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Flashcards in Tombazzi - Vascular GI Disorders Deck (61):

What are the main arteries involved in GI vascular support?

- Celiac trunk 

- Superior mesenteric artery (SMA): provides vascular support for pancreatico-duodenal area, small intestine, and right colon 

- IMA 

- NOTE: SMA and IMA provide most of the vascular support for the large intestine 


Is ischemia/necrosis typically worse in the small bowel or large intestine?

- Small bowel: usually more severe and aggressive (with worse outcome) than ischemia of the colon because you may have only one vessel supplying large area of tissue

- More anastomoses in the colon 

- NOTE: vast network of collateral blood vessel gives substantial protection from ischemia or infarction in a setting of segmental vascular occlusion 


What general factors are involved in the regulation of the splanchnic circulation?

–- Autonomic nerves: SYM, PARA, enteric nerves

–- Cardiovascular control: cardiac output, arterial pressure, blood volume

–- Endocrine and paracrine systems

–- Digestive systems: vasodilators, metabolites, vasoactive paracrine secretion, local circulatory mechanisms (postprandial hyperemia)

- NOTE: the GI tract is not the same all of the time -> big difference b/t fasting and fed 


Name 6 hormones (and their stimuli) involved in regulation of GI bloodflow.


1. Catacholamines (adrenal medulla): oligemic shock

2. Ang II (renal JGA): heart failure 

3. Vasopressin (post pit): oligemic shock  


1. Gastrin (mucosal G cells): mealtimes 

2. CCK (intestinal mucosa I cells): mealtimes

3. Secretin (intestinal mucosa S cells): mealtimes


What is the pathophys of GI vascular disease? Prognostic factor?

- SEQUENCE: DEC mesenteric flow (sepsis, emboli)

1. Vasospasm: cytokines released 

2. Mucosal hypoxia 

3. Necrosis of villi: bleeding 

4. Edema of lamina propria: pain w/o ileus 

5. Infarction: ileus-sepsis -> bacteria living in GI tract can get into vasculature 

- Prognostic factor: TIME -> takes blood longer to get from jejunum to visible area (rectum) vs. rectal blood, which is much closer, so small bowel more likely to have transmural necrosis, and involvement of longer segment of bowel before detection 


What are 3 categorical causes of bowel ischemia?

- DEC arterial supply: emboli in SMA 

- DEC venous return 

- Low flow states: heart failure, hemorrhage, shock 

- NOTE: depending on the layers affected, infarcts are classified as:

1. Transmural

2. Mural

3. Mucosal 


What are some predisposing conditions to bowel ischemia?

- Arterial thrombosis: atherosclerosis, systemic vasculitis, oral contraceptives, angiographic procedures, hypercoagulable state

- Arterial embolism: cardiac vegetations, aortic atheroembolism

- Venous thrombosis: hypercoagulable states, oral contraceptives, Antithrombin III deficiency, postop, invasive neoplasm, cirrhosis

- Nonocclusive ischemia: cardiac failure, shock, dehydration, vasoconstrictive drugs

- OTHER: radiation injury, volvulus, stricture, hernias


What 3 things determine the effects of bowel ischemia?

- Severity of ischemia: DEC flow vs. no flow

- Length of ischemic TIME

- Amount of tissue involved


What are the 4 ischemic diseases of the GI tract?

- Ischemic colitis: lack of BLOOD FLOW to mucosa is the ultimate cause 

- Acute mesenteric ischemia 

- Chronic mesenteric ischemia 

- Venous mesenteric ischemia 

- NOTE: ischemia can present with a wide range of clinical presentations from transient bloody diarrhea to full-blown surgical emergency 

1.  Can occur in elderly w/known CV disease, but also YOUNG pts 2o to meds, previous abdominal surgery, or cocaine use


Ischemic colitis: presentation, PE, dx, tx, outcome

- PRESENTATION: hematochezia (bright red blood), diarrhea, abdominal pain (not severe)

- PE: abdominal tenderness

- DX: abdominal CT, colonoscopy (normal mucosa, then deep ulcer from R to L on attached image) 

- TX: generally conservative; treat CHF, and pt. will get better 

- OUTCOME: generally benign; depends on severity, extent, rapidity of onset, ability of bowel wall to resist bacterial infection, and status of collateral circulation 


What are some of the causes of ischemic colitis?

