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1

Causes of bloody diarrhoea

 ischaemic colitis
 campylobacter, shigella, salmonella, E. coli,
amoeba, pseudomembranous colitis
 UC, Crohn’s
 CRC, polyps

2

Causes of pus in stools

IBD, diverticulitis, abscess

3

Management for diarrhoea

Treat cause

Oral or IV rehydration

Codeine phosphate or loperamide after each loose stool

Anti-emetic if assoc. n/v: e.g. prochlorperazine

Abx (e.g. cipro) in infective diarrhoea → systemic illness

4

What is C.diff

 Gm+ve spore-forming anaerobe
 Release enterotoxins A and B
 Spores are v. robust and can survive for >40d

5

Risk factors for c.diff infection

 Abx: clindamycin, cefs, co-amox, ciprofloxacin
- up to 2m after
 ↑age
 In hospital: ↑ ̄c length of stay, ↑ ̄c C. diff +ve contact
 PPIs

6

Clinical presentation of infection with c.diff

 Asymptomatic
 Mild diarrhoea
 Colitis
 Pseudomembranous colitis
- fever, dehydration, abdo pain, bloody diarrhoea, mucus PR
 Fulminant colitis

7

Investigations for c.diff

 Bloods: ↑↑CRP, ↑↑WCC, ↓albumin, dehydration
 CDT ELISA -toxin A&B
 Stool culture

8

Complications of c.diff infection

 Paralytic ileus
 Toxic dilatation → perforation
 Multi-organ failure

9

Management of c.diff

Barrier nursing - put in side room
 Stop causative Abx
 Avoid antidiarrhoeals and opiates
 Enteric precautions

1st line: Metronidazole 2wk 2nd line: Vanc 125mg
Severe: Vanc 1st

Urgent colectomy may be needed if
 Toxic megacolon
 ↑ LDH
 Deteriorating condition

10

Causes of constipation

OPENED IT
Obstruction - mechanical (adhesion/hernia/ca) or post op ileus
Pain - fissure
Endocrine/ electrolytes - ↓T4, ↓Ca, ↓K, uraemia
Neuro - MS, Myelopathy, Cauda Equina
Elderly
Diet/ Dehydration
IBS
Toxins - opiods

11

Management of constipation

 Drink more
 ↑ dietary fibre

Bulking: ↑ faecal mass → ↑ peristalsis - fybogel (Ispaghula husk)
 CI: obstruction and faecal impaction

Osmotic: retain fluid in the bowel - Lactulose

Stimulant: ↑ intestinal motility and secretion - Senna
 CI: obstruction, acute colitis
 SE: abdo cramps

Softeners
 For painful anal condition - Liquid paraffin

Phosphate enema (osmotic)

Suppositories
 Glycerol (stimulant)

12

Diagnosis of IBS

Abdo discomfort / pain for ≥ 12wks which has 2 of:
 Relieved by defecation
 Change in stool frequency (D or C)
 Change in stool form: pellets, mucus

+2of:
 Urgency
 Incomplete evacuation
 Abdo bloating / distension
 Mucous PR
 Worsening symptoms after food

Exclusion criteria
 >40yrs
 Bloody stool
 Anorexia
 Wt. loss
 Diarrhoea at night

13

Management of IBS

Bloods - incl Coeliac and TSH
+/- colonoscopy

- Exclusion diets can be tried
- Fybogel for constipation and diarrhoea
- Antispasmodics for colic/bloating (e.g. mebeverine)
- Amitriptyline may be helpful
- CBT

14

Causes of dysphagia

Inflammatory
 Tonsillitis, pharyngitis
 Oesophagitis: GORD, candida
 Oral candidiasis
 Aphthous ulcers

Mechanical Block
- Luminal
 FB
 Large food bolus
- Mural
> Benign stricture
 Web (e.g. Plummer-Vinson)
 Oesophagitis
 Trauma (e.g. OGD)
> Malignant stricture- Pharynx, oesophagus, gastric
 Pharyngeal pouch
- Extra-mural
 Lung Ca
 Rolling hiatus hernia
 Mediastinal LNs (e.g. lymphoma)
 Retrosternal goitre
 Thoracic aortic aneurysm

Motility Disorders
- Local
Achalasia
 Diffuse oesophageal spasm
 Nutcracker oesophagus
 Bulbar / pseudobulbar palsy (CVA, MND)
- Systemic
 Systemic sclerosis / CREST
 MG

15

Presentation of dysphagia

 Dysphagia for liquids and solids at start
- Yes: motility disorder
- No, solids > liquids: stricture
 Difficulty making swallowing movement: bulbar palsy
 Odonophagia: Ca, oesophageal ulcer, spasm
 Intermittent: oesophageal spasm
 Constant and worsening: malignant stricture
 Neck bulges or gurgles on drinking: pharyngeal pouch

16

Signs that dysphagia could present with

 Cachexia
 Anaemia
 Virchow’s node (+ve = Troisier’s sign)
 Neurology
 Signs of systemic disease (e.g. scleroderma)

17

Investigations for dysphagia

URGENT upper GI endoscopy +- biopsy (if >55, with weight loss, abdo pain, dyspepsia)

 Bloods: FBC, U+E
 Barium swallow ± video fluoroscopy
 Oesophageal manometrry
 +- USS/EUS/CT thorax

18

Pathophysiology of achalasia

 Degeneration of myenteric plexus (Auerbach’s)
 ↓ peristalsis
 LOS fails to relax
- most commonly idiopathic

19

Presentation of achalasia

 Dysphagia: liquids and solids at same time
 Regurgitation
 Substernal cramps
 Wt. loss

20

Investigations for achalasia

 Ba swallow: dilated tapering oesophagus (Bird’s beak)
 Manometry: failure of relaxation + ↓ peristalsis
 CXR: may show widended mediastinum
 OGD: exclude malignancy

21

Rx of achalasia

 Med: CCBs, nitrates
 Int: endoscopic balloon dilatation, botulinum toxin injection
 Surg: Heller’s cardiomyotomy (open or endo)

22

Pharyngeal pouch pathophysiology

Outpouching of oesophagus between upper boarder of cricopharyngeus muscle and lower boarder of inferior constrictor of pharynx
 Weak area called Killian’s dehiscence.
 Defect usually occurs posteriorly but swelling usually bulges to left side of neck.
 Food debris → pouch expansion → oesophageal
compression → dysphagia.

23

Presentation and rx of a pharyngeal pouch

Pres: regurgitation, halitosis, gurgling sounds

Rx: excision, endoscopic stapling

24

Diffuse oesophageal spasm presentation

 Intermittent chest pain ± dysphagia
 Ba swallow shows corkscrew oesophagus

25

Nutcracker oesophagus presentation

 Intermittent dysphagia ± chest pain
↑ contraction pressure ̄c normal peristalsis

26

Causes of an oesophageal rupture

- Iatrogenic - endoscopy, biopsy, dilatation
- violent emesis (boerhaave's syndreom)
- carcinoma
- Trauma (surgical emphysema ±pneumothorax)

27

Features of oesophageal rupture

- Odonophagia
- Mediastinitis (tachypnoea, dyspnoea, fever, shock)
- surgical emphysema

28

management of oesophageal rupture

PPI, Abx, NGT

29

Symptoms of dyspepsia

 Epigastric pain
 Bloating
 Heartburn
ALARM
 Anaemia
 Loss of wt.
 Anorexia
 Recent onset progressive symptoms
 Melaena or haematemesis
 Swallowing difficulty

30

Causes of dyspepsia

 Inflammation: GORD, gastritis, PUD
 Ca: oesophageal, gastric
 Functional: non-ulcer dyspepsia

31

Management of new onset dyspepsia

OGD if >55 or ALARMS
- Try conservative for 4 weeks
> stop NSAIDS, CCBS
> Lose wt., stop smoking, ↓ EtOH
> Avoid hot drinks and spicy food
> OTC - Antacids/gaviscon

- Test for H. pylori if no improvement: breath or serology
 +ve → eradication therapy
 -ve → PPI trial for 4wks

OGD if no improvement

32

Eradication therapy for H.Pylori

Triple therapy for 1 week
- `PPI
- Amoxicillin
- Clarithromycin

33

Presentation of Duodenal Ulcers v gastric ulcers

DU
Epigastric pain:
 Before meals and at night
 Relieved by eating or milk
GU
 Epigastric pain:
 Worse on eating
 Relieved by antacids
 Wt. loss

34

Risk factors for PUD

H. pylori (90%)
 Drugs: NSAIDs, steroids
 Smoking
 EtOH
 gastric emptying (↑ DU, ↓GU)
 Blood group O (PU)
 Stress --> Cushings, burns, sepsis, trauma

35

Complications of PUD

Haemorrhage
 Haematemeis or melaena
 Fe deficiency anaemia

Perforation
 Peritonitis and distension, vomiting

Gastric Outflow Obstruction
 Vomiting, colic, distension, succission splash

Malignancy
 ↑ risk ̄c H. pylori

36

Investigations for PUD

 Bloods: FBC, urea (↑ in haemorrhage)
 C13 breath test
 OGD (stop PPIs >2wks before)
 Campylobacter-like organism test (CLO) / urease test for H. pylori (urea --> CO2 + ammonia - neutralises stomach acid)
 Biopsy ulcer to check for Ca
 Gastrin levels if Zollinger-Ellison suspected

37

Conservative Management of PUD

 Lose wt.
 Stop smoking and ↓ EtOH
 Avoid hot drinks and spicy food
 Stop drugs: NSAIDs, steroids
 OTC antacids

38

Medical management of PUD

 OTC antacids: Gaviscon, Mg trisilicate
 H. pylori eradication
 Full-dose acid suppression for 1-2mo
 PPIs: lansoprazole 30mg OD
 H2RAs: ranitidine 300mg nocte
 Low-dose acid suppression PRN

39

Surgical management of PUD

 No acid → no ulcer
 Acid secretion
stimulated by gastrin and vagus N.

Vagotomy +/- antrectomy ( distal half of stomach removed)

Subtotal gastrectomy

40

Complications of gastric surgery

Physical
 Stump leakage
 Abdominal fullness
 Reflux or bilious vomiting (improves ̄c time)
 Stricture

Metabolic
- Dumping syndrome
 Abdo distension, flushing, n/v
Early: osmotic hypovolaemia
 Late: reactive hypoglycaemia
- Blind loop syndrome → malabsorption, diarrhoea
 Overgrowth of bacteria in duodenal stump
 Anaemia: Fe + B12
 Osteoporosis
- Wt. loss: malabsorption of ↓ calories intake

41

Pathophysiology of GORD

LOS dysfunction → reflux of gastric contents → oesophagitis.

