Short gut syndrome is a condition in which the small intestine is less than 200cm in adults and not long as normal in children (neonate’s is 250 cm) resulting in massive malabsorption. This 200 cm must be viable; able to perform the normal functions (Siebert, 1980). This shortness of the small intestines may be due to surgical removal of part of small intestines due to other medical conditions that need surgical interventions or due to congenital defects. SGS can lead to malabsorption syndrome as the remaining or existing surface area of the gut is less for normal absorption of nutrients. In adults the normal length of the small intestines is an average of 600cm (range of 260-800cm). any disease, condition or injury that lads to loss of 50%+ of the small intestines creates a risk of developing short gut syndrome (Andorsky & Lund et al. 2001).
Short gut syndrome occurs in neonates as a result of congenital malformations during intrauterine growth. Congenital abnormalities of the small intestines lead to reduction of the length of the small intestines and poor development of the gut surfaces which are very important in normal functions of the gut: absorption of nutrients. Other causes of neonatal short gut syndrome are necrotizing enterocolitis, intestinal atresias and midgut volvulus. In older infants and children, the most common cause of SGS is intussusception with ischemic small-intestinal injury. Currently, in adults, the most common causes according to Khursheed, (2002) are Crohn disease, radiation enteritis, mesenteric vascular accidents, trauma, and recurrent intestinal obstruction. Surgical procedures involving the small intestines is also another cause of SGS mostly in cases where by the surgical procure results into reduction of the length of the gut or greatly reduces the absorption surface area of the gut (Buchman & Scolapio, 2003).
Short gut syndrome have varied severe out comes. These include malabsorption, steatorrhea, fluid and electrolyte imbalances, and malnutrition and nutritional disorders such as megaloblastic anaemia and weight loss. The short gut syndrome has the following symptoms; diarrhea, cramping, bloating, heart burn, malnutrition due to malabsorption of nutrients, dehydration as a result of the small intestines failure to reabsorb water.
Short gut syndrome does have potential complications for children of which the following are the commonest; megaloblastic anaemia, ileal bacterial overgrowth, gastric hypersecretion, failure to thrive and osmotic diarrhea. Megaloblastic anaemia is as a result of failure of the small intestines to absorb vitamin B12, folic acid and iron which are very important in the synthesis of red blood cells. Vitamin B12 is absorbed in ileam while iron is absorbed in duodenum. Insufficiency of Vitamin B12 and folic acid leads to synthesis of abnormally large red blood cells that can not perform the normal functions of RBCs; oxygen and carbon dioxide transport. The children normally present with dyspnoea, palour, edema of the extremities, fatigue. Ileal bacterial growth occurs due to reduced/compromised intestinal motility, dilated segments of gut and/or missing ileocecal valve. Reduced intestinal motility also leads to accumulation of bacteria in the small intestines as they are not swept away giving the bacteria time for replication within the small intestines. Malabsorption of nutrients means that the bacteria have the much needed nutrients creating a conducive environment for replication. This leads to bacterial overgrowth (growth above normal levels), that results in to malabsorption due to inflammation of the intestinal wall and rapid deconjugation of bile acids hence not enough for fat absorption. Symptoms include bloating, cramps, diarrhea, GIT hemorrhage, foul smelling stools and flatus and building up of D-lactic acid in blood. Failure to thrive is a complication caused by multiple factors which include malabsorption of nutrients, diarrhea, anaemia, malnutrition and dehydration. Children need constant supply of nutrients for growth and development and factor that may interfere with this leads to deficiency states in which the child fails to develop and grow. These children are normally small for age and present with muscle wasting, weak feeble cry, fatigue, and anorexia, lethargy and weight loss. Osmotic diarrhea arises from malabsorption and accumulation of fluids and nutrients such as vitamins, lactose, iron, carbohydrates and proteins in the bowel causing an increase in the osmolarity of the bowel. These nutrients draw in water into the bowel. Electrolytes such as magnesium, calcium and sodium that are also retained in the small intestines cause osmotic diarrhea. Gastric hyper secretion is the excessive formation of gastric juices especially its acid component. Hypersecretion creates a low pH in bowel causing inactivation of lipase, precipitation of bile salts and bowel mucosal damage (Vanderhoof, 1997).
References
- Andorsky D.J., & Lund D.P., et al. (2001). Nutritional and other postoperative management of neonates with short bowel syndrome correlates with clinical outcomes. J Pediatr, 139(1): 27-33.
- Buchman A. L., Scolapio (2003). AGA technical review on short bowel syndrome and intestinal transplantation. Gastroenterology,124:1111–1134.
- Khursheed, N. J., (2002). Short bowel syndrome : a nutritional and medical approach. Canadian medical association journal, (10), 166; 1297
- Siebert J.R., (1980). Small intestine length in infants and children. Am J Dis Child, 18: 593–596.
- Vanderhoof J.A., (1997). Short-bowel syndrome in children and adults. Gastroenterology 113:1767–1778.