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GI emergencies Flashcards

1
Q

What is peritonitis?

A
  • Inflammation of serosal membrane that lines abdominal cavity
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2
Q

How does peritonitis occur?

A
  • Peritoneal cavity is normally sterile
  • Can occur spontaneously (primary)
  • Or due to breakdown of peritoneal membranes leading to foreign substances entering cavity (secondary)
  • Can be infectious or sterile
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3
Q

Summarise the structure of the peritoneal cavity

A
  • Space between visceral and parietal layers of peritoneum
  • Visceral and parietal components are continuous
  • Parietal peritoneum lines abdominal wall
  • Visceral peritoneum is any part that does not line abdominal wall
  • Cavity contains a small amount of fluid
  • Divided into greater sac and lesser sac
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4
Q

Which demographic of patients are more commonly affected by primary peritonitis?

A
  • Patients with end stage liver disease
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5
Q

What is spontaneous bacterial peritonitis?

A
  • Infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition
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6
Q

What is ascites?

A
  • Pathological collection of fluid within peritoneal cavity
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7
Q

In cirrhosis, what causes ascites?

A
  • Portal hypertension
  • Causes increased hydrostatic pressure in veins draining the gut
  • Decreased liver function results in less albumin production
  • Decreased intravascular oncotic pressure
  • Results in net movement of fluid into peritoneal cavity
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8
Q

What are the symptoms of primary peritonitis?

A
  • Abdominal pain
  • Fever
  • Vomiting
  • Commonly symptoms are mild
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9
Q

How is primary peritonitis diagnosed?

A
  • Aspirating ascitic fluid
  • Neutrophil count >250 cells/mm^3
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10
Q

What is secondary peritonitis?

A
  • Result of an inflammatory process in peritoneal cavity
  • Secondary to inflammation, perforation, or gangrene of an intra-abdominal or retroperitoneal structure
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11
Q

What are common causes of secondary bacterial peritonitis?

A
  • Peptic ulcer disease (perforated)
  • Appendicitis (perforated)
  • Diverticulitis (perforated)
  • Post surgery
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12
Q

What are the non-bacterial causes of secondary peritonitis?

A
  • Tubal pregnancy that bleeds (ectopic pregnancy)
  • Ovarian cyst
  • Blood is highly irritant to peritoneal
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13
Q

What is the clinical presentation of peritonitis?

A
  • Abdominal pain is most common symptom
  • May come on acutely or gradually
  • Diffuse abdominal pain common in perforated viscera
  • Patients often lie very still as any movement makes pain worse
  • Often have knees flexed and shallow breathing
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14
Q

What are the treatments for peritonitis?

A
  • Control infectious source - surgery
  • Eliminate bacteria and toxins - antibacterial therapy
  • Maintain organ system function - intensive care
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15
Q

What is bowel obstruction?

A
  • Mechanical or functional problem that inhibits normal movement of gut contents
  • Can affect large and small intestine
  • Can affect all ages
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16
Q

What are common causes of bowel obstruction in children?

A
  • Intussusception
  • Intestinal atresia
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17
Q

What are common causes of bowel obstruction in adults?

A
  • Adhesions
  • Incarcerated hernias
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18
Q

What is intussusception?

A
  • When one part of the gut ‘telescopes’ into an adjacent section
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19
Q

What causes intussusception?

A
  • Cause not well known
  • Potential motility issues
  • Lead point (mass precipitating telescoping action) e.g. Meckel’s diverticulum or enlarged lymph node
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20
Q

What can bowel obstruction result in?

A
  • Can even prolapse out of rectum
  • Get oedema as soon as lymphatic and venous drainage is impaired
  • Can lead to infarction because arterial supply is impeded
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21
Q

What are the classic symptoms of intussusception?

A
  • Abdominal pain
  • Vomiting
  • Haematochezia
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22
Q

How is intussusception treated?

