Low Fiber Diet

Legend:
↑ Stool transit time
(↓ colonic motility)
Pathophysiology (light blue)
Mechanism (light orange)
Signs/symptoms/lab finding (light green)
Complication (light yellow)

Inherent weakness Stool build-up,

in the muscle layers ↑ pressure in
of the colonic wall colonic lumen

These regions are

Mucosal and submucosal layers of the colon Diverticula most commonly form
perceived in the left
wall herniates through the circular muscle in the descending and sigmoid
layer, creating colonic diverticula colon lower quadrant (LLQ) of
the abdomen

Continued stress on diverticula causes micro-

perforations → bacterial infection Triggers cytokines release Fever

- Persistent LLQ pain, abdominal

Inflammation of diverticula reaches parietal Irritation of parietal peritoneum
guarding and peritoneal signs
peritoneum → stimulation of somatic nerves
- Constipation/obstipation

Clotting of blood in the blood vessels feeding

diverticula No bleeding (unlike diverticulosis)

Inflamed vessels are more Dehydration (low JPV, ↑ resting

Continued inflammation of diverticula causes
permeable & leak fluid from the HR, orthostatic hypotension)
complications over time
blood into the colon

Complete bowel Fistulae (through Colonic fibrosis → Abscesses

perforation bladder, vagina, GI strictures,
(medical skin or gut) colonic obstruction
emergency)
Explanation:
The development of diverticula in the colon typically occurs in parallel rows
between the taenia coli. The pathogenesis of the disorder involves three
major areas: (1) structural abnormalities of the colonic wall, (2) disordered
intestinal motility, and (3) deficiencies of dietary fiber.
Previously, practitioners thought that obstruction of colonic diverticulum
with fecaliths led to increased pressure within the diverticulum and
subsequent perforation. They now theorized that increased luminal
pressure is due to food particles that lead to erosion of the diverticular
wall. This causes focal inflammation and necrosis of the region, causing
perforation. Surrounding mesenteric fat may easily contain micro-
perforations. This can result in local abscess formation, fistulization of
adjacent organs, or intestinal obstruction. Ultimately, frank bowel wall
perforations can lead to peritonitis and death without rapid diagnosis and
treatment (Schieffer, 2018).
The underlying pathological mechanisms that cause the formation of
colonic diverticula remain unclear. These are likely to be the result of
complex interactions between age, diet, colonic microbiota, genetic
factors, colonic motility, and changes in colonic structure. In this paper, we
focused on the roles of inflammation and colonic motility as part of the
physiopathology of diverticulosis.

Refrences:
Matrana, M. R., & Margolin, D. A. (2009). Epidemiology and pathophysiology of diverticular disease. Clinics in colon and rectal surgery, 22(3), 141–146.
https://doi.org/10.1055/s-0029-1236157

Linzay CD, Pandit S. Acute Diverticulitis. [Updated 2020 Nov 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK459316/

Elisei W, Tursi A: The Pathophysiology of Colonic Diverticulosis: Inflammation versus Constipation? Inflamm Intest Dis 2018;3:55-60. doi: 10.1159/000489173