42

Risk factors for GORD

 Hiatus hernia
 Smoking
 EtOH
 Obesity
 Pregnancy
 Drugs: anti-AChM, nitrates, CCB, TCAs
 Iatrogenic: Heller’s myotomy

43

Symptoms of GORD

Oesophageal
 Heartburn
 Related to meals
 Worse lying down / stooping
 Relieved by antacids
 Belching
 Acid brash, water brash
 Odonophagia
 Hoarseness

Extra-oesophageal
 Nocturnal asthma
 Chronic cough
 Laryngitis, sinusitis

44

Anti- reflux mechanisms

- LOS
- Angle of His
- Pressure in abdominal cavity higher than thoracic
- R crus of diaphragm acts as a sling around oesophagus

45

Complications of GORD

 Oesophagitis: heartburn
 Ulceration: rarely → haematemesis, melaena, ↓Fe
 Benign stricture: dysphagia
 Barrett’s oesophagus
- metaplasia of squamous to gastric columnar epithelium and goblet cell
 Oesophageal adenocarcinoma
- Metaplasia → dysplasia → adenocarcinoma

46

Differential diagnosis of GO reflux

Oesophagitis
 Infection: CMV, candida
 IBD
 Caustic substances / burns
PUD
Oesophageal Ca

47

Investigations for GORD

Isolated - no Ix
Bloods: FBC
CXR: hiatus hernia may be seen
OGD if:
 >55yrs
 Symptoms >4wks
 Dysphagia
 Persistent symptoms despite Rx
 Wt. loss
 OGD allows grading by Los Angeles (A-D)
Classification
Ba swallow: hiatus hernia, dysmotility 24h pH testing ± manometry
 pH <4 for >4hrs (demeester score)

48

Conservative management of GORD

 Lose wt.
 Raise head of bed
 Small regular meals ≥ 3h before bed
 Stop smoking and ↓ EtOH
 Avoid hot drinks and spicy food
 Stop drugs: NSAIDs, steroids, CCBs, nitrates

49

Medical management of GORD

 OTC antacids: Gaviscon, Mg trisilicate
 1: Full-dose PPI for 1-2mo
 Lansoprazole 30mg OD
 2: No response → double dose PPI BD
 3: No response: add an H2RA
 Ranitidine 300mg nocte
 Control: low-dose acid suppression PRN

50

Surgical management, indications and complications of GORD

Nissen Fundoplication - Mobilise gastric fundus and wrap around lower
oesophagus
- Indications: all 3 of:
 Severe symptoms
 Refractory to medical therapy
 Confirmed reflux (pH monitoring)

Complications
- Gas-bloat syn.: inability to belch / vomit
- Dysphagia if wrap too tight
OTHER
Radiofrequency ablation. magnetic beads

51

Classifications of hiatus hernias

Sliding (80%)
 GOJ slides up into chest
 assoc.GORD

Rolling (15%)
 GOJ remains in abdomen but a bulge of stomach rolls into chest alongside the oesophagus
 LOS remains intact so GORD uncommon
 Can → strangulation

Mixed (5%)

52

Gastric volvulus symptoms

Borchardt's triad
- severe epigastric pain
- retching without vom
- inability to pass NG tube

53

Ix for hiatus hernia

OGD: assess for oesophagitis and upwards displacement GOJ

CXR: gas bubble and fluid level in chest

24h pH + manometry: exclude dysmotility or achalsia

Ba Swallow

54

Rx of hiatus hernias

Lose wt.

Rx reflux

Surgery if intractable symptoms despite medical Rx OR rolling
- funoplication/ curoplasty

55

Risk factors for hiatus hernia

Age (reduced diaphragm tone)
raised intra-abdo pressure
0 pregnancy
0 obesity
0 ascites

56

Differentials of Haematemesis

VINTAGE

Varices
Inflammation (PUD/ oesopha/gastr- itis)
Neoplasia (oesoph/gastric)
Trauma (Mallory-weiss/ Boerhavve)
Angiodysplasia/ HHT/ Dieulafoy lesion
Generalised bleeding diathesis - warfarin, thrombolytics, CRF
Epistaxis

57

Difference between mallory-weiss and boerhaave's

Mallory-Weiss - mucosal Tear
Boerhaave’s Syndrome - Full-thickness tear
 2cm proximal to LOS

58

Signs on examination after an Upper GI bleed

 Signs of CLD - telangectasia, purpura, jaundice
 PR:melaena
 Shock?
- Cool, clammy, CRT>2s
- ↓BP (<100) or postural hypotension (>20 drop)
- ↓ urine output (<30ml/h)
- Tachycardia
- ↓GCS
- ↓ JVP

59

What is the Rockall score

Prediction of re-bleeding and mortality after Upper GI bleed
- Initial score pre-endoscopy
 Age
 Shock: BP, pulse
 Comorbidities
- Final score post-endoscopy
> Final Dx + evidence of recent haemorrhage
 Active bleeding
 Visible vessel
 Adherent clot

Initial score ≥3 or final >6 are indications for surgery

60

Pathology of oesophageal varices

Portal HTN → dilated veins @ sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins

61

Causes of portal hypertension

Pre-hepatic: portal vein thrombosis

Hepatic: cirrhosis (80% in UK), schisto (commonest
worldwide), sarcoidosis.

Post-hepatic: Budd-Chiari, RHF, constrict pericarditis

62

Management of oesophageal varices

- bleed prevention
 1: β-B, repeat endoscopic banding
 2: β-B, repeat banding, TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt)
- IR creates artificial channel between hepatic vein and portal vein → ↓ portal pressure.

63

Management of an Upper GI bleed

- Head-down
- High flow oxygen & protect airway
- 2 x 14G cannulae + IV bolus
- Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match 6u, ABG, glucose

- if remains shocked - o- blood
- notify surgeons if severe

IF VARICEAL BLEED - Terlipressin IV (splanchnic vasopressor)
 Prophylactic Abx: e.g. ciprofloxacin 1g/24h

Urgent endoscopy
- Haemostasis of vessel or ulcer:
 Adr injection; Thermal coagulation; Fibrin glue; Endoclips

Variceal bleeding:
 2 of: banding, sclerotherapy, adrenaline,
coagulation
 Balloon tamponade ̄c
 TIPSS

64

Indications for surgery after Upper GI bleed

 Re-bleeding
 Bleeding despite transfusing 6u
 Uncontrollable bleeding at endoscopy
 Initial Rockall score ≥3, or final >6.

65

Risk factors for oesophageal cancer

- alcohol
- smoking
- achalasia
- GORD
- Fatty diet
- Low vit A/C

66

Pathophysiology of oesophageal cancer

- 65% adenocarcinoma - lower 3rd
- 35% SCC - upper and middle 3rd

67

Presentation of oesophageal cancer

- Progressive dysphagia
- weight loss
- retrostrenal chest pain and dyspepsia
- lymphadenopathy
- hoarseness (recurrent laryngeal n invasion)
- cough +/- aspiratino pneumonia
- odonophagia
- mets - jaunice, hepatomegaly, ascites

68

Ix for oesophageal cancer

OGD + biopsy
- Bloods
- Staging CT
EUS - t stage

69

Staging used for oesophageal cancer

TMN
T1 - submucosa
T2 - muscularis propria
T3 - adventitia
T4 - adjacent structures

70

Causes of perforation

Inflammatory
- chemical - PUD, Foreign body
- infection - appendicitis, diverticulitis, meckels, cholecystitis,
- ischaemia - mesenteric,, obstructive Ca, Bezoar, faeces
- colitis - fistula, toxic megacolon

Traumatic
- iatrogenic - surgery. endoscopy
- penetrating force
- direct rupture - booerhavve/ mallory weiss

71

Ix for perforated GIT

- Blood - FBC, Amylase, CRP, clotting, ABG
- urine dipstick
- Erect CXR (erect 15min)
- AXR - (riglers and psoas sign)
- CT scan

72

Mx of Perforated PU

- A-E
- NBM
- fluid resuscitation
- catheter +/- CVP line
- analgesia
- Abx
- NGT

+/- surgery is systemically unwell - abdominal washout and repair (patch - DU); may require gastrectomy

73

Ix for gastric outflow obstruction

- ABG - hypercholraemic hypokalaemic met alkalosis
- AXR (dilated gastric air bubble air fluid level, collapsed distal bowel)
- OGD

74

Rx for gastric outflow obstruction

- correct metabolic abnormalities
- benign --> endscopic ballow dilation/ gastroenterostomy
- malignant - stent/ resection

75

Risk factors for gastric cancer

- atrophic gastritis - pernicious anaemia, h.pylori)
- diet high nitrates
- smoking and alcohol
- blood group A
- low social class
- familial - E cadherin abnormality
- partial gastrectomy

76

Pathology of gastric cancer

Mainly adenocarcinomas, located on gastric antrum

77

Symptoms of gastric cancer

- weight loss + anorexia
- dyspepsia
- dysphagia
- n & v

78

Signs of gastric cancer

- anaemia
- epigastric mass
- jaundice
- ascites
- hepatomegaly
- virchow's node
- acanthosis nigricans

79

Complications of gastric cancer

- perforation
- upper Gi bleed - haematemesis, melaena
- gastric outlet obstruction

80

Ix for gastric cancer

URGENT OGD + biopsy
- CXR/USS/ CT - mets
Staging - CT CAP

81

Complications of gastrectomy

- death
- anastomotic leak
- poor QoL
- Vit B12 def
- re-operation

82

describe the excretion of bilirubin

Hb → unconjugated to BR by splenic macrophages
 uBR → cBR by BR-UDP-glucuronyl transferase in liver
 Secreted in bile then cBR → urobilinogen (colourless)
 Some urobilinogen is reabsorbed, returned to liver and re-excreted into bile.
 Some reabsorbed urobilinogen is excreted into the urine
 The urobilinogen that remains in the GIT is converted to stercobilin (brown) and excreted.

83

Causes of pre-hepatic jaundice

Excess BR production
 Haemolytic anaemia
 Ineffective erythropoiesis
 e.g. thalassaemia

84

Causes of Hepatic jaundice

Unconjugated
↓ BR Uptake
 Drugs: contrast, RMP  CCF
↓ BR Conjugation
 Hypothyroidism
 Gilbert’s (AD)
 Crigler-Najjar (AR)
Neonatal jaundice is both ↑ production + ↓ conjug.