A
  • Air enema
  • Surgery
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23
Q

What are the most common symptoms of small bowel obstruction?

A
  • Nausea and vomiting (can contain bile) are most common symptom
  • Abdominal distension
  • Absolute constipation (late)
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24
Q

What can cause small bowel obstruction?

A
  • Intra-abdominal adhesions
  • Hernias (incarcerated groin hernias most common)
  • IBD (repeated inflammation/healing causes narrowing)
25
Q

What are intra-abdominal adhesions?

A
  • Abnormal fibrous bands between organs, or tissues, or both in abdominal cavity that are normally separated
26
Q

What causes intra-abdominal adhesions?

A
  • Arise after more than 50% of abdominal surgeries
  • Damage to mesothelium - capillary bleeding leads to exudation of fibrinogen
27
Q

What are the consequences of adhesions?

A
  • Abdominal pain
  • secondary infertility
28
Q

How is small bowel obstruction diagnosed?

A
  • History - abdominal pain is crampy/intermittent
  • Physical examination - abdominal distension, increased/absent bowel sounds, presence of hernia
  • Imaging - CT abdo and pelvis
29
Q

Which demographic of patients is most commonly affected by large bowel obstruction?

A
  • Typically affects older generation
30
Q

What are common causes of large bowel obstruction?

A
  • Colon cancer
  • Diverticular disease causing strictures
  • Volvulus - sigmoid (older patients) or caecal (younger patients and rarer)
31
Q

What are the symptoms of large bowel obstruction?

A
  • Appear gradually if caused by cancer but are abrupt with volvulus
  • Change in bowel habit
  • Abdominal distension
  • Crampy abdominal pain
  • Nausea/vomiting
32
Q

What is a volvulus?

A
  • Part of colon twists around mesentery
  • Most common in sigmoid colon and caecum
  • Results in obstruction
  • Caecal volvulus results in obstruction of large and small bowel
33
Q

What causes volvulus?

A
  • Overloaded sigmoid colon e.g. due to constipation
  • Extra mass elongates sigmoid colon
  • High fibre diet also results in sigmoid overload and twisting
34
Q

How is volvulus investigated?

A
  • CT abdo and pelvis
35
Q

Compare ages in small vs large bowel obstruction

A
  • Small bowel obstruction more common in younger age group
  • Large bowel obstruction more common in older age group
36
Q

Why is competence of the ileo-caecal valve important in bowel obstruction?

A
  • If valve is very competent, obstruction is made worse
  • Pressure increases in colon, making ischaemia and perforation more likely
37
Q

Compare the symptoms of large and small bowel obstructions

A
  • Abdominal pain is colicky for both but lasts longer in large bowel obstruction
  • Vomiting occurs relatively early in small bowel obstruction and relatively late in large bowel obstruction
  • Constipation occurs relatively late in small bowel obstruction but relatively early in large bowel obstruction
38
Q

How is bowel obstruction imaged?

A
  • CT scan
39
Q

What might a presentation of acute mesenteric ischaemia look like?

A
  • Intermittent diffuse abdominal pain
  • Worse after eating
  • Present for a while but recently worsened
  • Significant weight loss
40
Q

What is acute mesenteric ischaemia?

A
  • Symptomatic reduction of blood supply to GI tract
  • Worse after meals because blood is diverted to gut
41
Q

Which area of the gut is most commonly affected by acute mesenteric ischaemia?

A
  • Splenic flexure: superior and inferior mesenteric artery watershed
  • Rectosigmoid junction: inferior mesenteric and hypogastric artery watershed
42
Q

Outline arterial compromise of acute mesenteric ischaemia

A
  • Occlusion in 70% of cases
  • Arterial embolism/thrombosis usually affects SMA
  • Vasculitis can narrow artery (not acute)
  • Low cardiac output can also cause ischaemia
43
Q

Outline venous compromise of acute mesenteric ischaemia?

