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Surgery block (Y3) > General surgery (5) (Common conditions) > Flashcards

General surgery (5) (Common conditions) Flashcards

1
Q

GI bleeds can be split up into

A

upper GI bleeds

lower GI bleeds

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2
Q

upper GI bleed key symptoms

A

haematemesis and melaena

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3
Q

upper GI bleed emergencies

A
  • Oesophageal varices
  • Gastric ulceration
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4
Q

upper GI bleed non-emergency

A
  • Mallory Weiss tear
  • Oesophagitis
  • Other causes
    • Gastritis
    • Gastric malignancy
    • Meckel’s diverticulum
    • Vascular malformation
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5
Q

presentation of UGI bleed

A
  • Haematemesis
    • ‘Vomiting blood’ – caused by bleeding from the upper portion of the GI tract. Wide range of causes depending on the site of blood loss and the tissue bleeding.
    • Coffee ground vomiting- digested blood
  • Melaena – tar like, black greasy and offensive stools caused by digested blood- oxidised
  • Haemodynamic instability
  • Epigastric pain
  • Jaundice for ascites in decompensated lived disease
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6
Q

history taking for UGI bleed

A
  • Timing, frequency, and the volume of bleeding
  • History of dyspepsia, dysphagia, or odynophagia
  • Past medical history and smoking and alcohol status
  • Use of steroids, NSAIDs, anticoagulants, or bisphosphonates
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7
Q

examination of UGI bleed

A

On examination, it is important to assess specifically for epigastric tenderness or peritonism, as well as features suggestive of a potential underlying cause, such as evidence of varices or liver stigmata

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8
Q

general mageemnt of all upper GI bleeds

A
  • ABATED
  • Bloods
  • A – ABCDE approach to immediate resuscitation
  • B – Bloods
  • A – Access (ideally 2 large bore cannula)
  • T – Transfuse (group and save, if varices 4units blood cross-matched))
  • E – Endoscopy (arrange urgent endoscopy within 24 hours)
  • D – Drugs (stop anticoagulants and NSAIDs)
  • Haemoglobin (FBC)
  • Urea (U&Es)
  • Coagulation (INR, FBC for platelets)
  • Liver disease (LFTs)
  • Crossmatch 2 units of blood
  • Transfusion blood, platelets (if <50) and prothrombin complex concentrate (if on warfarin) in patients with massive hameorrhage
  • Definitive investigation/treatment: Esophagogastroduodenoscopy (OGD) (within 12h)– stops bleedings
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9
Q

upper GI bleed sign on blood test

A

raised urea

Blood is full of proteins (i.e Hemeglobin, Immunoglobins) which are absorbed in the GI tract. Since it is an upper GI bleed (above the ligament of treitz) there is time for adequate absorption.

  • Blood Urea Nitrogen (BUN) reflects the end product of the metabolic breakdown of protein
  • Hence when there is bleeding => protein breakdown & absorption => increase in Urea
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10
Q

oesophageal varices

A
  • anastomosis between azygous and left gastric vein
    • Upper 2/3 drains into oesophageal veins- goes through the azygous drains into the superior vena cava
    • Distal portion drains into the left gastric vein- drains into the portal vein
      • At the junction where there are veins draining into the main systemic circulation (SVC) is where the pressure builds up.
      • Veins are superficial- therefore become dilatedà easy to rupture
      • Significant Haematemesis
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11
Q

RF for oesophageal varcies

A

alcoholic liver disease causing portal hypertension

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12
Q

managemetn of oesophageal varcies

A
  • Same as general upper GI bleed
  • Additional steps: management should be swift and performed at the same time as active resuscitation, including the use of blood products and prophylactic antibiotics
    • Endoscopic banding is the most definitive method of management* however can be technically difficult
    • Vasopressors (e.g. terlipressin) should also be started, acting to reduce splanchnic blood flow and hence reduce bleeding
    • Long term management warrants repeated banding of the varices and long-term beta-blocker therapy
    • Prophylactic broad spectrum antibiotics
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13
Q

scoring systems for upper GI bleed

A

glasgow-blatchford score

rockall score

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14
Q

Glasgow-Blatchford score

A

Scoring system in suspected upper GI bleed on their initial presentation. It scores patient based on their clinical presentation. It establishes their risk of having an upper GI bleed to help you make a plan (for example whether to discharge them or not).