- NON-OCCLUSIVE: may be spontaneous, and either subclinical or produce mild symptoms

1. More malignant forms: hypotension, cardiac failure, sepsis

- OCCLUSIVE: thrombosis or embolization of the mesenteric arteries

1. Ligation of IMA during aortic reconstruction or colon resection

2. Diffuse disease of small vessels: diabetes mellitus, vasculitis 

- VENOUS outflow obstruction: intra-abdominal inflammatory processes, hypercoagulability states


- Extrinsic and intrinsic OBSTRUCTION: adhesions, tumor, volvulus, rectal prolapse


What areas of the colon are most commonly affected by ischemic colitis?

- Watershed areas that have limited collateral

1. Splenic flexure

2. Rectosigmoid area

- Rectum is generally NOT involved 


What is the clinical presentation of AMI?

- Early abdominal pain w/o ileus: SEVERE pain out of proportion to physical exam (unlike ischemic colitis)

- Peritoneal signs only in advanced disease, when damage is all the way through the mucosa 

- Not always blood 

- Medical/surgical EMERGENCY: delay in dx and tx may result in bowel necrosis 


What is the etiology of AMI?

- OCCLUSIVE: embolism generally coming from atherosclerotic plaques at origin of SMA (a-fib may facilitate this) 

1. Aortic dissection

2. Neoplasm 

3. Vasculitis

- NON-OCCLUSIVE: significant reduction in mesenteric flow secondary to cardiac failure or hypovolemic shock      


How is AMI diagnosed and treated? Outcome?

- DX: x -ray, CT (thickened bowel wall - thumb printing in attached image; ileus, portal vein gas), MRI 

1. Angiography: can dx and vasodilate this way; sensitivity 70-100%, specificity 100% 

- TX: ICU mgmt, vasodilators by angiography, surgery

- OUTCOME: poor -> need to do surgery in time 

1. Air in portal vein = complete necrosis of section of small bowel, which is a very bad sign 

2. Time from onset to death can vary depending on CV sufficiency of pt (generally, about 12 hrs)


What do you see here?

- Axial CT image

- Segment of DEC enhancement of the small bowel wall (arrows)

- Compare to the more normally enhancing loops (arrowheads)

- Gross image of ischemic bowel attached here 


What is this? Gross features?

- Ischemic bowel: turns grey, then becomes dark red as it gets congested, ischemic, and hemorrhagic 

- "Dusky bowel" may be salvageable, but often infarcted bowel that needs to be removed surgically 

1. Salvageable early, but gets darker/closer to black as it becomes necrotic & beyond salvage

- Dark appearance b/c combo of hemorrhage into lumen and wall of intestine 

- GROSS: geographic ulcers, pseudomembranes, submucosal edema, and strictures


What is this? Describe the characteristic histo findings.

Ischemic colitis: almost looks like it's "melting;" things furthest from blood supply affected first 

- MICRO findings: superficial mucosal necrosis

1. Hyalinized lamina propria: pink

2. Withered or atrophic crypts

3. Pseudomembranes

4. Chronic ulcers and strictures


What do you see here? What is this a feature of?

Pseudomembrane in ischemic bowel: can look like C. diff, but not going to have this “deep death” in C. diff

1. Even glands start to get withered look

2. Lamina propria will not have ischemic hyalinization and melted appearance in C. diff 

- Gross appearance attached here


What is this? Pathophys?

Pseudomembranous colitis: adherent layer of inflam cells and debris and denuded surface epi  

- Dense infiltrate of neutros: superficial lamina propria

- Superficially damaged crypts distended by a muco-purulent exudate that forms an eruption (volcano)

1. Exudates coalesce into pseudomembranes

- Lamina propria will NOT show hyalinization like ischemia

- PATHOPHYS: disruption of normal colonic microbiota by AB's allows C. difficile overgrowth

1. Almost any antibiotic may be responsible

2. Immuno­suppression is a predisposing factor


What are the distinguishing features b/t ischemic colitis and acute mesenteric ischemia?