Hepatocellular Dysfunction
 Congen: HH, Wilson’s, α1ATD
 Infection: Hep A/B/C, CMV, EBV
 Toxin: EtOH, drugs
 AIH
 Neoplasia: HCC, mets
 Vasc: Budd-Chiari1

85

Causes of post-hepatic jaundice

Obstruction
 Stones
 Ca pancreas
 Drugs - OCP, sulfonylureas
 PBC
 PSC
 Biliary atresia
 Choledochal cyst
 Cholangio Ca
Inflammatory LN at porta hepatis - TB/ Ca
Mirizzi's syndrome

86

Ix for Jaundice

- Urine
 pre - No BR (acholuric); ↑ urobilinogen; ↑Hb if intravascular haemolysis
 hepatic - ↑BR; ↑ urobilinogen
 post- ↑↑BR; No urobilinogen

- LFTs
 pre - ↑uBR; ↑AST; ↑LDH
 hepatic - ↑ cBR (usually); ↑AST:↑ALT; >2=EtOH/ <1=Viral; ↑ GGT (EtOH, obstruction); ↑ALP; Function: ↓ albumin, ↑ PT
 post- ↑↑cBR; ↑AST,↑ALT; ↑↑ALP; ↑GGT

- Other
 pre - FBC and film, Coombs, Hb electrophoresis
 hepatic - FBC, Ab, a1AT, Liver biopsy
 post - Abdo US (dilated ducts >6mm), ERCP/MRCP; Ab

87

Causes of liver failure

- cirrhosis
- acute
 Infection: Hep A/B, CMV, EBV, leptospirosis
 Toxin: EtOH, paracetamol, isoniazid, halothane
 Vasc: Budd-Chiari
 Other: Wilson’s, AIH
 Obs: eclampsia, acute fatty liver of pregnancy

88

Signs of liver failure

 Jaundice
 Oedema + ascites
 Bruising
 Encephalopathy
 Aterixis
 Constructional apraxia (5-pointed star)
 Fetor hepaticus
Signs of cirrhosis / chronic liver disease

89

Ix for liver failure

Blood
 FBC: infection, GI bleed, ↓ MCV (EtOH)
 U+E - ↓U, ↑Cr: hepatorenal syndrome. Urea synth in liver -->poor test of renal function
 LFT
- AST:ALT > 2 = EtOH
- AST:ALT < 1 = Viral
- Albumin: ↓ in chronic liver failure
- PT: ↑ in acute liver failure
 Clotting: ↑INR
 Glucose
 ABG: metabolic acidosis
 Cause: Ferritin, α1AT, caeruloplasmin, Abs,
paracetamol levels

Microbiology
 Hep, CMV, EBV serology
 Blood and urine culture
 Ascites MCS + SAAG

Radiology
 CXR
 Abdo US + portal vein duplex

90

Pathophysiology and classification of hepatorenal syndrome

 Cirrhosis → splanchnic arterial vasodilatation → effective circulatory volume → RAS activation → renal arterial vasoconstriction.
 Persistent underfilling of renal circulation → failure

 Type 1: rapidly progressive deterioration (survival
<2wks)
 Type 2: steady deterioration (survival ~6mo)

91

Rx of hepatorenal syndrome

 IV albumin + splanchnic vasoconstrictors (terlipressin)
 Haemodialysis as supportive Rx
 Liver Tx is Rx of choice

92

Mx of liver failure

 Manage in ITU
 Rx underlying cause: e.g. NAC in paracetamol OD
 Good nutrition: e.g. via NGT ̄c high carbs
 Thiamine supplements
 Prophylactic PPIs vs. stress ulcers

Monitor - fluids, bloods, glucose

93

Complications of liver failure

 Bleeding: Vit K, platelets, FFP, blood
 Sepsis: tazocin (avoid gent: nephrotoxicity)
 Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
 Hypoglycaemia: regular BMs, IV glucose if <2mM
 Encephalopathy: avoid sedatives, lactulose ± enemas,
rifaximin
 Seizures: lorazepam
 Cerebral oedema: mannitol

94

Drugs to avoid prescribing in liver failure

opiates, oral hypoglycaemics, Na-containing IVI

- Warfarin effects ↑

- Hepatotoxic drugs: paracetamol, methotrexate,
isoniazid, salicylates, tetracycline

95

Poor prognostic factors in liver failure

 Grade 3/4 hepatic encephalopathy
 Age >40yrs
 Albumin <30g/L
 ↑INR
 Drug-induced liver failure

96

Criteria for liver transplant

Kings college

Paracetamol-induced
pH< 7.3 24h after ingestion
Or all of:
PT > 100s
Cr > 300uM
Grade 3/4 encephalopathy

Non-paracetamol
PT > 100s
Or 3 out of 5 of:
Drug-induced
Age <10 or >40
>1wk from jaundice to encephalopathy
PT > 50s
BR ≥ 300uM

97

Pathophysiology of cirrhosis

Irreversible loss of hepatic architecture with bridging fibrosis and nodular regeneration

98

Signs of cirrhosis

Hands
 Clubbing (± periostitis)
 Leuconychia (↓ albumin)
 Terry’s nails (white proximally, red distally)
 Palmer erythema
 Dupuytron’s contracture

Face
 Pallor: ACD
 Xanthelasma: PBC
 Parotid enlargement (esp. ̄c EtOH due to dehydration increasing salvia production)

Trunk
 Spider naevi (>5, fill from centre)
 Gynaecomastia
 Loss of 2O sexual hair

Abdo
 Striae
 Hepatomegaly (may be small in late disease)
 Splenomegaly
 Dilated superficial veins (Caput medusa)
 Testicular atrophy

Hyperdynamic circualtion

99

Complications of cirrhosis

- Decompensation --> heptatic failure (jaundice, encephalopathy, ↓Albumin, bruising (↑INR), hypoglycaemia)

- Spontaneous bacterial peritonitis

- Portal hypertension
Splenomegaly
Ascites
Varices - oeosphgeal, caput medusa, piles
Encephalopathy

- ↑ risk of HCC

100

Ix to find cause of cirrhosis

 EtOH: ↑MCV, ↑GGT
 NASH: hyperlipidaemia, ↑ glucose
 Infection: Hep, CMV, EBV serology
 Genetic: Ferritin, α1AT, caeruloplasmin (↓ in Wilson’s)
 Abs
 Ca: α-fetoprotein

Abdo US + PV Duplex
 Small / large liver
 Focal lesions
 Reversed portal vein flow
 Ascites - Ascitic Tap + MCS
- PMN >250mm3 indicates SBP

Liver biopsy

101

Different Ab in cirrhosis

 AIH: SMA, SLA, LKM, ANA
 PBC: AMA
 PSC: ANCA, ANA
 Ig: ↑IgG – AIH, ↑IgM – PBC

102

Mx of cirrhosis

Good nutrition
EtOH abstinence
Colestyramine for pruritus
Screening
 HCC: US & AFP every 3-6 m
 Oesophageal varices: endoscopy +/- banding

Specific
 HCV: Interferon-α
 PBC: Ursodeoxycholic acid
 Wilson’s: Penicillamine

Decompensation
 Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
 Coagulopathy: Vit K, platelets, FFP, blood
 Encephalopathy: avoid sedatives, lactulose ± enemas,
rifaximin
 Sepsis / SBP: tazocin (avoid gent: nephrotoxicity)
 Hepatorenal syndrome: IV albumin + terlipressin

103

What is the Child-Pugh Grading score

Grades Cirrhosis
 Predicts risk of bleeding, mortality and need for Tx

 Graded A-C using severity of 5 factors
 Albumin
 Bilirubin
 Clotting
 Distension: Ascites
 Encephalopathy

Score >8 = significant risk of variceal bleeding

104

Where are the portosystemic anastomoses

Oesophageal varices
- Left and short gastric veins
and Inf. oesophageal veins

Caput medusae
Peri-umbilical veins and Superficial abdo wall veins

Haemorrhoids
Sup. rectal veins and Inf. and mid. Rectal veins

105

Pathophysiology of Encephalopathy

 ↓Hepatic metabolic function
 Diversion of toxins from liver directly into systemic
system.
 Ammonia accumulates and pass to brain where
astrocytes clear it causing glutamate → glutamine
 ↑ glutamine → osmotic imbalance → cerebral oedema

106

Classification of Encephalopathy

 1: Confused – irritable, mild confusion, sleep inversion
 2: Drowsy – ↑ disorientated, slurred speech, asterixis
 3: Stupor – rousable, incoherence
 4: Coma – unrousable, ± extensor plantars

107

Presentation of encephalopathy

 Asterixis, ataxia
 Confusion
 Dysarthria
 Constructional apraxia
 Seizures

108

Precipitants of encephalopathy

HEPATICS
 Haemorrhage: e.g. varices
 Electrolytes: ↓K, ↓Na
 Poisons: diuretics, sedatives, anaesthetics
 Alcohol
 Tumour: HCC
 Infection: SBP , pneumonia, UTI, HDV
 Constipation (commonest cause)
 Sugar (glucose) ↓: e.g. low calorie diet

109

Management of encephalopathy

20 degrees head up
- Correct any precipitants
 Avoid sedatives
 Lactulose ± PO4 enemas to ↓ nitrogen-forming bowel
bacteria → 2-4 soft stools/d
 Consider rifaximin PO to kill intestinal microflora

110

Pathophysiology of ascites

Back-pressure → fluid exudation
 ↓ effective circulating volume → RAS activation
 (In cirrhosis: ↓ albumin → ↓ plasma oncotic pressure
and aldosterone metabolism impaired)

111

Symptoms of ascites

Distension → abdominal discomfort and anorexia
 Dyspnoea
 ↓ venous return

112

Ix for ascites

Bloods: FBC, U+E, LFTs, INR, chronic hepatitis screen

US: confirm ascites, liver echogenicity, PV duplex

Ascitic tap
 MCS and AFB
 Cytology
 Chemistry: albumin, LDH, glucose, protein
 SAAG = serum albumin – ascites albumin

Liver biopsy

113

Management of ascites

 Daily wt. aiming for ≤0.5kg/d reduction
 Fluid restrict <1.5L/d and low Na diet
 Spironolactone + frusemide (if response poor)
 Therapeutic paracentesis ̄c albumin infusion (100ml
20% albumin /L drained)
- Respiratory compromise
- Pain / discomfort
- Renal impairment
 Refractory: TIPSS

114

Spontaneous bacterial peritonitis
- causative organisms
- Ix
- management

- ascites and peritonitic abdomen
 E. coli, Klebsiella, Streps

Complicated by hepatorenal syn. in 30%

 Ix: ascitic PMN > 250mm3 + MC+S
 Rx: Tazocin or cefotaxime until sensitivities known
 Prophylaxis: high recurrence - cipro long-term

115

Presentation of an alcoholic

 Fatty liver → hepatitits → cirrhosis
 AST:ALT >2, ↑ GGT

GIT
 Gastritis, erosions
 PUD
 Varices
 Pancreatitis
 Carcinoma

CNS
 Poor memory / cognition
 Peripheral polyneuropathy (mainly sensory)
 Wernicke’s encephalopathy
- Confusion; Ophthalmoplegia (nystagmus, LR palsy); Ataxia
 Korsakoff’s: amnesia → confabulation
 Fits, falls

Heart
 Arrhythmias: e.g. AF
 Dilated cardiomyopathy
 ↑BP

Blood
 ↑MCV
 Folate deficiency →anaemia

116

Screening tool for alcoholics

CAGE
 Cut down?
 Annoyed by people’s criticisms
 Guilty about drinking
 Eye opener?