Using an online calculator is the easiest way to calculate the score. A score > 0 indicates high risk for an upper GI bleed. It takes into account various features indicating an upper GI bleed:

  • Drop in Hb
  • Rise in urea
    • Blood in GI tract gets broken down and urea is a by-product absorbed in the intestine
  • Blood pressure
  • Heart rate
  • Melaena
  • Syncope
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15
Q

Rockall score

A
  • Used in pts that have had an endoscopy to calc their risk of rebleeding and overall mortility .
  • Online calculator
    • Age
    • Features of shock (e.g. tachycardia or hypotension)
    • Co-morbidities
    • Cause of bleeding (e.g. Mallory-Weiss tear or malignancy)
    • Endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels
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16
Q

gastric ulceration

A

Most common cause of haematemesis.

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17
Q

gastric ulceration cause

A

Erosion of blood vessels supplying upper GI tract

  • Lesser curve of stomach (20%)
  • Posterior duodenum (40%)
    • Gastroduodenal artery most common
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18
Q

risk factors for gastric ulceration

A
  • Ulcer disease/ H.pylori positive
  • NSAID
  • Steroids
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19
Q

investigations for gastirc ulceration

A
  • Erect CXR if suspect peptic ulceration
    • May see pneumoperitoneum
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20
Q

signs of bowel perforation on xray

A
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21
Q

rigler sign

A

also known as the double-wall sign, is a sign of pneumoperitoneum seen on an abdominal radiograph when gas is outlining both sides of the bowel wall, i.e. gas within the bowel’s lumen and gas within the peritoneal cavity. It is seen with large amounts of pneumoperitoneum (>1000 mL).

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22
Q

management of gastric ulceration

A
  • Injection of adrenaline and cauterisation of bleeding
  • High dose IV PPI therapy (e.g. IV 40mg of omeprazole) to reduce acid secretion
  • +/- H.Pylori eradication therapy if necessary
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23
Q

mallory-weis tear

A

A relatively common phenomenon

  • Episodes of severe or recurrent vomiting, then followed by minor haematemesis.
  • Such forceful vomiting causes a tear in the epithelial lining of the oesophagus, resulting in a small bleed.
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24
Q

management of mallory-weiss tear

A
  • Most cases are benign and will resolve spontaneously, therefore providing the patient reassurance and monitoring is usually all that is required.
  • Any prolonged or worsening haematemesis warrants investigation with an OGD.
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25
Q

oesophagitis

A

Inflammation of intraluminal epithelial layer of the oesophagus

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26
Q

causes of oesophagitis

A
  • GORD
  • Infections e..g candia albicans
  • Medication (bisphosphonates)
  • Radiotherapy
  • Ingestion of toxic substance
  • Crohns disease
27
Q

lower GI bleed main symptoms

A

rectal bleeding (haemtochezia)

  • passage of fresh blood per rectum
28
Q

causes of lower GI bleed

A
  • Diverticular disease
  • Ischaemic or infective colitis
  • Haemorrhoids
  • Malignancy
  • IBD
  • Radiation proctitis
29
Q

history taking for lower GI bleed

A
  • Nature of bleeding, including duration, frequency, colour of the bleeding, relation to stool and defecation
  • Associated symptoms, including pain (especially association with defaecation), haematemesis, PR mucus, or previous episodes
  • Family history of bowel cancer or inflammatory bowel disease
30
Q

examination for lower GI bleed

A
  • The abdomen for any localised tenderness or masses palpable.
  • A PR examination is essential for every patient presenting with haematochezia, allowing assessment for any rectal masses and ongoing presence of blood
31
Q

investigations for LGI bleed

A
  • Bloods- FBC, U&Es, LFT, clotting
    • Acute bleed may not show reduced Hb levels, ongoing bleeding will
  • Group and save
  • Stool culture
  • Haemodynamically unstable
    • Stabilised before undergoing urgent CT angiogram
      • Can identify source of bleeding
  • Haemodynamically stable
    • Flexible sigmoidoscopy (exclude left colonic pathology)- can be outpatient
  • If PR bleeding back no abnormality found on colonoscopy- look for upper GI bleed- OGD
32
Q