- ISCHEMIC COLITIS: 90% >60-yo, acute is rare, mild pain, tenderness, bleeding, colonoscopy, conservative mgmt

- AMI: age varies, acute is typical, severe pain, tenderness NOT prominent early, bleeding uncommon, angiography 

1. Tenderness, bleeding appear late 

2. CT of abdomen helpful: look for thickening b/c this means EDEMA of the lamina propria

- BOTH: look for risk factors for ischemia in med hx 

- NOTE: this card is IMPORTANT


How does chronic mesenteric ischemia present? Risk factors, dx, and tx?

- PRESENTATION: abdominal pain after eating; usually in 1st hr after eating, and lasting for 2-3 hrs 

1. Weight loss in about 80% of pts due to food aversion: severe weight loss due to not eating 

- RISK FACTORS: frequently patients have a history of underlying atherosclerotic vascular disease

1. At least 2 of the 3 splanchnic arteries usually have significant occlusive disease 

- DX: CT, MRI, US, angiography (if you really suspect)

- TX: angioplasty (balloon inflation), stent placement, surgery  


What is venous mesenteric ischemia? Presentation, risk factors, dx, tx?

- Venous thrombosis = resistance in mesenteric vv blood flow, bowel wall edema, fluid efflux into bowel lumen, INC blood viscosity, and compromise of the arterial blood support 

- PRESENTATION: similar to AMI, but in several days instead of hours

- RISK FACTORS: hyper-coagulability status, like Factor V Leiden 

1. Portal HTN, abdominal infections, blunt abdominal trauma, pancreatitis, splenectomy and malignancy in the portal region 

- DX: abdominal CT, MRI, angiography

- TX: stent, surgery, anticoagulation


How is GI bleeding classified clinically?

- Upper GI vs. Lower GI: ligament of Treitz (artificial division) 

- Obscure bleeding: bleeding w/o clear source (obscure means we don't know where pt is bleeding)

- Obscure overt bleeding: macroscopic obscure bleeding (see blood) 

- Obscure occult bleeding: microscopic obscure bleeding -> may be chronic, and present as iron deficiency anemia 

1. Can’t see blood, but can measure it (test for it; think about CANCER)


What are the 2 clinical presentations of GI bleeding?

- MELENA: black, tarry, loose or sticky, malodorous stool caused by degraded blood in intestine

1. Generally indicates upper GI source, although it may originate in the right colon

- HEMATOCHEZIA: bright red blood from the rectum

1. May be mixed w/stools, and usually indicates lower GI lesions

2. When caused by upper GI source, it indicates a massive hemorrhage -> pt. w/upper GI bleed may have hematochezia if bleeding A LOT 


What is the epi of acute upper GI bleeding? 4 elements of mgmt?

- Most frequent form of GI bleeding: 5x more freq than lower GI 

- More common in men & elderly and 80% self-limited

- Mortality depends on the cause: pts w/continued or recurrent bleeding have mortality rates of 25-30%


1. Stabilization of hemodynamic status

2. Determine the source

3. Stop active bleeding

4. Prevent recurrent bleeding 


How is GI bleeding managed?

- INITIAL EVAL: history, PE, hemodynamic stability, IV access, lab

- TRIAGE: hemodynamic stability

- TRANSFUSIONS (Hb >7), optimize coagulation

1. Keep Hb >10 if pt. has severe atherosclerosis 

- MEDS: PPI in PUD, Octreotide in portal HTN (need to verify if pt. has liver disease; use at least 5 days)

- ENDOSCOPY: will tell you what is bleeding, chance of re-bleeding, and guide treatment

- ANGIOGRAPHY w/embolization, surgery (don’t call the surgeons very often)

- NOTE: this slide is IMPORTANT 


What are some of the causes of upper GI bleeding? What should you be looking for in history and PE?

- CAUSES: peptic ulcers, gastritis, duodenitis, tumors, vascular malformation, esophagitis, varices

- HISTORY: PUD, recent NSAID use, alcohol/caustic ingestion, cirrhosis, aortic graft surgery, cancer, coagulopathies, recent nose bleed, etc.

