Assessment of steatorrhoea

Last reviewed: 29 Oct 2020

Last updated: 10 Mar 2020

Steatorrhoea, an excess of fat in stools, indicates a problem with either fat digestion or fat absorption. There are few descriptive studies on steatorrhoea outside of patients with pancreatic disease 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 steatorrhoea.

Categories of steatorrhoea

Patients with steatorrhoea can be considered in 3 broad aetiological categories.

Pancreatic exocrine insufficiency. These patients have insufficient lipase and colipase to allow normal lipid hydrolysis. 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 due to small intestinal disease, surgery, or medications.