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.
Below the submucosal layer is the muscularis propria which is basically two layers of smooth muscle with the myenteric plexus, another part of the enteric nervous system, sandwiched between them.
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.
The superior mesenteric artery is the main supplier of blood to the small intestine.
Because the small intestine has a high demand for oxygen and nutrients to sustain digestion, it is highly susceptible to tissue injury from ischemia.
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.
Small bowel infarction happens when there’s a significant decrease in blood flow to the small intestine.
At the cellular level, ischemic injury can lead to the production of reactive oxygen species which can damage DNA, RNA, and proteins in the cell, leading to cell death.
If blood flow returns to the ischemic tissue, it’s called reperfusion.
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.
Severe damage to the small intestines can also cause a break in the epithelial lining of the small intestines, allowing bacteria in the lumen to get into the blood vessels in the wall.