- PE: hemodynamic stability, stigmata of cirrhosis, vascular lesions, hepatomegaly, lymph nodes, epigastric tenderness, rectal exam, etc. 


What is the chance of re-bleed in these ulcers?

- <1% chance of re-bleed


What is the chance of re-bleed in this ulcers?

- Stigmata of recent bleeding: big vessel growing in base of ulcer and pressing up

- Need to do something about this: 40-50% chance of re-bleed 

- Helps stratify pts by risk of re-bleeding 


What is the chance of re-bleed here?

- Clot, so chance for re-bleed 5-10%

- Want to remove clot and treat 


How can peptic ulcers be treated endoscopically to prevent bleeding?

- Temperature 

- Injection of saline 

- Clips


What are some of the damaging and protective factors for the gastric mucosa (image)?

- Gastric lumen has a pH of close to 1, more than a million times more acidic than the blood

- This harsh environment contributes to digestion, but also has the potential to damage the gastric mucosa


What is this? 3 layers?

Gastric ulcer: always have to consider malignancy as part of the differential -> require surveillance endoscopy to document ulcer healing

1. Cellular debris 

2. Fibrinoid necrosis

3. Granulation tissue

- Fibrosis in deeper, and more long-standing ulcers


What is going on here?

- Gastric erosions: superficial epithelial loss

- 16% of pts with upper GI bleeding 

- Break in mucosa that does not cross the muscularis mucosa -> endoscopically <3-5mm & w/o significant depth

1. NSAIDs, alcohol-related gastropathy, stress gastric erosions


What are esophageal varices? Causes? Tx?

- Venous blood from GI tract passes through liver, via portal vein, before returning to the heart -> portal HTN results in devo of collateral channels at sites where portal and caval systems communicate

- These collateral veins allow some drainage to occur, but also lead to devo of congested subepi and submucosal venous plexi in the distal esophagus and proximal stomach = varices

- CAUSES: cirrhosis, hepatic schistosomiasis

- TX: Octreotide if pt has liver disease: reduces splanchnic flow and volume feeding portal pressure 

1. Esophageal banding 


What is the mortality rate from variceal bleeding? Predictive factors?

- MORTALITY: 30-50% 


1. Pressure 

2. Size 

3. Color 


What is going on here?

- Esophageal banding: one of the txs for esophageal varices 


What do you see here? Gross appearance?

Esophageal varices: dilated varices beneath intact squamous mucosa 

- GROSS image: lower esophagus (turned inside out at autopsy)

1. Linear, dark blue submucosal dilated veins (varices) 

2. Superficial varices are prone to bleed (red) 


What are some of the txs for gastric varices?

- TIPS or glue injection (banding not as good) 

- Can be 1o from the stomach, or from esophageal varices 

1. Bleed less frequently than esophageal, but bleed very badly



What is TIPS?

- Transjugular intrahepatic portosystemic shunt: do this if you can't use glue for gastric varices tx 

Shunt b/t hepatic and portal vein: DEC pressure, and complete decompression of the varices

1. Leads to more encephalopathy b/c blood not being filtered through liver before making it to brain 


What are Mallory-Weiss tears? Boerhaave's syndrome?

- M-W: lacerations in region of GE junction caused by retching w/forceful gastric mucosa prolapse -> 5-10% of UGI hemorrhage

1. Hx of vomiting; resolves w/conservative mgmt (usually) and bleeding stops spontaneously in 80-90% of pts (<5% re-bleed)

2. No inflammation: just disruption of mucosa

3. Dx by endoscopy, and txs incl. hemodynamic stabilization and endoscopic tx (angiography or surgery rarely required)

- Boerhaave’s: very deep M-W -> surgery the only option to save patient’s life

1. Dx'd by CT 


What is going on here?

- GERD: 


Name 4 types of esophagitis/esophageal ulcers.


- Pill-induced ulcers (see attached images): think bisphosphonates 

- CMV 

- Herpes virus 

- NOTE: 8% of upper GI bleeding 


What is this?

Herpetic esophageal ulcer


What do you see here?

CMV esophagitis


What is this?