117

Features of alcohol withdrawal

0-72h after last drink
 Consider in new ward pt (≤3d) ̄c acute confusion

signs
- Confusion, fits, hallucinations: esp formication (DTs)
- ↑HR, ↓BP, tremor

118

Management of alcohol withdrawal

Tapering regimen of chlordiazepoxide PO / lorazepam IM

Thiamine

119

Management of alcholism

 Group therapy or self-help (e.g. AA)
 Baclofen: ↓ cravings
 Acamprosate: ↓ cravings
 Disulfiram: aversion therapy

120

Presentation of alcoholic hepatitis

 Anorexia
 D/V
 Tender hepatomegaly
 Ascites
 Severe: Jaundice, bleeding, encephalopathy

121

Ix findings in alcoholic hepatitis

 Bloods: ↑MCV, ↑GGT, AST:ALT>2
 Ascitic tap
 Abdo US + PV duplex

122

Management of alcoholic hepatitis

 Stop EtOH
 Rx withdrawal
 High dose B vitamins: Pabrinex
 Optimise nutrition
 Daily wt., LFT, U+E, INR
 Mx complications of failure

123

Score that predicts mortality in alcoholic hepatitis

Maddrey score predicts mortality
 Mild: 0-5% 30d mortality
 Severe: 50% 30d mortality
 1yr after admission: 40% mortality

124

Describe the different HBV Ab

 HBsAg +ve = current infection
(>6mo = chronic disease)

 HBeAg +ve = high infectivity

 Anti-HBc IgM = recent infection

 Anti-HBc IgG = past infection

 Anti-HBs = cleared infection or vaccinated

125

Presentation of hepatitis B

Prodromal phase
 Fever, malaise, arthralgia, nausea, anorexia
 Distaste for cigarettes

Icteric phase
 Jaundice, HSM, lymphadenopathy, cholestasis

Extra-hepatic features due to immune complexes
 Urticaria or vasculitic rash
 Cryoglobulinaemia
 PAN
 GN
 Arthritis

126

Types of viral hepatitis, causes and how they are spread

A- FO
Seafood, especially abroad
B- IV
Blood, body fluids, babies (vertical)
C- IV
Mainly blood. Less vertical cf. HCV
D- IV
Dependent on prior HBV infection
E- FO
Developing world

127

Management of viral hepatitis

A & E - supportive, avoid alcohol, +/- IFN α (fulminant hepatitis)
B - supportive, avoid alcohol, +/- PEGinterferon α2b (chronic disease)
C - PEGinterferon α2b + ribavirin

128

Risk factors for non-alcoholic fatty liver disease

 Obesity
 HTN
 T2DM
 Hyperlipidaemia

129

Presentation of NAFLD

 Mostly asymptomatic
 Hepatomegaly and RUQ discomfort may be present.

130

Ix and Mx for NAFLD

 BMI
 Glucose, fasting lipids
 ↑ transaminases: AST:ALT <1  Liver biopsy

Mx -
 Lose wt.
 Control HTN, DM and lipids

131

Pathophysiology of NAFLD

↑ Fat diet and ↓ exercise

hepatic steatosis

↓ FAA ox and ↑ lipogenesis and ↑ lipid export

Insulin resistance

132

What is Budd-Chiari syndrome and causes

Hepatic vein obstruction → ischaemia and hepatocyte damage → liver failure or insidious cirrhosis.

- hypercoagulable - myeloproliferative, OCP, Anti-PL
- Local tumour - HCC

133

Presentation of Budd-Chiari syndrome

 RUQ pain: stretching of Glisson’s capsule
 Hepatomegaly
 Ascites: SAAG ≥1.1g/dL
 Jaundice (and other features of liver failure)

134

Rx of Budd-Chiari syndrome

 Anticoagulate unless there are varices
 Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
 Other options: thrombolysis, angioplasty, TIPSS
 Transplant if fulminant hepatic failure or cirrhosis
 Rx underlying cause

135

Presentation of AI hepatitis

 Constitutional: fatigue, fever, malaise
 Cushingoid: hirsute, acne, striae
 Hepatitis
 HSM
 Fever
 Amenorrhoea
 Polyarthritis
 Pulmonary infiltration
 Pleurisy

136

Presentation of PBC

 Pruritus and fatigue
 Pigmentation of face
 Bones: osteoporosis, osteomalacia (↓ vit D)
 Big organs: HSM
 Cirrhosis and coagulopathy (↓ vit K)
 Cholesterol ↑: xanthelasma, xanthomata
 Steatorrhoea

Jaundice often occurs late

137

Pathology of PBC

Intrahepatic bile duct destruction by chronic
granulomatous inflammation → cirrhosis

138

Rx of PBC

Symptomatic
 Pruritus: colestyramine, naltrexone
 Diarrhoea: codeine phosphate
 Osteoporosis: bisphosphonates

Specific
 ADEK vitamins
 Ursodeoxcholic acid: ↓LFTs but no effect on mortality or need for transplant

Liver transplant
 End-stage disease or intractable pruritus
 Recurrence occurs in ~20% but doesn’t usually
→ graft failure.

139

Pathophysiology of PSC

Inflammation, fibrosis and strictures and intra- and
extra-hepatic ducts.

Chronic biliary obstruction → secondary biliary cirrhosis → liver failure

140

Presentation of PSC

Symptoms
 Jaundice
 Pruritus and fatigue
 Abdo pain

Signs
 Jaundice: dark urine, pale stools
 HSM

141

Complications and associations of PSC

 Bacterial cholangitis
 ↑ Cholangiocarcinoma
 ↑ CRC

ASSOCIATED UC
- pANCA +ve

142

Rx of PSC

NEED TRANSPLANT
 Pruritus: colestyramine, naltrexone
 Diarrhoea: codeine phosphate

 ADEK vitamins
 Ursodeoxycholic acid improves cholestasis only
 Abx for cholangitis
 Endoscopic stenting for dominant strictures
 Screening - Cholangiocarcinoma: US + Ca19-9 and CRC: colonoscopy

143

Signs and Symptoms of liver tumours

Symptoms
 Benign tumours are usually asymptomatic
 Systemic: fever, malaise, wt. loss, anorexia
 RUQ pain: stretching of Glisson’s capsule
 Jaundice is often late, except in cholangiocarcinoma
 May rupture → intraperitoneal haemorrhage

Signs
 Hepatomegaly: smooth or hard and irregular
 Signs of chronic liver disease
 Abdominal mass
 Hepatic bruit (HCC)

144

Pathology of liver tumours

90% of liver tumours are 2O metastases
 stomach, lung, colon, breast, uterus

90% of primary tumours are HCC.

145

Causes and Mx of HCC

 Viral hepatitis
 Cirrhosis: EtOH, HH, PBC
 Aflatoxins (produced by Aspergillus)

- resection
- chemo, percutaneous ablation and embolization

146

Causes of Cholangiocarcinoma

 Flukes (Clonorchis)
 PSC
 Congenital biliary cysts
 UC

147

Presentation and Mx of Cholangiocarcinoma

 Fever, malaise
 Abdominal pain, ascites, jaundice
 ↑BR, ↑↑ALP

Mx - resect; pallative stent

148

Indications for liver transplant in CLD

 Advanced cirrhosis
 HCC

149

Contra- indications for liver transplant in CLD

 Extra-hepatic malignancy
 Severe cardiorespiratory disease
 Systemic sepsis
 HIV infection
 Non-compliance ̄c drug therapy

150

Complications of liver transplant

Acute rejection (T-cell mediated)
 50% @ 5-10 days
 Pyrexia, tender hepatomegaly
 ↑ or change immunosuppressants
 Sepsis
 Hepatic artery thrombosis
 CMV infection
 Chronic rejection (6-9mo): shrinking bile ducts
 Disease recurrence (e.g. HBV)

151

Epidemiology of UC v CD

UC - 30s
Smoking protective TH2-mediated
CD - 20s
Smoking ↑ risk TH1/TH17-mediated

152

Macroscopic features of UC v CD

> UC
Rectum + colon ± backwash ileitis
Contiguous
No Strictures

> CD
Mouth to anus esp. terminal ileum
Skip lesions
Strictures

153

Microscopic features of UC v CD

> CD
Transmural Inflammation
Ulcers - Deep, thin, serpiginous → cobblestone mucosa
Marked Fibrosis
Granulomas
Fistulae

> UC
Mucosal Inflammation and Crypt Abscesses
Ulcers - Shallow, broad
Pseudoplyps

154

Presentation of UC v CD

Fatigue, anorexia, malaise
 +/- fever
 Abdominal tenderness

UC
 Diarrhoea
 Blood ± mucus PR
 Abdominal discomfort
 Tenesmus, faecal urgency

CD
 Diarrhoea (not usually bloody)
 Abdominal pain
 Wt. loss
 RIF mass,
 Perianal abscess, fistulae, tag
 anal/rectal stricture

155

Extra-intestinal features of IBD

Apthous ulcers
Pyoderma gangrenosum
Iritis
Erythema nodosum
Sacroilitis
Arthralgia/AS
Clubbing, Ca - Cholang, gall/renal stones

156

Complications of UC

 Toxic megacolon
- Diameter >6cm
- Risk of perforation
 Bleeding
 Malignancy
- CRC and Cholangiocarcinoma
 Strictures → obstruction
 Venous thrombosis

