General - presentations Flashcards

1
Q

Bowel obstruction

A

Mechanical blockage of the bowel, whereby a structural pathology physically blocks the passage of intestinal contents
Once bowel segment has become occluded, gross dilatation of the proximal limb of the bowel occurs
There becomes an increased peristalsis of the bowel -> in turn leads to secretion of large volumes of electrolyte-rich fluid into the bowel
(when bowel is adynamic and not working properly, this typically either an ileus/pseudo-obstruction)

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2
Q

Closed loop obstruction

A

In patients with a mechanical bowel obstruction, if there is a second separate obstructing point proximally = closed-loop obstruction
Surgical emergency as if not corrected, the bowel will continue to distend within a closed segment of bowel -> stretching the bowel wall until it becomes ischaemic & this can further lead to perforation

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3
Q

Bowel obstruction aetiology

A

Small bowel – adhesions or hernia
Large bowel – malignancy, diverticular disease or volvulus
Intraluminal – gallstone ileus, ingested foreign body, faecal impaction
Mural – cancer, inflammatory strictures, intussusception, diverticular strictures, Meckel’s diverticulum, lymphoma
Extramural – hernias, adhesions, peritoneal metastasis, volvulus

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4
Q

Bowel obstruction clinical features

A

Abdominal pain – colicky/cramping in nature
Vomiting – early is proximal obstruction and late in distal obstruction
Abdominal distension
Absolute constipation – occurring early in distal obstruction & late is proximal obstruction
Examination – evidence of underlying cause, assess patient’s fluid status, palpate for focal tenderness, tinkling bowel sounds

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5
Q

Bowel obstruction investigations

A

Lab test – routine urgent bloods, group and save, venous blood gas
Imaging
- CT scan with intravenous contrast of the abdomen and pelvis is the imaging modality of choice in suspected bowel obstruction
- AXR is still used in some settings as the initial investigation for bowel obstruction
o Small bowel obstruction – dilated bowel (> 3cm), central abdominal location & valvulae conniventes visible (lines completely crossing the bowel)
o Large bowel obstruction – dilated bowel (> 6cm, or >9cm at caecum), peripheral location and haustral lines visible (lines not completely crossing the bowel)

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6
Q

Bowel obstruction conservative management

A

Absence of signs of ischaemia/perforation, initial management for cases of adhesional bowel obstruction is conservative – drip and suck management:
- Make the patient NBM and insert a NGT to decompress the bowel
- Start IV fluids and correct any electrolyte disturbances
- Urinary catheter and fluid balance
- Analgesia as required with suitable anti-emetics
Water soluble contrast study can be performed in cases that do not resolve initially with conservative management

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7
Q

Bowel obstruction surgical management

A

Surgical intervention is indicated in patients with:
- Suspicion of intestinal ischaemia or closed loop bowel obstruction
- Cause that requires surgical correction
- If patients fail to improve with conservative measures (typically after > 48 hours)
Generally will warrant a laparotomy, defunctioning stoma may be required if the re-joining of the obstructed bowel is not possible

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8
Q

Bowel obstruction complications

A

Bowel ischaemia
Bowel perforation – faecal peritonitis
Severely intravascularly fluid deplete – resulting in AKI and other end-organ injury if mismanaged

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9
Q

Haematemesis

A

Vomiting fresh blood, occurs as a result of bleeding occurring in any part of the upper gastrointestinal tract

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10
Q

Haematemesis differentials

A

Oesophageal varices
Peptic ulcer disease
Mallory-weiss tear
Oesophagitis
Other causes – gastric cancer or oesophageal cancer or vascular malformations

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11
Q

Haematemesis clinical features

A

Features of haematemesis – timing, frequency & volume
Associated symptoms – dyspepsia, dysphagia, melaena, weight loss
Past medical history – including the smoking and alcohol status
Drug history – use of steroids, NSAIDs, anticoagulants or bisphosphonates

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12
Q

Haematemesis investigations

A

Initial investigations – routine blood tests, to help investigate for underlying causes and to stratify patient risk, group and save requested
Further investigations – gastroscopy for further assessment, urgency by which an OGD is performed should be determined by the patients Glasgow-Blatchford bleeding score
- CT angiogram can be performed if OGD is normal and ongoing bleeding