- Dieulafoy lesion: idiopathic, dilated submucosal vessel overlying the epithelium without ulcer

- Caliber of the artery is 1-3 mm, usually proximal stomach

- Bleeding can be profuse -> really scared with these because only see vessel if acutely bleeding 


What do you see here? Tx?

- Gastric antral vascular ectasia (GAVE): ectatic and saculated mucosal vessels

- Bleeding usually chronic and occult: mild bleeding, but can cause chronic anemia

- Idiopathic, but more frequent in pts with portal HTN (but not required)

- TX: endoscopic -> argon photocoagulation (burn), in similar manner to vascular ectasias 


What are these?

- Chronic bleeding, frequently occult

- Present as iron deficiency anemia

- Frequently multiple 

- TX: endoscopic -> pts with chronic renal insufficiency (treat with argon photocoagulation, APC: burn)


What is this?

- Neoplasm 

- 2-5% of UGI hemorrhage: usually self-limited 


What is the etiology of small bowel bleeding (pie chart)?

- AVM: arteriovenous malformations


What are these for?

- Capsule endoscopy: best procedure available to study small intestine mucosa

- Extremely helpful in investigation in pts with occult bleeding

- Vascular malformation on left, and cancerous nodule on right (attached images) 


What are the MCC's of acute and chronic lower GI bleeding?

- ACUTE: diverticulosis (more severe), angiodysplasia (usually less severe)

- CHRONIC: hemorrhoids and neoplasia (until proven otherwise)

- Less common than UGI bleeding; mortality 3.6 %

- REMEMBER: lower GI bleeding is that from below the ligament of Treitz


What are the features of diverticular bleeding?

- MCC of severe acute bleeding in lower GI tract

- 3% of pts with diverticulosis and 70% of bleeding from right side of colon

- Acute, painless, maroon to bright red hematochezia

- Bleeding is often significant and 25-35% will have a new episode of bleeding


What do you see here? Tx?

Diverticulosis = colonic outpouchings: pit-like areas with fecal matter inside 

- Not true diverticulum like Meckel’s because doesn’t include serosa and muscular layer

- Bleeding from penetration of a colonic artery into the dome of a diverticula

1. Often significant, but stops spontaneously in 70-80% of patients

- TX: hemodynamic stabilization and endoscopic tx

1. Angiography w/embolization and surgery are options in pts with persistent bleeding

- MCC of lower GI bleeding

- Diverticulitis: inflammation; can perforate too b/c right at the serosa


What is this? Causes?

Angiodysplasia: malformed submucosal and mucosal blood vessels, including vascular ectasias and Dieulafoy lesions 

- CAUSES: advanced age

1. Chronic renal failure

2. Osler-Weber-Rendu: same as hereditary hemorrhagic telangiectasias 

3. Prior radiation therapy, i.e., for prostate cancer 


What is the epi of angiodysplasia? Where do they occur?

- Slow intermittent blood loss: not as severe as diverticulosis

- 67% of patient are >70 years of age

- Primary cecum and right side colon


What do you see here?

- Angiodysplasia: malformed submucosal and mucosal blood vessels

- Ectatic nests of dilated, torturous vessels (veins, venules, and capillaries) that are prone to rupture w/hemorrhage into colonic lumen

- Cecum and ascending colon; look similar to hemorrhoids histologically

- FRONT IMAGE: eroded surface w/some granulation tissue: pt. was probably bleeding at some point


What are these?

- Hemorrhoids: thin-walled, dilated anal and perianal submucosal veins attributed to persistently high venous pressure from constipation, pregnancy or portal HTN

- Can cause pain or mild rectal bleeding

- Anus and lower rectum

- Big thing going to be LOCATION for differentiating these from angiodysplasia 

- FRONT IMAGE: can see transition from squamous to glandular epithelium in rectum 


What do you think is going on here?

- Malignancy: colon cancer should be always considered in the differential of lower GI bleeding

- Most common presentation is occult GI bleeding

- Always consider colon malignancy in patients >50 presenting with iron deficiency anemia


What are the risk factors for severe peptic ulcer bleeding?

- Size 

- Location

- Stigmata