157

Complications of CD

Fistulae
- Entero-enteric/colonic → diarrhoea
- Enterovesical → frequency, UTI
- “pepperpot” anus

Strictures → obstruction
Abscesses
 Abdominal
 Anorectal

Malabsorption
 Fat → Steatorrhoea, gallstones
 B12 → megaloblastic anaemia
 Vit D → osteomalacia
 Protein → oedema

Toxic megacolon and Ca may occur (< cf. UC)

158

Ix findings in UC

 FBC: ↓Hb, ↑WCC
 LFT: ↓albumin
 ↑CRP/ESR
 Blood cultures

Stool
 MCS: exclude Campy, Shigella, Salmonella, C.diff

Imaging
 AXR: megacolon (>6cm), wall thickening
 CXR: perforation
 CT
 Ba / gastrograffin enema
- Lead-pipe: no haustra
- Thumbprinting: mucosal thickening
- Pseudopolyps: regenerating mucosal island

Ileocolonoscopy + regional biopsy (at least 2 from 5 sites)

159

Classification of UC severity

Mild
Fewer than 4 motions/ day; small amount of blood

Moderate
4-6 motions/ day; mild-severe blood

Severe
6 + motions a day. Visible blood
+ 1 of:
Pyrexia
HR >90
Anaemia
Erythrocyte sedimentation rate (mm/hour) > 30

160

Management of acute severe UC

 Resus: Admit, IV hydration, NBM
 Hydrocortisone: IV 100mg QDS + PR; switch to oral when improve then taper
(IV ciclosporin if CI)
 Transfuse if required
 Thromboprophylaxis: LMWH
 Monitoring
- Bloods: FBC, ESR, CRP, U+E
- Vitals + stool chart
- Twice daily examination
- ± AXR

161

Medical management of UC

Inducing Remission
- 5- ASAs (Mesalasine
- Prednisolone
+/- suppositories/enemas
- Infliximab if steroid sparing

Maintaining remission
1)Sulfasalazine/mesalasine (PO/ Topical)
2) Azathioprine/ Mercaptopiurine PO
3) Inflixmab

162

Indications for emergency and elective surgery

 Toxic megacolon
 Perforation
 Massive haemorrhage
 Failure to respond to medical Rx

Elective - Chronic symptoms despite medical therapy
- Carcinoma or high-grade dysplasia

163

Surgical management of UC
- emergency
- elective

Total / subtotal colectomy --> end ileostomy ± mucus fistula

After ~3mo
 Completion proctectomy + Ileal-pouch anal anastomosis (IPAA) or end ileostomy
 Ileorectal anastomosis (IRA)

Elective
 Panproctocolectomy --> end ileostomy or IPAA
 Total colectomy --> IRA

164

Complications after UC surgery

Abdominal
 SBO
 Anastomotic stricture
 Pelvic abscess
Stoma: retraction, stenosis, prolapse, dermatitis
Pouch
 Pouchitis (50%) (abdo pain, bloody diarrhoea, nausea)
metronidazole + cipro
 ↓ female fertility
 Faecal leakage

165

Ix for CD

Bloods
 FBC: ↓Hb, ↑WCC
 LFT: ↓albumin
 ↑CRP/ESR
 Haematinics: Fe, B12, Folate
 Blood cultures

Stool
 MCS: exclude Campy, Shigella, Salmonella, C.diff

Imaging
 AXR: obstruction, sacroileitis
 CXR: perforation
 MRI - severity, pelvic disease and fistula
 Small bowel follow-through or enteroclysis
- Skip lesions
- Cobblestoning: ulceration + mural oedema
- String sign of Kantor: narrow terminal ileum

Endoscopy
 Ileocolonoscopy + regional biopsy

166

Management of a severe CD attack

↑temp, ↑HR, ↑ESR, ↑CRP, ↑WCC, ↓albumin

 Resus: Admit, NBM, IV hydration
 Hydrocortisone: IV + PR if rectal disease (switch oral when can)
 Abx: metronidazole PO or IV
 Thromboprophylaxis: LMWH
 Dietician Review - Elemental diet; Consider parenteral nutrition
 Monitoring
- Vitals + stool chart
- Daily examination

No improvement --> methotrexate +/- infliximab

167

Medical management of CD

Inducing remission
1) Sulfasalazine
2) prednisolone
3) methotrxate
4) infliximab

Maintaining remission
1) azathioprine or mercaptopurine
2) methotrexate
3) Infliximab / adalimumab

168

Indications for surgery in CD

Emergency
 Failure to respond to medical Rx
 Intestinal obstruction or perforation
 Massive haemorrhage

Elective
 Abscess or fistula
 Perianal disease
 Chronic ill health  Carcinoma

169

Surgical management of CD
and its complications

 Limited resection: e.g. ileocaecal
 Stricturoplasty
 Defunction distal disease ̄c temporary loop ileostomy

Complications
 Stoma complications
 Enterocutaneous fistulae
 Anastomotic leak or stricture
 Short gut syndrome (Steatorrhoea
; ADEK and B12 malabsorption; Bile acid depletion → gallstones; Hyperoxaluria → renal stones)

170

Presentation of coeliac disease

GLIAD

GI malabsorption - fatigue and weakness
- n/v/d, abdo distension, colic, flatus, weight loss, steatorrhoea, vit def

Lymphoma and carcinoma
Immune associations - T1DM, IgA def
Anaemia
Dermatitis herpetiformis and apthous ulcers

171

Ix findings in coeliac disease

- Anaemia, ↓alb, vitamin def
- Anti-endomysial IgA Ab and anti-TTG IgG, Anti-gliadin

172

Definition of true and false diverticulum

Diverticulum is an outpouching of tubular structure
- true - composed of complete wall
- false - composed of only mucosa

173

Pathophysiology of diverticular disease

- Associated with raised intraluminal pressure (low fibre diet, no osmotic effect keeping stool wet)
- mucosa herniates through muscularis propria at points of weakness where perforating arteries enter
- most often sigmoid

174

Symptoms of diverticular disease

- altered bowel habit +/- left sided colic (relieved by defecation)
- nausea
- flatulence

175

Presentation of diverticulitis

- abdominal pain and tenderness (often LIF, localised peritonitis)
- pyrexia

176

Pathophysiology of diverticulitis

- inspissated faeces --> obstruction of diverticulum

177

Complications

- perforation (sudden onset chest pain, peritonitis and shock - air under diaphragm)
- haemorrhage (PR bleed)
- abscess (swinging fever, leukocytosis)
- fistulae
- strictures

178

Management of acute diverticulitis

- mild - bowel rest (fluids only) + co-amox
- admit if unwell, cant tolerate fluids and uncontrolled pain

medical
- NBM
- IV fluids
- Analgesia
- Abx - cefuroxime and metronidazole

Surgery - if perforation haemorrhage, stricture/ obstruction
- hartmanns / resection

179

Hinchley grading of perforation due to diverticulitis

1) small confined pericolic abscess
2) large abscess extending into pelvis
2) generalised purulent peritonitis
3) generalised faecal peritonitis

180

Symptoms of B3 (niacin) deficiency

Diarrhoea, Dermatitis, Dementia

181

Different types of gallstones

Cholesterol Stones: 20%
 Large
 Often solitary
 Formation ↑ according to Admirand’s Trangle
- ↓ bile salts
- ↓ lecithin
- ↑ cholesterol

Pigment Stones: 5%
 Small, black, gritty, fragile
 Calcium bilirubinate
 Associated c¯ haemolysis

Mixed Stones: 75%
 Often multiple
 Cholesterol is the major component

182

Risk factors for gallstones

 Female
 OCP, pregnancy
 ↑ age
 High fat diet and obesity
 Racial: e.g. American Indian tribes
 Loss of terminal ileum (↓ bile salts)

183

Complications of gallstones

In the Gallbladder
1. Biliary Colic
2. Acute cholecystitis ± empyema
3. Chronic cholecytsitis
4. Mucocele
5. Carcinoma
6. Mirizzi’s syndrome

In the CBD
1. Obstructive jaundice
2. Pancreatitis
3. Cholangitis

In the Gut
1. Gallstone ileus

184

Pathogenesis and presentation of biliary colic

Gallbladder spasm against a stone impacted in the neck of the gallbladder – Hartmann’s Pouch.

 RUQ pain radiating → back (scapular region)
 Assoc. c¯ sweating, pallor, n/v
 Attacks may be ppted. by fatty food and last <6h
 o/e may be tenderness in right hypochondrium
 ± jaundice if stones passes in to CB

185

Differentials of biliary colic

Pancreatitis

Cholecystitis

Bowel Perforation

186

Ix for gallstone disease

 Urine: bilirubin, urobilinogen, Hb
 Bloods: FBC, U+E, amylase, LFTs, G+S, clotting, CRP

Imaging
 AXR: 10% of gallstones are radio-opaque
- pneumobilia - gas froming infection
 eCXR: look for perforation
 US:
- Stones: acoustic shadow
- Dilated ducts: >6mm
- Inflamed GB: wall oedema

 If Dx uncertain after US - HIDA cholescintigraphy: shows failure of GB filling
(requires functioning liver)

 If dilated ducts seen on US → MRCP

187

Management of biliary colic

Conservative
 Rehydrate and NBM
 Opioid analgesia: morphine 5-10mg/2h max
 High recurrence rate - surgical Rx favoured

Surgical
 As for conservative + either:
 Urgent lap chole (same admission)
 Elective lap chole @ 6-12wks

188

Differences between biliary colic, acute cholecystitis and Ascending cholangitis

All - RUQ
Fever - Acute cholecystitis and ascending cholangitis
Jaundice - Ascending cholangitis

189

Pathogenesis of acute cholecystitis

Stone or sludge impaction in Hartmann’s pouch
 → chemical and / or bacterial inflammation

190

Complications of acute cholecystitis

1. recurrence
2. Gangrene and rarely perforation
3. Chronic cholecystitis
4. Empyema

191

Symptoms and signs of Acute Cholecystitis

Symptoms
 Severe RUQ pain
- Continuous
- Radiates to right scapula and epigastrium
 Fever
 Vomiting
Signs
 Local peritonism in RUQ
 Tachycardia c¯ shallow breathing
 ± jaundice
 Murphy’s sign
- 2 fingers over the GB and ask pt. to breath in → pain and breath catch. Must be –ve on the L

192

Management of acute cholecystitis

Conservative
 NBM
 Fluid resuscitation
 Analgesia: paracetamol, diclofenac, codeine
 Abx: cefuroxime and metronidazole
 80-90% settle over 24-48h
 Deterioration: perforation, empyema