management of lower GI bleed: conservative

A
  • Young, haemodynamically stable patients with low risk score can be discharged and investigated as outpatient
33
Q

unstable rectal bleed management

A
  • Standard A to E
    • IV fluid
    • Blood products
      • Hb <70 requires transufsiion of packed red blood cells (unless pt has CVD, then Hb <80 used)
    • Reversal of any anti-coagulation
    • Potential management
      • Endoscopic haemostasis methods
        • Injection (diluted adrenaline)
        • Contact and non-contact thermal devices (bipolar electrocoagulation)
        • Mechanical therapies (endoscopic clips and band ligation)
      • Arterial embolization possible in those with identified bleeding point (termed a ‘blush’ of sufficient size on angiogram
34
Q

surgery for LGI bleed

A
  • Rarely required
  • May be considered in pt with ongoing GI bleeding (requiring continued transfusion), where endoscopic and radiographic treatment has failed
35
Q

scoring system used in LGI bleeds

A

Used to help stratify patients presenting with a lower GI bleed to determine if outpatient management is feasible.

Factors used to determine the Oakland score are

  • Age
  • Sex
  • Previous Admissions for Lower GI bleeding
  • PR findings
  • Heart Rate
  • Systolic Blood Pressure
  • Haemoglobin Concentration.
36
Q

GI perforation

A

May occur at any anatomical location from the upper oesophagus to the anorectal junction.

  • Delay in resuscitation and definitive surgery will progress rapidly into
    • septic shock
    • multi organ dysfunction,
    • death, hence it should be one of the first
  • diagnoses considered in all patients who present with acute abdominal pain.
37
Q

causes of GI perforation

A
38
Q

presentation of GI perforation

A
  • Pain- peritonism- rigid abdomen
    • Rapid onset
    • Sharp
    • Localised or generalised (implies diffuse contamination)
  • Systemically unwell- signs of sepssi
    • Malaise
    • Vomiting
    • Lethargy
39
Q

investigations for GI perforation

A
  • Blood test (FBC, U&Es, LFTS, CRP, clotting and G&S)
    • Raised WCC and CRP common features, amylase often mildly elevated
  • Imaging
    • CT scan gold standard- confirms frew air and location
    • CXR (not used as much)
      • Air under diaphragm
      • Rigler sign- both sides of bowel visible- pneumoperitoneum
40
Q

management of GI perforation: general approach

A
  • Broad spec antibiotics early
  • NBM
  • NG tube considered
  • IV resus
  • Analgesia
41
Q

conservative management of GI perforation

A

Select physiologically well patients may be managed conservatively, including patients with:

  • Localised diverticular perforation* with only localised peritonitis and tenderness, and no evidence of generalised contamination on imaging
  • Patients with a sealed upper GI perforation on CT imaging without generalised peritonism
  • Elderly frail patients with extensive co-morbidities who would be very unlikely to survive surgery

*An estimated size less than 5cm on CT scan is an accepted cut off for conservative treatment in these patients, who may respond to antibiotics alone or may be amenable to guided percutaneous drainage

42
Q

The key aspects of any surgical intervention for a GI perforation are:

A
  • Identification of the underlying cause
  • Appropriate management of perforation
  • Thorough washout- VERY IMPORTANTwhen is surgery considered for GI perforation
43
Q

surgical technique for peptic ulcer perforation

A

can be accessed typically via an upper midline incision (or laparoscopically if feasible) and a patch of omentum (termed a “Graham patch”) is tacked loosely over the ulcer, which would otherwise be difficult to oversew due to tissue inflammation

44
Q

surgical technique for small bowel perforation

A
  • can be accessed via a midline laparotomy; small perforations can be oversewn if the bowel is viable, yet any doubt about condition of bowel should lead to bowel resection +/- primary anastomosis +/- stoma formation
45
Q

surgical treatment for large bowel perforation

A

can be accessed via midline laparotomy; anastomosis in the presence of faecal contamination and an unstable patient is not recommended, so a resection with stoma formation is often the preferred option

46
Q

IBD comparison

A
47
Q

crohns disease

A

The disease typically follows a remitting and relapsing course. Severe exacerbations may be life- threatening, causing severe systemic upset, bowel perforation, or rarely death.

