Auer Ch 35 Intestinal Injury

Front 1

Causes of intestinal injury:

Back 1

simple (non-strangulating) luminal occlusion, strangulating obstruction, non-obstructive conditions such as infarction

Front 2

Mechanism of injury related to non-strangulating obstruction:

Back 2

increased intraluminal pressure (from distention), direct compression of the wall by the obstruction leads to local occlusion of vascular supply

Front 3

Result of increased intraluminal pressure:

Back 3

intramural vascular compression

Front 4

Strangulating obstruction results from:

Back 4

occlusion of the intestinal lumen as well as vascular supply

Front 5

Types of strangulating obstruction:

Back 5

hemorrhagic, ischemic

Front 6

Hemorrhagic strangulating obstruction:

Back 6

venous supply is occluded earlier than the arterial supply, resulting in continued supply of blood to the injured region, without patent outflow

Front 7

Ischemic strangulating obstruction:

Back 7

arterial and venous supply are occluded at the same time

Front 8

Why is HSO is more prevalent than ISO?

Back 8

wall of the vein is thinner and more compliant than the wall of the artery

Front 9

Result of HSO:

Back 9

ischemic injury to the affected region but also congestion of the tissues with blood

Front 10

Result of ISO:

Back 10

rapid degeneration of the mucosa

Front 11

Most common cause of intestinal infarction:

Back 11

cranial mesenteric arterits, result of migration of strongylus vulgaris

Front 12

MOA of cranial mesenteric arteritis infarction:

Back 12

Inflammation of the artery with or without evidence of thrombus

Front 13

Mechanisms of intestinal injury:

Back 13

luminal distention, mucosal ischemia, and reperfusion

Front 14

Manifestation of distention and decompression injury:

Back 14

epithelial sloughing

Front 15

Degree of injury to the mucosa by luminal distention is related to:

Back 15

degree of distention and the length of distension

Front 16

Blood supply to the villi:

Back 16

countercurrent exchange system, central arteriole located in core of villus, arborizes at tip, venous drainage via venules at periphery

Front 17

Oxygen flow in villi:

Back 17

preferentially from central arteriole toward the venules

Front 18

Result of villi vascular anatomy:

Back 18

relatively hypoxic tip, sensitivity to ischemic injury

Front 19

When is hypoxia at the villus tip exacerbated?

Back 19

arterial blood supply is limited

Front 20

MOA of hypoxia induced mucosal injury:

Back 20

loss of oxidative phosphorylation, decreased supply of ATP to Na/K-ATPase, anaerobic metabolism results in lactic acid accumulation and lowered cellular pH, damaging cellular membranes and causing detachment of epithelial cells from the basement membrane

Front 21

Function of Na/K ATPase pumps in intestinal mucosa:

Back 21

regulate ion, nutrient transport across the mucosal epithelium

Front 22

Result of separation of epithelium from basement membrane:

Back 22

fluid filled space at the tip of the villus, exacerbate further separation along the length of the villus toward the crypts

Front 23

Why are crypts are more resilient to hypoxic injury?

Back 23

vascular supply is independent of the countercurrent exchange supplying the villi

Front 24

MOA of reperfusion injury:

Back 24

xanthine dehydrogenase converted to xanthine oxidase, hypoxanthine accumulates, when reperfusion occurs, accumulated XO degrades hypoxanthine to superoxide

Front 25

Effects of superoxide:

Back 25

generates neutrophil chemoattractants, interacts with lipid membranes to trigger AA metabolism and formation of leukotriene B4, production of more reactive oxygen metabolites occurs with neutrophil influx

Front 26

Potential sites of inhibition of reperfusion:

Back 26

Allopurinol is XO inhibitor, superoxide dismutase inhibits superoxide, monoclonal antibodies directed against neutrophil adhesion molecules, DMSO scavenges reactive oxygen metabolites

Front 27

Determination of intestinal viability:

Back 27

clinical assessment of the bowel, fluorescein dye, surface oximetry, Doppler ultrasonography, luminal pressure measurements, histopathology

Front 28

Clinical assessment of viability:

Back 28

mucosal and serosal color, wall thickness, peristalsis, and mesenteric arterial pulsation

Front 29

Non-viable intestine:

Back 29

dark color, dull serosa appearance, with lack of rehydration of the surface with lavage solutions

Front 30

Fluorescein dye dose:

Back 30

administered IV at a dose of 6.6 to 15 mg/kg

Front 31

Advantages and disadvantages of fluorescein dye:

Back 31

predicts viability with ischemic stranglulating obstruction but is not as effective with hemorrhagic obstructions, dye perfusion affected by systemic cardiovascular status and degree of intestinal distention

Front 32

Surface oximetry:

Back 32

indirect measurement of tissue perfusion, measured as surface oxygen partial pressure (PSO2)

Front 33

Use of surface oximetry:

Back 33

predicting horses that will survive but inaccurate for predicting non-survival

Front 34

Normal oximetry value range:

Back 34

55 to 71 mmHg

Front 35

What oximetry value associated with increase likelihood of death?

Back 35

20 mmHg or less indicated a 7.4 increase in likelihood of death

Front 36

Limits of surface oximetry:

Back 36

patient’s cardiovascular status, applied focally and unlikely to predict accurately regional viability

Front 37

Advantage and disadvantage of Doppler ultrasound:

Back 37

more accurate than clinical assessment, fluorescein dye methods in hemorrhagic strangulating obstructions but poorer than the other methods for ischemic strangulating obstructions

Front 38

Disadvantage of intraluminal pressure measurements:

Back 38

limited value in SI strangulating obstructions because of the variability in degree of distention and length of time of distention

Front 39

Use of intraluminal pressure measurements:

Back 39

predict viability with LCV

Front 40

Histopathology parameters assessed for intestinal viability:

Back 40

loss of surface epithelium, loss of glandular epithelium, and width of the crypts and interstitial space between crypts.

Front 41

Histological non-viable tissue parameters:

Back 41

interstitium to crypt ratio of greater than 3 (normal is 1,) loss of glandular epithelium of greater than 50%