nasogastric drainage despite water soluble contrast reaching the colon

Failure of the obstruction to relieve by 48 hours post presentation

A

The correct answer here is “c) developing peritonitis and rising blood lactate levels.” This is because if the patient develops peritonitis then it is an indicator of possible perforation and the rising lactate levels suggest worsening shock and possibly can indicate bowel ischaemia which can happen with obstruction if it is not relieved. This is a clear indication for surgery. Vomiting and constipation are hugely variable with SBO because it will depend on the level of obstruction and the longevity of symptoms but in itself does not help with prognosis. Similarly, obstruction of the proximal small bowel does not predict a higher chance of surgery as long as one is confident it is adhesional. Answer d) is potentially confusing but is representative of the mixed clinical picture that we so often see with SBO. The fact that the water soluble contrast has reached the colon means that, by definition, it has managed to traverse the entire small bowel suggesting the obstruction has relieved, and it may well be that the NG drainage has just yet to settle. Clearly if this persists then one would need to consider if the obstruction is still present or has re-occurred, however again this on its own in the initial period after the contrast passes would not predict surgical intervention. If adhesional SBO has not relieved by 72 hours (not 48 as is the option) then this is predictive of a higher chance of failure of conservative management and therefore surgery is more likely to be needed.

195
Q

A patient presents with an obstructing sigmoid colon cancer. Her abdomen becomes significantly distended and she develops significant pain in the right iliac fossa. What is likely the cause of this picture?

Due to the obstruction the patient has developed acute appendicitis

She has an incompetent ileocaecal valve and the pain is due to reflux of colonic material back into the terminal ileum

Her sigmoid is so long with the obstruction that she is feeling the pain in the RIF instead of the left side

She likely has a closed loop obstruction with competent ileocaecal valve and her caecum is at risk of perforation

The sigmoid tumour is locally advanced and invading the right side of the pelvis causing ureteric obstruction

A

The correct answer here is “d) She likely has a closed loop obstruction with competent ileocaecal valve and her caecum is at risk of perforation.” A competent ileocaecal valve (in about 50% of the population) means that passage of faecal material can only go into the colon and cannot reflux back into the small bowel. If the colon is obstructed then this is important because the pressure will build much faster than if faeces can reflux back into the small bowel. The caecum has the widest diameter and the thinnest wall within the colon and therefore the wall tension will be highest (Laplace’s law) and hence the caecum is most likely to perforate if there is an obstruction – indicative by the RIF pain in this case. As mentioned in the lecture, a sudden relief of the RIF pain in this context can suggest that the caecum has ruptured, but regardless intervention is needed urgently. Answer b) is incorrect because this suggests the obstruction is not a closed loop and there is therefore more time to deal with the situation. If one diagnosis explains everything then it is not normally necessary to look for a second pathology and whilst statistically possible, acute appendicitis (answer a)) would not be likely here. Pains from the site of obstruction itself would not be likely as mentioned above (answer c)) and although colorectal cancers can cause ureteric obstruction (e)) this would not likely to present with this clinical picture.

196
Q

A 67 year old smoker presents with significant abdominal pain and vomiting. He has had no previous surgery. Examining him, he is noted to be in atrial fibrillation which was not previously known about and his abdomen is slightly distended but soft and no masses are felt. He is tender throughout but not significantly so, although he is requiring significant doses of morphine for his pain. His blood tests show a raised WBC and lactate.

Adhesional small bowel obstruction

Small bowel ischaemia

Closed loop large bowel obstruction

Perforated peptic ulcer

Acute diverticulitis

A

The answer is “b) Small bowel ischaemia.” He has a number of risk factors for vascular disease (smoker; new onset AF) which raises the possibility of a vascular issue. He also seems to have pain which is out of proportion with the clinical findings (that his abdomen is soft but he is requiring significant doses of pain relief). This is a diagnosis which is very hard to make clinically and therefore a high index of suspicion is needed. Adhesional bowel obstruction does not usually cause such significant pain unless there are complications, and he has had no previous surgery which makes this much less likely. A closed loop LBO would likely result in significant abdominal distension but vomiting is not invariable and a perforated peptic ulcer would likely have more abdominal signs such as peritonitis and tenderness and acute diverticulitis would likely be more localised, but again more tenderness would be expected and lactate levels would not necessarily be high unless the patient is dehydrated.

197
Q

A patient is day 6 following an open anterior resection with defunctioning ileostomy. She has been persistently vomiting for 3 days and an NG tube was placed the previous day which has drained >2L bilious fluid since insertion. Her stoma has not produced anything since surgery.

What is the most likely diagnosis here? Also, consider how you might rule the other differentials out
Hide answer choices

Paralytic ileus
Correct answer

Adhesional small bowel obstruction

Obstruction of the stoma from the abdominal muscle being too tight

Incorrect orientation of the stoma

Small bowel obstruction from herniation into the surgical wound

A

It is important to note that all of these are potential diagnoses for this patient and the questions is what is most likely. With that in mind, the correct answer is “a) paralytic ileus” as the patient is in the early days after an open colorectal procedure. Looking at the rest of the possible diagnoses, they are less likely, but if the ileus seems to be persisting longer than expected (most are resolved within 14 days and most sooner than that), then a review of the other differentials is needed. Early adhesional SBO is very unusual but sometimes is seen. This is seen on a CT as a focal area of obstruction rather than a more widespread small bowel distention without specific site of hold up seen with ileus. If the muscle incision through which the stoma is pulled (and even more unusually the skin) are too tight then the stoma may not work and sometimes a stoma will need revision to increase the size of the aperture – there may also be oedema in the SB in the stoma which worsens the problem, but a CT will show dilatation to the stoma and then collapsed bowel beyond. Getting the stoma the wrong way round in this type of surgery would be unusual but in other situations, such as performing a trephine to pull out a defunctioning stoma without being able to check the orientation of the bowel within the abdomen, they can be twisted which can result in obstruction. Again, a CT will show the issue to be at the stoma rather than elsewhere, and sometimes this is not fully appreciated until the patient is in theatre for a revision. Once again, early hernias are unusual but need consideration if an apparent ileus is prolonged. It is thought that larger (10-12mm) laparoscopic port sites are more at risk of this than smaller (5mm) ones, but some surgeons do not close these defects. It is also possible for small bowel to be caught up in a wound closure stitch or to slide up into the wound between stitches, but this is unusual and CT will confirm any potential site of herniation with obstruction.

Year 3 Surgery (15 decks)

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