Diverticula, or a single diverticulum, is this pouch that forms along the walls of a hollow structure in the body, kind of like a cave. Usually we talk about these caves or pouches in the context of the large intestine, so it’d be a colonic diverticula, but it can also happen in the small intestine as well as other hollow structures in the body. The walls of the large intestine are made up of several layers, starting with the inner layer, the mucosa, then the submucosa, then the muscle layer, and finally serosa. Sometimes these little out-pouches include all the layers, from mucosa to serosa, and these are true diverticula, and sometimes only the mucosa and submucosa poke through the muscle layer, and these would be called pseudo or false diverticula, where the muscle layer isn’t included and the mucosa and submucosa are covered only by serosa. Most of the time, diverticula in the large intestine are false diverticula.
It’s thought that the formation of colonic diverticula is a result of high pressures that literally push the walls such that they bubble out and form these pouches. Now remember that the large intestine has this smooth muscle layer, right? And it’s able to contract using that muscle layer, just like any other muscle we contract, except that we can’t consciously control these because it’s smooth muscle rather than skeletal muscle. This smooth muscle contraction accomplishes a couple things, like mixing ingested food and moving digested food toward the end of the line. Whenever it contracts, though, higher pressures are generated inside the lumen, since it’s sort of like being squeezed and compressing the air inside, and normally you’d imagine that the higher pressure would be equally felt throughout the lumen, right? Well, it’s thought that the contractions in patients with diverticula are exaggerated or abnormal in some way, which causes an unequal distribution of pressure with some specific areas having really high pressures during contractions. It’s not quite clear exactly what leads to these abnormal contractions, but some studies suggest it may have to do with the smooth muscle itself.
Now let’s take a step back and think about something called Laplace’s law which says that the pressure on the wall of a cylinder is proportional to the inverse of its diameter, so as diameter decreases, pressure increases. In other words, a really small cylinder is going to feel a lot more pressure on its walls than a really large cylinder. Similarly, since the sigmoid colon is the smallest portion of the colon in diameter, it’s subject to relatively high pressures according the Laplace’s law, basically the spot in the large intestine where the walls get pushed on the hardest. The sigmoid colon is therefore where most diverticula form. Additionally, diverticula tend to form in the spots where the blood vessels that supply the intestinal walls traverses the muscle layer, this spot is slightly weaker, making it more likely for diverticula to form. As that diverticula forms, that blood vessel responsible for wall weakness becomes separated from the intestinal lumen only by mucosa, and is therefore subject to injury and predisposed to rupture, meaning blood gets into the large intestine, which would then be passed with stool—this is known as hematochezia or rectal bleeding, and this bleeding is usually painless.
Other associations with diverticula include things that either increase stress on the walls of the intestine, or decrease the strength of the intestinal walls. Fiber helps stool move more easily through the colon, so diets low in fiber can lead to constipation and make it harder for the colon to move small, hard stool. Having said that, the exact relationship between fiber and having diverticula (with and without symptoms) is not very clear, but dietary fiber is associated with a decreased risk of symptomatic diverticular disease, and on the flip side a diet high in fatty foods and red meat is associated with an increased risk of symptomatic diverticular disease. There are also genetic causes of diverticula like Marfan syndrome and Ehlers-danlos which are genetic disorders that affect connective tissue. Without strong connective tissue supporting and strengthening the colon wall, diverticula can begin to form.
Having diverticula in the colon is called diverticulosis, and most of the time, people won’t even know that they have diverticulosis because they don’t have any symptoms. Sometimes, people with diverticulosis have vague stomach pain, and occasionally the diverticula might bleed, but most of the time, when there are no symptoms, diverticulosis is discovered during a colonoscopy or CT scan that might be done for another reason entirely. Sometimes, though, the diverticula can become inflamed and this is known as diverticulitis, -itis meaning inflammation, right? Although inflammation can happen when fecal matter, or fecaliths, become lodged in the diverticula, this is thought to actually be less common, and really inflammation is thought to happen more often due to erosion of the diverticular wall from higher luminal pressures. Erosion and inflammation most commonly causes pain in the left lower quadrant. Diverticulitis is usually not associated with hematochezia, or rectal bleeding, since the blood vessels become scarred from inflammation, and therefore rectal bleeding is more associated with diverticulosis.
Sometimes, if the diverticula becomes distended enough, it may rupture and form a fistula, which is a connection with an adjacent organ or structure. Since it sits pretty close to the bladder, a fistula connecting the large intestine to the bladder may form, called a colovesicular fistula, and this might result in air or stool in the urine. Which as you might imagine...is not a good thing.
Treatment for diverticulitis may involve antibiotics to limit bacterial overgrowth, and some may recommend a high-fiber diet after patients have recovered. In more severe cases, though, the affected area of the colon might be surgically removed.
Resources edit
http://www.aafp.org/afp/2005/1001/p1229.html
http://emedicine.medscape.com/article/173388-overview#a6