Assessment of steatorrhoea

Last reviewed:October 2019

Last updated:June 2018

Summary

Steatorrhoea, an excess of fat in stools, can be thought of in terms of problems in either fat digestion or fat absorption. Descriptive studies on steatorrhoea outside of patients with pancreatic disease are infrequent in the medical literature and thus much of our understanding of fat malabsorption comes from this population.

Normal fat absorption

Normal fat absorption involves a complex mixture of digestive enzymes, bile salts, and an intact intestinal mucosa to enable uptake of these hydrophobic complexes. After ingestion, dietary lipids are initially emulsified in the stomach and then hydrolysed by the action of gastric and pancreatic lipase and colipase. The hydrolysed lipids are then aggregated into micelles or liposomes with the addition of bile salts in the duodenum and jejunum.[1] These micelles are absorbed across the intact intestinal villi by both active and passive processes. Finally, they are packaged into chylomicrons within intestinal epithelial cells and transported to the circulation via the lymphatic system.[2]

More than 90% of daily dietary fat is absorbed into the general circulation, but any defects in the processes can reduce this uptake and lead to fatty diarrhoea.

Categories of steatorrhoea

Patients with evidence of steatorrhoea can be thought of in 3 broad aetiological categories.

Pancreatic insufficiency steatorrhoea due to insufficient lipase and colipase to allow normal lipid hydrolysis (pancreatic exocrine insufficiency). This most commonly occurs due to chronic pancreatic inflammation and loss of acinar cells.
Bile salt deficiency due to impaired production or secretion, or reduced circulating bile acids.
Malabsorption steatorrhoea due to small intestinal disease, surgery, or medications.