A
  • Mesenteric venous thrombosis (5-10%)
  • Systemic coagulopathy, malignancy
44
Q

What are the symptoms of acute mesenteric ischaemia?

A
  • Most cases are in more elderly patients with cardiovascular risk factors
  • Can be difficult to diagnose - symptoms are non-specific
  • Abdominal pain is disproportionate to clinical findings
  • Nausea and vomiting often present
  • Pain often left sided because blood supply to splenic flexure is most fragile
45
Q

What are the investigations for acute mesenteric ischaemia?

A
  • Blood tests for metabolic acidosis/increased lactate levels
  • CT abdo/pelvis
  • CT angiography
46
Q

How is acute mesenteric ischaemia treated?

A
  • Surgery - resection of ischaemic bowel (bypass graft)
  • Thrombolysis/angioplasty
  • Mortality is high
47
Q

Outline peptic ulceration

A
  • Cause of 20-50% upper GI bleeding
  • Disruption in gastric/duodenal mucosa going through to submucosa
  • Duodenal ulcers most common
  • Gastro-duodenal artery most commonly affected
  • Gastric ulcers commonly found in lesser curve or antrum of stomach
48
Q

Summarise portal hypertension

A
  • Caused by anything that slows blood through portal vein
  • Due to pressure than 10 mmHg
  • Can cause issues in sites of porto-systemic anastomosis are areas that have venous drainage through portal vein and systemic veins
49
Q

Outline venous drainage of oesophagus

A
  • Portal drainage - oesophageal veins drain into left gastric vein which then drains into portal vein
  • Oesophageal veins drain into azygous vein, drains into superior vena cava
50
Q

How are oesophageal varices treated?

A
  • Transjugular intrahepatic portosystemic shunt
  • Expandable metal placed within liver to bridge portal vein into hepatic vein
  • Decompresses portal vein pressure
  • Reduction in variceal pressure and ascites
  • Terlipressin (reduces portal venous pressure)
51
Q

What is an abdominal aortic aneurysm?

A
  • Permanent pathological dilation of aorta
  • Diameter >1.5 times expected (3cm or more)
  • More than 90% of aneurysms originate below renal arteries
52
Q

What usually causes AAAs?

A
  • Due to degeneration of media layer of arterial wall
  • Made up of smooth muscle cells with elastin and collagen
  • AAAs form due to degradation of elastin and collagen
  • Lumen gradually starts to dilate
  • Most AAAs are asymptomatic
53
Q

What are the risk factors for AAAs?

A
  • Male
  • Inherited risk
  • Increasing age
  • Smoking
54
Q

What are the symptoms of AAAs?

A
  • Normally asymptomatic until acute expansion or rupture
  • Can cause symptoms by compressing other nearby structures e.g. stomach, bladder, vertebra
  • E.g. nausea, urinary frequency, back pain
55
Q

How does a ruptured AAA present?

A
  • Abdominal pain (+/- flank and groin pain)
  • Back pain
  • Pulsatile abdominal mass
  • Transient hypotension
  • Syncope
  • Retroperitoneum can temporarily tamponade the bleed
  • Sudden cardiovascular collapse
56
Q

How do ruptured AAAs get diagnosed?

A
  • Presence of pulsatile abdominal mass
  • Ultrasonography (non-invasive, very sensitive, very specific)
  • CT
57
Q

How is an AAA treated?

A
  • Smoking cessation
  • Hypertension control
  • Surveillance of AAA - if greater than 5.5 cm - refer to vascular surgeon
  • Surgery
  • Endovascular repair - relining aorta using an endograft
58
Q

Outline how surgery is used to treat AAA?

A
  • Stent inserted through femoral artery to seal renal arteries and common iliacs
  • Or open surgical repair
  • Clamp aorta
  • Open aneurysm to remove thrombus and debris
  • Suture in a synthetic graft to replace diseased segment

GI tract (23 decks)

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