Surgical
 May be elective surgery @ 6-12wks (↓ inflam)
 If <72h, may perform lap chole in acute phase

Empyema
 High fever
 RUQ mass
 Percutaneous drainage: cholecystostomy

193

Symptoms of chronic cholecystitis

Flatulent Dyspepsia
 Vague upper abdominal discomfort
 Distension, bloating
 Nausea
 Flatulence, burping
 Symptoms exacerbated by fatty foods
- CCK release stimulates gallbladder

194

Differentials of chronic cholecystitis

 PUD
 IBS
 Hiatus hernia
 Chronic pancreatitis

195

Ix findings from chronic cholecystitis

 AXR: porcelain gallbladder
 US: stones, fibrotic, shrunken gallbladder

196

Mx of chronic cholecystitis

 Medical - Bile salts (not very effective)
 Surgical
- Elective cholecystectomy
- ERCP first if US shows dilated ducts and stones

197

What is a mucocele

Neck of gallbladder blocked by stone but contents
remains sterile
 Can be very large → palpable mass
 May become infected → empyema

198

What is Mirizzi's syndrome

Large stone in GB presses on the common hepatic duct
→ obstructive jaundice.
 Stone may erode through into the ducts

199

Pathogenesis, symptoms and mx of gallstone ileus

Large stone (>2.5cm) erodes from GB → duodenum
through a cholecysto-duodenal fistula secondary to chonic inflam.
 May impact in distal ileum → obstruction

Symptoms
Rigler’s Triad:
 Pneumobiliia
 Small bowel obstruction
 Gallstone in RLQ

Mx - stone removal via enterotomy

200

management of gallstones

Conservative
 Monitor LFTs: passage of stone may → resolution
 Vitamins ADEK
 Analgesia
 Cholestyramine

Interventional
 If: no resolution, worsening LFTs or cholangitis
 ERCP c¯ sphincterotomy and stone extraction

Surgical
 Open / lap stone removal c¯ T tube placement
 T tube cholangiogram 8d later to confirm
stone removal.
 Delayed cholecystectomy to prevent recurrence

201

Features of ascending cholangitis

Charcot’s triad: fever/rigors, RUQ pain, jaundice

Reynolds pentad: Charcot’s triad + shock + confusion

202

Management of ascending cholangitis

 Cef and met
 1st: ERCP
 2nd: Open or lap stone removal c¯ T tube drain

203

Risk factors for pancreatic carcinoma

 Smoking
 Inflammation: chronic pancreatitis
 Nutrition: ↑fat diet
 EtOH
 DM

204

Pathology of pancreatic carcinoma

90% ductal adenocarcinomas
 Present late, metastasise early
- Direct extension to local structures
- Lymphatics
- Blood → liver and lungs
 60% located in head, 25% body, 15% tail

205

Presentation of pancreatic carcinoma

 Typically male >60yrs
 Painless obstructive jaundice: dark urine, pale stools
 Epigastric pain: radiates to back, relieved sitting
forward
 Anorexia, wt. loss and malabsorption
 Acute pancreatitis
 Sudden onset DM in the elderly

206

Signs of pancreatic carcinoma

 Palpable gallbladder
 Jaundice
 Epigastric mass
 Thrombophlebitis migrans (Trousseau Sign)
 Splenomegaly: PV thrombosis → portal HTN
 Ascites

207

Courvoisier’s Law

In the presence of painless obstructive jaundice, a
palpable gallbladder is unlikely to be due to stones.

208

Ix for pancreatic carcinoma

Bloods: cholestatic LFTs, ↑Ca19-9 (90% sens), ↑Ca

Imaging
 US: pancreatic mass, dilated ducts, hepatic
mets, guide biopsy
 EUS: better than CT/MRI for staging
 CXR: mets
 Laparoscopy: mets, staging

ERCP
 Shows anatomy
 Allows stenting
 Biopsy of peri-ampullary lesions

209

Rx of pancreatic carcinoma

Surgery
 Fit, no mets, tumour ≤3cm (≤10% of pts)
 Whipple’s pancreaticoduodenectomy
 Distal pancreatectomy
 Post-op chemo delays progression
 5ys = 5-14%

Palliation
 Endoscopic / percutaneous stenting of CBD
 Palliative bypass surgery:
– cholecystojejunostomy + gastrojejunostomy
 Pain relief – may need coeliac plexus block

210

Pathophysiology of acute pancreatitis

Pancreatic enzymes released and activated in vicious
circle → multi-stage process.

1. Oedema + fluid shift + vomiting → hypovolaemic
shock while enzymes → autodigestion and fat necrosis

2. Vessel autodigestion → retroperitoneal haemorrhage

3. Inflammation → pancreatic necrosis

4. Super-added infection: 50% of pts. c¯ necrosis

211

Causes of acute pancreatitis

Aetiology
 Gallstones (45%)
 Ethanol (25%)
 Trauma

 Steroids
 Mumps + Coxsackie B
 Autoimmune: e.g. PAN
 Scorpion (Trinidadian)
 Hyperlipidaemia (I and V), ↑Ca, Hypothermia
 ERCP: 5% risk
 Drugs: e.g. thiazides, azathioprine

 Idiopathic (20%): ?microstones

212

Symptoms and signs of acute pancreatitis

Symptoms
 Severe epigastric pain → back
- May be relieved by sitting forward
 Vomiting
Signs
 ↑HR, ↑RR
 Fever
 Hypovolaemia → shock
 Epigastric tenderness
 Jaundice
 Ileus → absent bowel sounds
 Grey Turners: flank
 Cullens: periumbilical (tracks up Falciform)

213

Criteria used for acute pancreatitis

Glasgow (IMRIE)
- assess severity and predict mortality
1 = mild; 2 = mod; 3 = severe

PaO2 <8kPa
 Age >55yrs
 Neutrophils >15 x109/L
 Ca2+ <2mM
 Renal function U>16mM
 Enzymes LDH>600iu/L
AST>200 iu/L
 Albumin <32g/L
 Sugar >10mM

214

Criteria for diagnosis of acute pancreatitis

- 2/3
1) CT
2) Amylase x 3
3) epigastric pain radiatating to back

215

Ix findings in acute pancreatitis

Bloods
 FBC: ↑WCC
 ↑amylase (>1000 / 3x ULN) and ↑lipase - ↑ in 80%
- Returns to normal by 5-7d
 U+E: dehydration and renal failure
 LFTs: cholestatic picture, ↑AST, ↑LDH
 Ca2+: ↓
 Glucose: ↑
 CRP: monitor progress, >150 after 48hrs = sev
 ABG: ↓O2 suggests ARDS

Urine: glucose, ↑cBR, ↓urobilinogen

Imaging
 CXR: ARDS, exclude perfed DU
 AXR: sentinel loop, pancreatic calcification
 US: Gallstones and dilated ducts, inflammation
 Contrast CT: Balthazar Severity Score

216

Conservative Mx of acute pancreatitis

Manage @ appropriate level: e.g. ITU if severe
 Constant reassessment is key
 Hrly TPR, UO
 Daily FBC, U+E, Ca2+, glucose, amylase ABG

Fluid Resuscitation
- Aggressive fluid resus: keep UO >30ml/h
- Catheter ± CVP
Pancreatic Rest
 NBM
 NGT if vomiting
 TPN may be required if severe to prevent catabolism
Analgesia
- Pethidine via PCA
- Or morphine 5-10mg/2h max
Antibiotics
 Not routinely given if mild
 Used if suspicion of infection or before ERCP
 Penems often used: e.g. meropenem, imipenem

OTHER
-ARDS: O2 therapy or ventilation
-EtOH withdrawal: chlordiazepoxide

217

Interventional and surgical management for pancreatitis

ERCP + spincheterotomy --> If pancreatitis c¯ dilated ducts 2O to gallstones

Surgery
 Laparotomy + necrosectomy (pancreatic debridement)
 Laparotomy + peritoneal lavage
 Laparostomy: abdomen left open c¯ sterile packs in ITU

218

Indications for surgery in acute pancreatitis

 Infected pancreatic necrosis
 Pseudocyst or abscess
 Unsure Dx

219

Early complications of acute pancreatitis

Systemic
 Respiratory: ARDS, pleural effusion
 Shock: hypovolaemic or septic
 Renal failure
 DIC
 Metabolic
 ↓ Ca2+
 ↑ glucose
 Metabolic acidosis

220

Late complications of acute pancreatitis

>1wk: Local
 Pancreatic necrosis
 Pancreatic infection
 Pancreatic abscess
- May form in pseudocyst or in pancreas --> Open or percutaneous drainage
 Bleeding: e.g. from splenic artery --> May require embolisation
 Thrombosis --> Splenic A., GDA or colic branches of SMA
= May → bowel necrosis
- Portal vein → portal HTN
 Fistula formation --> Pancreato-cutaneous → skin breakdown

221

What is a pancreatic pseudocysts and how is it managed

Collection of pancreatic fluid in the lesser sac surrounded by granulation tissue
 4-6wks after acute attack
 Persisting abdominal pain
 Epigastric mass → early satiety

Complications
 Infection → abscess
 Obstruction of duodenum or CBD
Ix --> Persistently ↑ amylase ± LFTs
 DO US / CT

Rx
 <6cm: spontaneous resolution
 >6cm - Endoscopic cyst-gastrostomy OR Percutaneous drainage under US/CT

222

Causes of Chronic Pancreatitis

AGITS
 Alcohol (70%)
 Genetic - CF
 Immune - Lymphoplasmacytic sclerosing pancreatitis (↑IgG4)
 Triglycerides ↑
 Structural - Obstruction by tumour

223

Presentation of Chronic Pancreatitis

Epigastric pain
 Bores through to back
 Relieved by sitting back or hot water bottle → erythema ab igne
 Exacerbated by fatty food or EtOH

Steatorrhoea and wt. loss
DM: polyuria, polydipsia
Epigastric mass: pseudocyst

224

Ix for chronic pancreatitis

↑ glucose

↓ faecal elastase: ↓ exocrine function

US: pseudocyst

AXR: speckled pancreatic calcifications

CT: pancreatic calcifications

225

Management of acute pancreatitis

Diet
 No EtOH
 ↓ fat, ↑ carb
Drugs
 Analgesia: may need coeliac plexus block
 Enzyme supplements: pancreatin (Creon)
 ADEK vitamins
 DM Rx
Surgery
- Indications
 Unremitting pain
 Wt. loss
 Duct blockage
--> Whipple’s/ endoscopic stenting

