Lecture 18- GI emergencies 2/2 Flashcards

1
Q

Acute mesenteric ischemia

A

Symptomatic reduction in blood supply to GI tract

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2
Q
  • Risk factors of acute mesenteric ischemia
    *
A

More common in females (75%) and if you have a history of peripheral vascular disease

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3
Q

causes of acute mesenteric ischaemia

A
  • Acute occlusion (70%)
  • Non-occlusive mesenteric ischaemia (20%)
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4
Q

Acute occlusion (70%)

A

Arterial embolism in the SMA (50%)- midgut

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5
Q

Non-occlusive mesenteric ischaemia (20%)

A
  • Low CO
  • Mesenteric venous thrombosis (5-10%)
  • Systemic coagulopathy and malignancy
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6
Q

most cases of acute mesenteric ischaemia are in

A

lderly patients. With CVD risk factors.

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7
Q
  • Symptoms of acute mesenteric ischaemia
A
    • Can be difficult to diagnose because symptoms can be fairly non-specific
      • Abdominal pain disproportionate to the clinical findings
        • Classic pain- comes on 30 mins after eating and lasts 4 hours
      • Nausea and vomiting

Pain on left hand side

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8
Q
  • why Pain on left hand side in acute mesenteric ischaemia-
A
  • blood supply to the splenic flexure (point where transverse colon turns into the descending colon) is more fragile
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9
Q

AMI Investigations

*

A
  • Blood tests
    • Metabolic acidosis / increased lactate levels- ischaemic drugs
  • Erect chest x-ray- check for perforation (gas under the diaphragm)
  • CT angiography (90% sensitivity)- intravenous contrast
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10
Q

Treatment AMI

A
  • Surgery- resection of ischaemic bowel–> bypass graft
  • Thrombolysis/angioplasty
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11
Q

Prognosis of AMI

*

A
  • Mortality is high (arterial thrombosis’s up to 70% mortality)
    • Often older pts with comorbidities
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12
Q

2 examples of major upper GI bleeding

A
  1. peptic ulceration
  2. oesophageal varices
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13
Q

peptic ulceration causes …….% of acute upper GI bleeding

A

20-50%

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14
Q

what is peptic ulceration

A
  • Disruption in gastric/duodenal mucosa that extends through the muscularis mucosa
  • Greater than 5mm diameter
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15
Q

which type of ulcer is most common

A
  • Duodenal ulcers most common
    • First part of duodenum
    • Gastro-duodenal artery lies behind first part of duodenum
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16
Q

where are peptic ulcers found in the stomach

A
  • Lesser curve and antrum common sites
17
Q

gastric ulcer erosion is especially dangerous if it erosed the

A

splenic artery

18
Q

what are oesophageal varices

A

porto-systmeic anastomosis

  • 12-14% of acure upper GI bleeding
19
Q

explain how oesophageal varices occur and how they can lead to major upper GI bleeding

A
  • an example of porto-systemic anastomosis
  • they are often caused by portal hypertension
    • back flow of blood from the portal vein –> left gastric –> which drains the distal portion of the oesophagus
  • oesophagus also draine dby the azygous vein
  • left gastric vein and azygous anastomose
  • these anastomes distend with blood – rupture –> bleed
20
Q

causes of oesophageal varices

A

portal hypertension

  • Caused by anything that slows blood flow through portal vein
    • Pre-hepatic (portal vein thrombosis)
    • Hepatic (cirrhosis schistosomiasis)
    • Post hepatic causes (hepatic vein thrombosis, RHF)
21
Q
  • Normal pressure in portal vein
A
  • 5-10mm Hg
    • Problem happens around 10 mmHg
22
Q
  • porto-systemic anastomoses are areas that
A

have venous drainage through portal vein and systemic veins e.g. the distal portion of the oesophagus

23
Q

Treatment of oesophageal varices

A
  • Fluid resus
  • If bleeding not controlled by banding
    • Transjugular intrahepatic portosystemic shunt (TIPS)
  • Drug treatment
    • Terlipressin- reduces portal venous pressure
24
Q

Transjugular intrahepatic portosystemic shunt (TIPS)

A
  • expandable metal is palced within the liver
  • bridge the portal vein to the hepatic vein
  • decrompresses protal vein pressyre
  • reduction in variccal pressure
  • reduction in ascites
25
Q

Abdominal aortic aneurysm – AAA

A

A permanent pathological dilation of the aorta with a diameter >1.5 times the expected anteroposterior (AP) diameter of that segment, given the patients sex and body size. The most commonly adopted threshold is 3cm or more. More than 90% of aneurysms originate below the renal arteries.

26
Q

MOA of AAA

A
  • Usually due to the degeneration of the media layer of the arterial wall
    • Media- smooth muscle cells with elastin and collagen
      • AAA forms due to degradation of elastin and collagen

Lumen gradually starts to dilate

27
Q

AAA Risk factors

A
  • Male
  • Inherited risk
  • Increasing age
  • Smoking
28
Q

AAA Symptoms

A
  • Most are asymptomatic until acute expansion or rupture
  • pulsating mass or feeling is stomach
  • Can cause symptoms by compressing other nearby structures
    • Stomach (nausea)
    • Bladder (urinary frequency)
    • Vertebra (back pain)
29
Q

Symptoms of a ruptures AAA

A
  • Abdominal pain
  • Back pain
  • shortness of breath
  • Pulsatile abdominal mass- surgical referral
  • Transient hypotension–> syncope
  • Sudden cardiovascular collapse – 65% of ruptures AAA die before hospital
30
Q

why transient hypotension (esp in early AAA rupture)

A
  • Retroperitoneum can temporarily tamponade the bleeding
    • syncope
31
Q
A
32
Q

diagnosis of AAA

A
  • Physical exam
    • Presence of pulsatile abdominal mass (less than 50%)
  • Ultrasonography
    • Non invasive and in the right hands very sensitive and specific
    • Can also detect free peritoneal blood
  • Computed tomography (CT)
    • Can detect a lot of surrounding anatomy that may be relevant
      • Planning for elective surgery
  • Plain x-rays
    • If aneurysm has calcified then can be seen on plain X-ray
33
Q

non surgical treatment of AAA

A

smoking cessation

hypertension control

34
Q
  • Surveillance of AAA
A
  • Less than 5.5 cm (most grow slowly enough to not need treatment)
  • More than 5.5cm- refer to surgeons
35
Q

surgery to repair AAA (2 ways)

A
  1. endovascular repair
  2. open surgical repair
36
Q
  • endovascular repair
A

Insert wire through femoral artery and over that wire you pass an endograft- this will expand and hook into place- seal below renal arteries and above common iliacs

37
Q
  • open surgical repair
A
  • Clamp aorta
  • Open the aneurysm (remove thrombus and debris)
  • Suture in a synthetic graft to replace diseased segment
38
Q

types of AAA

A

90% of AAA’s are infrarenal