48
Q

RF for Crohns disease

A
  • Caucasian
  • Family history
  • younger
  • smoking
49
Q

pathophysiology of crohns

A
  • Aetiology unknown
  • Familial and environmental links
  • Smoking increases risk
50
Q

characteristic features of crohns

A
  • Transmural inflammation
    • Deep ulcers and fissures- cobblestone appearance
      • Fistula risk
  • Effect entire GI tract
  • Skip lesions of inflammation
  • Granulomas
51
Q

presentation of crohns

A
  • Episodic abdominal pain and diarrhoea
  • Blood and mucus in diarrhoea
  • Systemic symptoms
    • Malaise
    • Anorexia
    • Low grade fever
    • Malnourishment due to malabsorption
  • Oral to perianal involvement e.g. aphthous ulcers or perianal disease
  • Extra-intestinal
    • Enteropathic arthritis
    • Metabolic bone disease (malabsorption)
    • Erythema nodosum
    • Anterior uveitis
    • Primary sclerosing cholangitis
    • Cholangiocarcinoma
    • Renal stones
52
Q

complications of crohns

A

fistula, stricture, GI malignancy, malabsorption, osteoporosis

53
Q

investigations for crohns

A
  • Bloods
    • FBC, albumin, CRP, WCC
  • Faecal calprotectin
  • Imaging
    • Colonoscopy is gold standard
      • Biopsy taken
      • Montreal score used to quantify disease extent
    • CT abdomen
      • Warranted in severe crohns
        • To show bowel obstruction, perforation etc
    • MRI
      • To assess disease severity both with small bowel involvement and presence of enteric fistulae and or peri-anal disease
54
Q

management of crohns

A
  • Inducing remission
    • Fluid resus
    • Nutrition support
    • Prophylactic heparin (prothrombotic state of IBD flare)
    • medication corticosteroid, followed by mesalazine or azathioprine or biologics like infiliximab
    • avoid colonscopy in flare- risk of perforation
  • Maintaining remission
    • azathioprine
    • smoking cessation
    • colonoscopy surveillance
  • Surgical management (failed medical management or severe complications)
    • Ileocaecal resection (removal of terminal ileum and caecum with primary anastomosis)
    • Small bowel resection or large bowel resection
    • Surgery for peri-anal disease (e.g. abscess drainage, seton insertion, or laying open of fistulae)
    • Stricturoplasty (division of a stricture that is causing bowel obstruction
55
Q

ulcerative colitis

A

Most common form of IBD

56
Q

RF of UC

A
  • Caucasian
  • Family history
57
Q

pathophysiology of UC

A
  • Aetiology unknown
  • Familial and environmental links
  • Smoking protective
58
Q

Characteristic features of UC

A
  • Diffuse continual mucosal inflammation
  • Colon only
    • Beginning in rectum and spreading proximally
    • Crypt abscesses and goblet cell hypoplasia
59
Q

presentation of UC

A
  • Insidious in onset
  • Bloody diarrhoea
  • Proctitis- inflammation is confined to rectum only
    • PR bleeding and mucus, frequency and urgency, tenesmus
    • Dehydration and electrolyte imbalance- widespread colonic involvement
60
Q

extra-intestinal features of UC

A
  • Enteropathic arthritis
  • Erythema nodousm
  • Anterior uveitits
  • Primary sclerosing cholangitis
61
Q

complications of UC

A

fulminant colitits toxic megacolon, colonic perforation, death

62
Q

investigations for UC

A
  • Bloods
    • FBC, albumin, CRP, WCC
  • Faecal calprotectin
  • Imaging
    • Colonoscopy is gold standard
      • Biopsy taken
      • Montreal score used to quantify disease extent
    • AXR/CT abdomen
      • Warranted in severe exacerbation
        • To show bowel obstruction, perforation etc
63
Q

features of IBD on AXR

A
  • Thumbprinting: mucosal thickening of the haustra due to inflammation and oedema causing them to appear like thumbprints projecting into the lumen.
  • Lead-pipe (featureless) colon: loss of normal haustral markings secondary to chronic colitis.
  • Toxic megacolon: colonic dilatation without obstruction associated with colitis.

Surgery block (Y3) (38 decks)

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