226

Complications of chronic pancreatitis

 Pseudocyst
 DM
 Pancreatic Ca
 Pancreatic swelling → biliary obstruction
 Splenic vein thrombosis → splenomegaly

227

Differentials of upper abdominal pain

- cholecystitis (R)
- pyelonephritis
- uteric colic
- hepatitis (R)
- pneumonia
- gastric ulcer (L)

228

Differentials of RIF pain

 appendicitis
 Cholecystitis
 Diverticulitis
 Meckel’s diverticulitis
 Cyst accident: torsion, rupture, haemorrhage
 testicular torsion
 Salpingitis / PID
 Ruptured ectopic
 Mesenteric adenitis
 UTI
 Crohn’s
 Inguinal hernia

229

Causes of LLQ psin

-ureteric colic
- inguinal hernia
- IBD
- UTI
- Gynaecological
- testicular torsion
- diverticulitis

230

Causes of epigastic pain

- PUD
- Cholecystitis
- Pancreatitis
- MI

231

Causes of Peri-umbilical pain

- SI obstruction
- LI obstruction
- Appendicitis
- AAA

232

Features of carcinoid syndrome

FIVE HT
 Flushing: paroxysmal, upper body ± wheals
 Intestinal: diarrhoea
 Valve fibrosis: tricuspid regurg and pulmonary stenosis
 whEEze: bronchoconstriction
 Hepatic involvement: bypassed 1st pass metabolism
 Tryptophan deficiency → pellagra (3Ds)

233

Pathogenesis of acute appendicitis

Obstruction of the appendix
 Faecolith most commonly
 Lymphoid hyperplasia post-infection
 Tumour (e.g. caecal Ca, carcinoid)
 Worms (e.g. Ascaris lumbicoides, Schisto)

Gut organisms → infection behind obstruction → oedema → ischaemia → necrosis → perforation
 Peritonitis
 Abscess
 Appendix mass

234

symptoms of acute appendicitis

Colicky abdo pain
 Central (visceral irritation)→ localised in RIF ) parietal irritation)
 Worse on movement

 Anorexia
 Nausea (vomiting is rarely prominent)
 Constipation / diarrhoea

235

Signs of appendicitis

 Low-grade pyrexia: 37.5 – 38.5
 ↑HR, shallow breathing
 Foetor oris
 Guarding and tenderness: @ McBurney’s point
- +ve cough / percussion tenderness
 Appendix mass may be palpable in RIF
 Pain PR suggests pelvic appendix.
Rovsing’s Sign
 Pressure in LIF → more pain in RIF
Psoas Sign
 Pain on extending the hip: retrocaecal appendix

236

Management of acute appendicitis

- Urine dip - Pregnancy test and exclude UTI
- US - exclude gynae and visialise appendix
- fluids
- abx - cef + met
- analgesia

If uncertain - observe
If certain - appendicetomy

237

Complications of acute appendicitis

> Appendix Mass - Abx + NBM
 Resolution of mass → interval appendicectomy
 Exclude a colonic tumour: colonoscopy

> Appendix Abscess
 Mass enlarges, pt. deteriorates - Abx + NBM
 CT-guided percutaneous drainage
 If no resolution, surgery may involve right hemicolectomy.

> Perforation - peritonitis

238

Commonest causes of Small and Large bowel obstruction
- + a non-mechanical cause

SBO
 Adhesions: 60%
 Hernia
 Neoplasm - mets/ lymphoma
LBO
 Colorectal Neoplasia: 60%
 Diverticular stricture: 20%
 Volvulus: 5%

- paralytic ileus

239

Causes of paralytic ileus

 Post-op - bowel handling/ anesthesia
 Peritonitis
 Pancreatitis/ localised inflammation
 TCAs
 Pseudo-obstruction
 Metabolic: ↓K, ↓Na, ↓Mg, uraemia
 Mesenteric ischaemia

240

Presentation of SB v LB obstruction

SBO
Early - Vom and mild distension.
Late - Absolute constipation
Colicky pain every 2-3 minutes

LBO
Early - Abdo pain and distension with absolute constipation
Late - Vomiting and can be faeculant
Colicky Pain every 10-15 minutes

- constant pain --> strangulation

241

Signs of bowel obstruction

 ↑HR: hypovolaemia, strangulation
 Dehydration, hypovolaemia
 Fever- inflam disease or strangulation
 Surgical scars
 Hernias
 Mass: neoplastic or inflammatory
 Bowel sounds
- ↑: mechanical obstruction
- ↓: ileus
 PR
- Empty rectum; Rectal mass; Hard impacted stool; Blood from higher pathology

242

Ix for bowel obstruction

Bloods
 FBC: ↑WCC
 U+E: dehydration, electrolyte abnormalities
 Amylase: ↑↑ if strangulation/ perforation
 VBG: ↑ lactate - strangulation
 G+S, clotting: ?surgery

Imaging
 Erect CXR
 AXR: ± erect film for fluid levels
 CT: can show transition point

Gastrograffin studies
 Look for mechanical obstruction: no free flow
 Follow through or enema
 Follow through may relieve mild mechanical
obstruction: usually adhesional

Colonoscopy
 Can be used in some cases
 Risk of perforation
 May be used therapeutically to stent

243

Findings on AXR of SBO v LBO

SBO
≥3cm; central; Valvulae coniventes; many loops, and many, short fluid levels; LB Gas Absent

LBO
≥6cm (caecum ≥9- emergency if ileocaecal valve working); Peripheral;
Haustra; LB Gas Present; few loops; Few, long fluid levels

244

medical management of bowel obstruction

 NBM
 IV fluids: aggressive as pt. may be v. dehydrated
 NGT: decompress upper GIT, stops vomiting, prevents
aspiration
 Catheterise: monitor UO

 Analgesia: may require strong opioid
 Antibiotics: cef+met if strangulation or perforation
 Gastrograffin study: oral or via NGT
 Consider need for parenteral nutrition

 Regular clinical examination is necessary to ensure that
the pt. is not deteriorating.
- ↑ distension/ pain/ tenderness/ ↑ HR/ ↑RR
 Repeat imaging and bloods

245

Indications for surgery in bowel obstruction

 Closed loop obstruction
 Obstructing neoplasm
 Strangulation / perforation → sepsis, peritonitis
 Failure of conservative Mx (up to 72h)

246

Surgical management of. bowel obstruction

SBO: adhesiolysis

LBO
 Hartmann’s (proctosigmoidectomy)
 Colectomy + 1° anastomosis + on table lavage
 Palliative bypass procedure
 Transverse loop colostomy or loop ileostomy
 Caecostomy

247

Types of stoma

Colostomy - flush to skin; LIF
- loop --> entire loop of colon exteriorised and both proximal and distal end open into common stoma opening and are not transected
- end --> created from proximal end of colon, distal end stapled/ sewn shut and remains as blind pouch

Ileostomy; RIF; spout as enzymes toxic to skin
- loop - Loop SI brought out, colon ann rectum removed
- end - colon and rectum removed, and of ileum brought out

248

Pathophysiology of a sigmoid volvulus and sign on AXR

 Long mesentery c¯ narrow base predisposes to torsion
 Usually due to sigmoid elongation 2° to chronic
constipation
 ↑ risk in neuropsych pts.: MS, PD, psychiatric
 Disease or Rx interferes c¯ intestinal motility
→ closed loop obstruction

- coffee bean sign on AXR

249

Mx of sigmoid volvulus

Sigmoidoscopy and flatus tube
insertion

2) Sigmoid colectomy if Failed endoscopic decompression/ Bowel necrosis

250

Presentation and Prevention of paralytic ileus

Presentation
 Distension
 Constipation ± vomiting
 Absent bowel sounds

Prevention
 ↓ bowel handling
 Laparoscopic approach
 Peritoneal lavage after peritonitis
 Unstarched gloves

251

Mx of paralytic ileus

 NBM
 IV fluids: aggressive as pt. may be v. dehydrated
 NGT: decompress upper GIT, stops vomiting, prevents
aspiration
 Catheterise: monitor UO

Correct any underlying causes
 Drugs
 Metabolic abnormalities
+/- parenteral nutrition

252

What is obstruction and mx

Clinical signs of mechanical obstruction but no
obstructing lesion found
 Usually distension only: no colic
- assoc elderly, CR disorders, hip arthroplasty and trauma

Mx - neostigmine and colonoscopic decompressino

253

Pathology and. Presentation of L v R colorectal carcinoma

ADENOCARCINOMA

Left
 Altered bowel habit
 PR mass (60%)
 Obstruction (25%)
 Bleeding / mucus PR
 Tenesmus
Right
 Anaemia
 Wt. loss
 Abdominal pain

Either
 Abdominal mass
 Perforation
 Haemorrhage
 Fistula

254

Ix for colorectal carcinoma

Bloods
 FBC: Hb - anaemia
 LFTs: mets
 Tumour Marker: CEA (carcinoembryonic Ag) (to monotor disease progression)

Imaging
 CXR: lung mets
 US liver: mets
 CT and MRI (rectal and liver)- staging
 Endoanal US: staging rectal tumours

Endoscopy + Biopsy
 Flexi sig: 65% of tumours accessible
 Colonoscopy

255

Staging and grading of colorectal carcinomas

Dukes
A Confined to bowel wall
B Through bowel wall but no LNs
C Regional LNs
D Distant mets

TNM
 TIS: carcinoma in situ
 T1: submucosa
 T2: muscularis propria
 T3: subserosa
 T4: through the serosa to adjacent organs
 N1: 1-3 nodes
 N2: >4 nodes

Grade - low - high based on Dysplasia, mitotic index, hyperchromatism

256

Surgical management of colorectal carcinomas

o R Hemicolectomy
o Left Hemicolectomy
o Sigmoidcolectomy (Sigmoid colon tumours)
o Anterior Resection (High rectal tumours >5cm from the anus)
o Abdominoperineal (AP) Resection (Low rectal tumours <5cm from the anus)

257

Screening for colorectal carcinoma

FOB Testing
 60-75yrs -  Home FOB testing every 2yrs: ~1/50 have +ve FOB
 Colonoscopy if +ve: ~1/10 have Ca

Flexi Sig
 55-60yrs
 Once only flexi Sig

258

Risk factors for CRC

- FAP
- age (>60yrs)
- Fhx
- IBD
- ↓ fibre diet; ↑processed meat intake
- smoking
- ↑ alcohol intake.