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13
Q

Glasgow-blatchford bleeding score

A

Used to risk stratify patients admitting with an upper GI bleed, based purely on clinical and biochemical parameters
Allows for appropriate management of further investigations
Scores >/= 6 have been associated with a >50% risk of needing an intervention

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14
Q

Haematemesis management

A

A to E approach should be used to stabilise the patient
Most cases will warrant a gastroscopy from which a range of therapeutic options ar available depending on the underlying causes suspected or confirmed:
- Peptic ulcer disease – injections of adrenaline and cauterisation of the bleeding during endoscopy, then patients on high dose intravenous PPI therapy to reduce gastric acid secretion
- Oesophageal varices – management should be swift & performed at the same time as active resus (endoscopic banding)
Surgical intervention is rarely required in upper GI bleeds, where endoscopic and interventional treatments have failed

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15
Q

Dysphagia

A

Refers to difficulty in swallowing
Occurs from any abnormal delay in the transit of liquids or solids during the oropharyngeal or oesophageal stages of swallowing
Either a transient delay or a fixed delay

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16
Q

Dysphagia aetiology

A

Mechanical – oesophageal cancer, gastric cancer of head & neck cancer, benign oesophageal strictures, extrinsic compression, pharyngeal pouch, foreign body & oesophageal web
Motility – cerebrovascular accident, achalasia, diffuse oesophageal spasm, myasthenia gravis & muscular dystrophy

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17
Q

Dysphagia clinical features

A

Exact nature of the symptoms, including duration & frequency
Further symptoms – reflux/dyspepsia, hoarse voice or referred pain, significant weight loss
Should be differentiated from odynophagia
General examination – assess for overt motor dysfunction, resting tremor or dysarthria
Examine the mouth, neck & abdomen

18
Q

Dysphagia investigations

A

Routine bloods
First line investigation – upper GI endoscopy, this will assess for any mechanical cause & exclude upper GI malignancy
Any further investigations will depend on the suspected underlying cause
Manometry testing – assesses the motor function of the upper oesophageal sphincter, the oesophageal sphincter & the lower oesophageal sphincter

19
Q

Dysphagia management

A

Treatment of the underlying cause
Patients with dysphagia are often significantly malnourished
Referral to a speech and language therapist
Patients with cancer – MDT meeting
Motility disorders – medical management is trialled first before either endoscopic/surgical intervention
Neurological disorders – best managed by a neurologist

20
Q

Gastric outlet obstruction

A

Mechanical obstruction of the proximal gastrointestinal tract, occurring at some level between the gastric pylorus and the proximal duodenum, resulting in an inability in the stomach to empty

21
Q

Gastric outlet obstruction aetiology

A

Peptic ulcer disease
Gastric cancer
Small bowel cancer
Iatrogenic
Bouveret syndrome
Gastric bezoar

22
Q

Gastric outlet obstruction clinical features

A

Epigastric pain
Postprandial vomiting
Early satiety
Examination – significant dehydration & often hypovolaemic, tender and distended upper abdomen, localised peritonism/guarding can be present

23
Q

Bouveret syndrome

A

Gastric outlet obstruction secondary to a gallstone impacted at the pylorus or proximal duodenum
Occurs in patients with a cholecystoduodenal fistula, typically developing from episodes of recurrent cholecystitis

24
Q

Gastric outlet obstruction investigations

A

Should have routine bloods performed and a clotting screen and group & save
Abdominal plain film radiograph, but most cases will warrant a CT scan with IV contrast for confirmation of GOO
Upper GI endoscopy

25
Q

Gastric outlet obstruction management

A

Resuscitative IV fluids
NGT to decompress the stomach & patient started on IV PPI
Endoscopy – dilate benign stricturing where feasible or remove any luminal obstruction
Surgical intervention – mainstay of treatment in most cases

