AssessmentsSmall bowel ischemia and infarction
Small bowel ischemia and infarction
USMLE® Step 1 style questions USMLE
USMLE® Step 2 style questions USMLE
A 77-year-old woman comes to the emergency department because of acute abdominal pain. She rates the pain a 10 on a 10-point scale and localizes it to her umbilicus. She also says she experiences nausea and vomiting. She denies diarrhea or constipation. She has a past medical history of congestive heart failure. She has never had any surgeries. She has a 10-pack-year history of smoking cigarettes. Her temperature is 37.0ºC (98.6ºF), pulse is 80/min, respirations are 16/min, and blood pressure is 120/90 mm Hg. Physical examination shows a soft, nontender, nondistended abdomen with no rebound tenderness or guarding. The lower extremities have 1+ pitting edema.
Now, the small intestine is made of several layers.
The innermost layer is the mucosal layer and it’s composed of a few of its own layers.
The first layer is the epithelial lining and it faces the lumen; next is the lamina propria, which is rich with blood and lymph vessels; and finally the muscularis mucosae, which has smooth muscle.
Deep to this mucosal layer is the submucosal layer, which has connective tissue with proteins like collagen and elastin, as well as glands, and additional blood vessels.
The submucosal layer also contains the Meissner plexus which is a part of the enteric nervous system.
These muscles are particularly important in helping to move food through the bowel.
Finally, there’s the serosal layer which is the outermost layer of the small intestines that faces the abdominal cavity.
To reduce the risk of that happening, the mesenteric arteries branch and reconnect at points forming collateral circulation.
That’s protective because if blood flow is reduced in one pathway, then the tissue can still receive blood through another pathway.
Unfortunately, though, that process can cause further injury - called reperfusion injury.
In reperfusion injury, the influx of oxygen into an already damaged cell can be overwhelming and can cause even more oxidative stress, which worsens the cell damage.
As damaged cells release reactive oxygen species, it triggers an inflammatory response which attracts immune cells, like neutrophils.
The immune cells remove dead and damaged cells and release of cytokines, like Tumor necrosis factor-alpha.
Small bowel ischemia and infarction becomes more severe as the damage extends from just the mucosal layer, called a mucosal infarct, to all layers, known as a transmural infarction.