00:01
Welcome back. Thanks for joining me on this discussion of small intestines under the section of small
bowel obstruction. Let’s start with a clinical case. You see a patient who is 65 years old who has a
history of hysterectomy presenting to the emergency department with nausea, vomiting, and abdominal pain.
00:23
What’s on your differential diagnosis? I’ll give you a second to think about it. Of course, small bowel
obstruction. It’s very high on our differential diagnosis given her previous surgery. Across the US, small
bowel obstruction is a very, very common diagnosis. In fact, over 300,000 small bowel obstruction
procedures were performed on an annual basis. What are the etiologies of small bowel obstructions?
They include what I’ve already previously discussed, adhesions or scar tissue formed from previous surgery.
01:02
Here, you see the image of scar tissue attaching itself to the peritoneal lining. Of note, adhesions are
normal body response to healing.
01:11
Virtually, all patients that undergo intraabdominally surgery develop adhesions.
01:15
Tumors can cause small bowel obstruction. Much like our discussion during the
carcinoid tumor discussion, if the tumor is large enough in the small bowel, it can be a source
of obstruction. Volvulus, volvulus is a twisting of the small bowel usually along the mesentery.
01:34
You’ll notice from this picture that the intestines do not look very happy. Its blood supply looks like
it’s been compromised at some point. Reminder, back to the previous lectures about hernias,
both groin as well as ventral hernias, in this picture you see a patient with an ostomy bag and a large
loss of domain and hernia bulging from the abdominal wall. Common findings in both historical
and physical findings include crampy abdominal pain, nausea and vomiting, and obstipation,
again, inability to pass gas or have bowel movements. You’ll also notice that these findings are very similar
to many other surgical diagnoses, which is why it’s important to have a list of high-yield differential diagnoses.
02:27
On this slide, you’ll notice that small bowel obstruction causes crampy abdominal pain. But unlike appendicitis
or perforated duodenal ulcers, it’s difficult to localize to one quadrant. You’ll notice that most patients
with small bowel obstructions will present with general, mild abdominal pain that’s described
as crampy in nature. Clearly, this can worsen during the patient’s hospital course which may be
an indication for surgery. Let’s take a look at the labs. Common chemistries: One might find decrease
in the chloride; increase in the bicarb; increase in the creatinine; maybe, maybe not any changes
in the white blood cell count. Though typically, unless there is intestinal ischemia or compromised
bowel, the white count is typically normal. But remember, it is important to know that when you
have a patient with worsening abdominal pain, increased white count or leukocytosis associated with
the small bowel obstruction, one should start to begin thinking maybe the patient needs surgery
sooner rather than later.
03:39
It's classic findings of nausea, vomiting in a patient, particularly one
where you have placed a nasogastric tube. They’re hypovolemic because of large volume emesis and inability
to tolerate PO; hypokalemia, loss of potassium through emesis; hypochloremic metabolic alkalosis
with emesis due to the significant loss of chloride through stomach acids. This is important
to remember as a high-yield metabolic derangement of nausea/vomiting. The kidneys try to
preserve volume through the aldosterone mechanism which stimulates hydrogen and potassium
excretion worsening the previous hypokalemia. Here’s the mechanism of action of aldosterone.
04:27
Commit this to memory. It’s very important. In the distal collecting tubule, you’ll notice the
rectangular box simulates the tubule. In this three sodium, two potassium, one hydrogen pump,
you’ll notice that aldosterone tries to hold on to the sodium while sacrificing potassium
and hydrogen into the tubule which is then later excreted. This is also why patients have
a paradoxical aciduria despite a metabolic alkalosis. This slide is worthwhile to review.