26
Q

Gastrointestinal perforation aetiology

A

Upper GI tract – PUD, gastric cancer/oesophageal cancer, foreign body ingestion, excessive vomiting
Lower GI tract – diverticulitis, colorectal cancer, appendicitis/Meckel’s diverticulitis, foreign body insertion, severe colitis, toxic megacolon
Any part – iatrogenic, trauma, mesenteric ischaemia, obstructing lesions

27
Q

Gastrointestinal perforation clinical features

A

Abdominal pain – rapid onset and severe
Systemically unwell & may have associated malaise, vomiting or lethargy
Examination – look unwell & often have features of sepsis, usually have features of peritonism which may be localised or generalised

28
Q

Gastrointestinal perforation investigations

A

Laboratory tests – urgent blood tests, raised inflammatory markers
Imaging – CT scan with intravenous contrast, in suspected upper GI perforation, a CT scan with oral contrast may be used for upper GI perforation
eCXR and AXR
- eCXR: pneumoperitoneum
- AXR: Rigler’s sign (both sides of the bowel visible) or psoas sign (loss of the sharp delineation of the psoas muscle border)

29
Q

Gastrointestinal perforation surgical intervention

A

Intra-operative washout
Peptic ulcer perforation – a patch of omentum is tacked loosely over the ulcer
Small bowel perforation – bowel resection +/- primary anastomosis +/- stoma, small perforations can be managed by oversewing the defect
Large bowel perforation – can result in a large amount of contamination, bowel resection +/- stoma formation is typically the preferred option

30
Q

Gastrointestinal perforation conservative management indications

A

Localised diverticular perforation with only localised peritonitis and tenderness and no evidence of generalised contamination
Patients with a sealed upper GI perforation on CT without generalised peritonism
Elderly frail patients

31
Q

Malaena

A

Black, offensive tarry stools
Occurs as a result of upper gastrointestinal bleeding

32
Q

Malaena differentials

A

Peptic ulcer disease
Variceal bleeds
Upper GI malignancy
Other less common – gastritis, oesophagitis, Meckel’s diverticulum, small bowel tumours or vascular malformations

33
Q

Malaena clinical features

A

Colour and texture of the stool
Associated symptoms – including any haematemesis, abdominal pain, weight loss, dyspepsia/dysphagia
Past medical history – smoking and alcohol status
Drug history – use of steroids, NSAIDs, anticoagulants or iron tablets
DRE, full abdominal examination

34
Q

Malaena investigations

A

Initial investigations – routine blood tests
- Any drop in haemoglobin and rise in urea:creatinine ratio is very indicative of an upper GI bleeds
Further investigations – gastroscopy, if inconclusive: CT angiogram, colonoscopy

35
Q

Malaena management

A

Peptic ulcer disease – injections of adrenaline & cauterisation of the bleeding during endoscopy, IV PPI
Oesophageal varices – urgent endoscopy and concurrent resuscitation with blood products, alongside prophylactic antibiotics and somatostatin analogues (endoscopic banding is the most definitive management)
Upper GI malignancies – require biopsies to be taken and a definitive surgical management plan is required

36
Q

Rectal bleeding differentials

A

Diverticular disease
Ischaemic/infective colitis
Haemorrhoids
Malignancy
Angiodysplasia
Crohn’s disease
Ulcerative colitis

37
Q

Rectal bleeding clinical features

A

Nature of bleeding – duration, frequency & colour
Associated symptoms – pain, any haematemesis or malaena, any PR mucus, previous episodes or weight loss
Family history – bowel cancer or IBD
Examination – localised tenderness or palpable masses, PR examination

38
Q

Oakland score

A

Can be used to help stratify patients presenting with a lower GI bleed to determine if outpatient management is feasible

39
Q

Rectal bleeding investigations

A

Routine bloods, group & save, stool cultures
Urgent CT angiogram should be performed once stabilised
Patients with stable bleeds – require a colonoscopy for further assessment to exclude left-colonic pathology
Upper GI endoscopy if no abnormality identified on colonoscopy

40
Q

Rectal bleeding management

A

95% will settle spontaneously
Endoscopic haemostasis methods
Arterial embolisation
Surgical intervention – rarely required, may be considered in patient with ongoing lower GI bleeding instability where other treatments have failed