Blind loop syndrome (BLS), otherwise known as stagnant loop syndrome, is a rare malabsorptive disorder with growing clinical significance in the field of gastroenterology. This disease can evolve as a complication from multiple pathologies, including anatomic abnormalities, motility disorders, and inflammatory disease. This condition is further defined by its distinctive pathogenesis: stagnation of the small intestine causing pathologic bacterial overgrowth.

Under normal circumstances, the small bowel harbors a sparse amount of mixed flora in concentrations of less than 1,000 microorganisms/mL. However, static conditions can alter the population dynamic. In blind loop syndrome, stasis enables the proliferation of species like Bacteroides, E. coli, Streptococcus, and Lactobacillus in abnormally high concentrations. Consequently, this overgrowth affects digestion and absorption, resulting in malnutrition, B12 deficiency, and steatorrhea.


  • Anatomic Abnormalities (most prevalent)
  • Afferent loop syndrome (most commonly from Billroth II, Roux-en-Y, Whipple procedure)
  • Surgical complications (fistulas, strictures, scarring)
  • Anastomosis
  • Jejunal diverticulosis
  • Motility Disorders
  • Scleroderma
  • Parkinson disease
  • Diabetic patients.
  • Inflammatory Disease
  • Crohn disease
  • Radiation enteritis
  • Diverticulitis
  • Celiac diseases

EPIDEMIOLOGY:- There is insufficient epidemiological data, as the patient presentation can be vague, and the diagnosis is infrequently worked up or mistaken for alternative diagnoses.

PATHOPHYSIOLOGY: - In this disease process, the etiologies, as mentioned above, can cause stasis in a segment of the proximal small intestine. This dysfunction impairs peristaltic motility and impedes luminal flow. Throughout digestion, food is diverted around the stagnant length of the bowel, suitably referred to as the “blind loop.” Naturally, particulate builds up, serving as a focal point for bacterial proliferation.

The consensus of current literature points to Bacteroides, E. coli, Streptococcus, and Lactobacillus as the implicating species in BLS.However, there is debate on how these organisms disrupt cobalamin absorption to manifest this constellation of symptoms. One theory suggests that bacteria (i.e., Bacteroides) directly injure the alimentary tract through released toxins or harmful by-products of microbial metabolism.Another theory proposes that microbes (i.e., E. coli, Streptococcus) remove the available supply of vitamin B12 from the lumen for use during replication.

In addition to restricting the absorption of B12, microbial overgrowth also impairs fat absorption. Under normal conditions, conjugated bile salts are transported into the duodenum to solubilize dietary lipids. As food passes through the gut, the intestinal flora deconjugates a small percentage of bile salts/acids, which exit the body through the stool. However, in stagnant conditions, the population of bacteria drastically increases. Accordingly, more bacteria (notoriously anaerobes) yield a larger number of unconjugated bile salts/acids, manifesting as steatorrhea and fat-soluble deficiencies.


The medicines that can be thought of use are:-

  • Nat mur
  • Pulsatilla
  • Lycopodium
  • Bryonia
  • Carbo veg