259

Presentation of mesenteric ischaemia

 Triad
 Acute severe abdominal pain ± PR bleed
 Rapid hypovolaemia → shock
 No abdominal signs

260

Causes of mesenteric ischaemia

 Arterial: thrombotic (35%), embolic (35%)
 Non-occlusive (20%)
 Splanchnic vasoconstriction: e.g. 2O to shock
 Venous thrombosis (5%)
 Other: trauma, vasculitis, strangulation

261

Management of mesenteric ischaemia

- Fluids
- Abx
- LMWH
- Laparotomy to resect necrotic bowel

262

Presentation of Chronic Small Bowel Ischaemia

 Severe, colicky post-prandial abdo pain
 “gut claudication”
 PR bleeding
 Malabsorption
 Wt. loss

Mx --> angioplasty

263

Causes of Lower GI bleed

 Rectal: haemorrhoids, fissure
 Diverticulitis
 Neoplasm

Other
 Inflammation: IBD
 Infection: shigella, campylobacter, C. diff
 Polyps
 Large upper GI bleed (15% of lower GI bleeds)
 Angio: dysplasia, ischaemic colitis, HHT

264

Mx of Lower GI bleed

 Resuscitate
 Urinary catheter
 Abx: if evidence of sepsis or perf
 PPI: if upper GI bleed possible
 Keep bed bound: need to pass stool may be large bleed
→ collapse
 Stool chart
 Diet: keep on clear fluids (allows colonoscopy)
 Surgery: only if unremitting, massive bleed

265

Pathophysiology of Haemorrhoids

Anal cushion: mass of spongy vascular tissue - Positioned @ 3, 7 and 11 O’clock
 Where the 3 major arteries that feed the vascular plexuses enter the anal canal

 Gravity, straining (+pregnancy, portal HTN) → engorgement and enlargement of
anal cushions

 Hard stool disrupts CT around cushions.
 Cushions protrude and can be damaged by hard stool → bright red (capillary) bleeding.

266

Classification of haemorrhoids

 1st degree: never prolapse
 2nd: prolapse on defecation but spontaneously reduce
 3rd: prolapse on defecation but require digital reduction
 4th: remain permanently prolapsed

267

Symptoms of haemorrhoids

 Fresh painless PR bleeding
- Bright red
 Pruritis ani
 Lump in perianal area
 Severe pain = thrombosis

268

Mx of haemorrhoids

 ↑ fibre and fluid intake
 Stop straining @ stool

Medical
 Anusol: hydrocortisone
 Topical analgesics
 Laxatives: lactulose, Fybogel

Interventional
 Injection c¯ sclerosant - above dentate line - SE: impotence, prostatitis
 Barron’s banding → thrombosis and separation - SE: bleeding, infection
 Cryotherapy - SE: watery discharge post-procedure
 Infra-red coagulation

Surgical: Haemorrhoidectomy
 Excision of piles + ligation of vascular pedicles
 Lactulose + metronidazole 1wk pre-op
 Discharge c¯ laxatives post-op
- SE: bleeding, stenosis

269

Definition and causes of anal fissures

Tear of squamous epithelial lining in lower anal canal

 Mostly trauma 2 ° to the passage of hard stool
- Assoc. c¯ constipation
- Spasm of internal anal sphincter contributes to
pain and → ischaemia + poor healing
 Crohn’s
 Herpes
 Anal Ca

270

Presentation of anal fissures

 Intense anal pain
- Especially on defecation
- May prevent pt. from passing stools
- PR impossible
 Fresh rectal bleeding

271

Mx of anal fissures

 Soaks in warm bath
 Toileting advice
 Dietary advice: ↑ fibre and fluids

Medical
 Laxatives: lactulose + fybogel
 Topical → resolution in 75%
 Lignocaine/ GTN/ Diltiazem
 Botulinum injection

Surgical: Lateral partial sphincterotomy
 Division of internal anal sphincter @ 3 O’clock
- Complications
 Minor faecal/flatus incontinence (= GTN)/ Perianal abscess

272

Pathogenesis of Fistula in Ano

Abnormal connection between ano-rectal canal and the
skin.
- Usually occur 2° to perinanal sepsis
- Blockage of intramuscular glands → abscess → discharges to form a fistula
 Associations
CD, Diverticular disease, Rectal Ca, Immunosuppression

273

Goodsall's rule for Fistula's in Ano

Fistula anterior to anus track in a straight line (radial)

Fistula posterior to anus always have internal opening
at the 6 o’clock position → curved track

274

Presentation, Rx and Mx of Fistula in Ano

Persistent anal discharge
Perianal pain or discomfort


- Endoanal USS/ MRI

Mx - Low - Fistulotomy and excision --> Laid open to heal by 2° intention
- High - a seton – passed through fistula and gradually
tightened over months

275

Pathogenesis of peri-anal abscess

 Anal gland blockage → infection → abscess
E.g. coli, bacteroides
 May develop from skin infections
E.g. sebaceous gland or hair follicle OR Staphs

276

Presentation of peri-anal abscess

Throbbing perianal pain - Worse on sitting

Occasionally a purulent anal discharge

Fluctuant mass on PR

Septic signs: fever, tachycardia

277

Rx of peri-anal abscess

Abx may suffice if Rx instigated v. early in course

Most cases require EUA - I&D
 Wound packed
 Heals by 2O intention
 Daily dressing for 7-10d

278

Pathophysiology and risk factors of pilonidal sinus

Hair works its way beneath skin → foreign body
reaction → formation of abscess
 Usually occur in the natal cleft.

Risk Factors
 M>F=4:1
 Geo: Mediterranean, Middle east, Asians
 Often overweight c¯ poor personal hygiene (sweaty)
 Occupations c¯ lots of sitting: e.g. truck drivers

279

Presentation and Rx of pilonidal sinus

 Persistent discharge of purulent or clear fluid
 Recurrent pain
 Abscesses

Rx
 Hygiene advice
 Shave / remove hair from affected area
 Incision and drainage of abscesses
 Elective sinus excision

280

Pathology and Presentation of anal carcinoma

 80% SCCs
 Spread
 Above dentate line → internal iliac nodes
 Below dentate line → inguinal nodes

Associated HPV

Presentation
 Perianal pain and bleeding
 Pruritis ani
 Faecal incontinence

281

Ix and Rx of anal carcinoma

Ix
 ↓ Hb (ACD)
 Endoanal US
 Rectal EUA + biopsy
 CT / MRI: assess pelvic spread

Rx
 Chemoradiotherapy: most pts
 Surgery: reserved for
 Tumours that fail to respond to radiotherapy
 GI obstruction
 Small anal margin tumours w/o sphincter involvement

282

Rectal prolapse classification

Protrusion of rectal tissue through the anal canal.

Type 1: Mucosal Prolapse
 Partial prolapse of redundant mucosa
Type 2: Full Thickness Prolapse ( elderly)

283

Presentation of rectal prolapse

Mass extrudes from rectum on defecation
 May reduce spontaneously or require manual reduction
 May become oedematous and ulcerated → pain and bleeding
 Faecal soiling
 Assoc. c¯ vaginal prolapse and urinary incontinence
↓ sphincter tone on PR

284

Rx of rectal prolapse

Partial Prolapse
 Phenol injection
 Rubber band ligation
 Surgery: Delorme’s Procedure
Complete Prolapse
 Pelvic floor exercises/ Stool softeners
 Rectopexy or Delorme’s Procedure

285

Define a hernia

Protrusion of a viscus or part of a viscus through the walls of its containing cavity into an abnormal position

286

Classification of Inguinal hernias

Indirect
 80%: commoner in young
 Congenital patent processus vaginalis
 Emerge through deep ring
 Same 3 coverings as cord and descend into the scrotum
 Can strangulate

Direct
 20%: commoner in elderly
 Acquired ( ↑IAPe.g. Chronic cough/ constipation/ obesity)
 Emerge through Hesselbach’s triangle
 Can acquire internal and external spermatic fascia
 Rarely descend into scrotum
 Rarely strangulate

287

Clinical features of Inguinal hernias

Children
 Lump in groin which may descend into scrotum
 Exacerbated by crying
 Commonly obstruct

Adults
 Lump in groin, exacerbated by straining/cough
 May be clear ppting event: e.g. heavy lifting
 Dragging pain radiating to groin
 May present c¯ obstruction/strangulation

288

Mx of Inguinal hernia

Non-surgical
 Rx RFs: cough, constipation
 Lose weight
 Truss

Surgical
 Tension-free mesh and suture repair

289

Complications of inguinal hernias

Early
 Haematoma / seroma formation: 10%
 Intra-abdominal injury (lap)
 Infection: 1%
 Urinary retention

Late
 Recurrence (<2%)
 Ischaemic orchitis: 0.5%
 Chronic groin pain / paraesthesia: 5%

290

Femoral hernia pathology

Protrusion of viscus through femoral canal (bounded by femoral vein and lacunar ligament) into femoral triangle (inguinal ligament, adductus longus and sartorius)

- more common in females due to shape of pelvis
- acquires - increased intra-abdominal pressure

291

Clinical features of a femoral hernia

Painless groin lump
 inferior (and lateral) to the pubic tubercle.
 Cough impulse.
 Often irreducible (tight boarders)

Commonly present - obstruction or strangulation
 Tender, red and hot
 Abdo pain, distension, vomiting, constipation

292

Mx of femoral hernia

High risk of strangulation
Rx - herniotomy and heniorrhaphy

293

Differntials of femoral hernia

- low inguinal hernia
- femoral canal lipoma
- femoral LN
- saphena varix ( compressible, disappears when flat)

294

Definition and risk factors for incisional hernia

Hernia arises through a previously acquired defect
- non- pulsatile, reducible soft and non-tender swelling near site of previous wound


Pre-operative
 ↑ age
 Obesity or malnutrition
 Comorbidities: DM, renal failure, malignancy
 Drugs: steroids, chemo, radio

Intra-operative
 Surgical technique/skill (major factor)
-Too small suture bites
- Inappropriate suture material
 Incision type (e.g. midline)
 Placing drains through wounds

Post-operative
 ↑ IAP: chronic cough, straining, post-op ileus
 Infection
 Haematoma

295

Mx of incisional hernia

Conservative
 Manage RFs: e.g. constipation, cough
 Weight loss
 Elasticated corset or truss

Surgical
 Pre-Op
- Optimise cardiorespiratory function
- Encourage wt. loss
 Nylon mesh repair: open or lap