DANIEL L. CHAN
DVM, Dip. ACVECC, Dip. ECVECC, Dip. ACVN, MRCVS
Transitioning to Enteral Nutrition
Dan is Professor of Emergency and Critical Care Medicine and Clinical Nutrition at the Royal Veterinary College. He received his DVM from Cornell University in 1998
Transitioning to Enteral Nutrition
Dr. Dan Chan – Part 1
Transitioning to Enteral Nutrition
Dr. Dan Chan – Part 2
What happens when an animal doesn’t eat?
Enterocytes are the cells that line the small intestine absorbing all the bodies nutrients and fluids and protecting against pathogenic bacteria, helping maintain the immune function of the gastrointestinal tract. Without direct nutrition enterocytes atrophy within as little as 90minutes, and so 24hrs to 72hrs fasting can have a devastating effect to the integrity and motility of the GI barrier.
Know the cells of the Gastrointestinal tract:
- The intestinal epithelium is made up of four major types of cells – enterocytes, mucous cells, enteroendocrine cells and Paneth cells. These four cell types all originate from stem cells located in the ‘valleys at the bottom of the villi, named the crypts of Lieberkuhm.
- Secondary digestion and absorption of nutrient molecules takes place in the small intestine through a layer of finger-like villi.
- Enterocytes are simple, column-shaped epithelial cells found in the small intestine and also the colon. they are also known as ‘surface absorptive cells’ and are the workhouses of the intestine. Enterocytes are coontinuously formed and replenished from the stem cells that are located in the crypts between the villi. Enterocytes are ‘born’ at the bottom of the villus and take 2-5 days to slowly migrate up to the apex of the villus. Once they reach the apex, they are programmed to die. In contrast, red blood cells live for about 3 months in the circulation.
- Enterocytes are responsible for absorbing sugars, amino acids, water and electrolytes. They adhere tightly to eachother and therefore also serve as a physical barrier that prevents food and bacteria in the intestinal lumen from migrating freely into the systematic circulation.
- Each enterocyte also forms numerous tiny folded extensions of its cell membrane, about 1 micrometer long, that are termed microvilli or ‘striated border’. These folds increase the surface area for absorption. Enzymes located in these microvilli break down sugars and proteins into their final forms, ready for absorption and transport through the enterocyte.
- Mucous cells release mucin that acts as a protective barrier for the villi.
- Enteroendocrine cells are scatter throughout the stomach, pancreas and small intestine. They are responsible for producing various hormones that control gastroinintestinal functions, such as gastrin, chloecystokinin, insulin and glycagon.
- Paneth cells are the guardians for the stem cells. They can release substances that causelysis of bacteria. Paneth cells actually live for about 3 weeks and are located in the crypts.
Did you know?
The gi tract weighs 5% of total body weight and uses up to 20% of the oxygen supply. It’s a hardworking organ and has to work even harder during illness as metabolism actually increases. #feeddontfast. Early enteral nutrition EEN helps speed recovery, reduce hospitalization time and can make the difference in reducing mortality with acute GI patients. Classic advise was to fast critically ill patients for up to 48 to 72hrs, but this led to complications where the gi barrier started to breakdown causing a leaky gut – bacterial translocation would lead to potential problems of sirs, sepsis or mods.
Todays approach is to recommend enteral nutrition as soon as the patient is able to tolerate a prescribed diet. These diets are usually high in fat and protein, designed to provide full RER resting energy requirments unti the patient is able to eat normal food again. Within the first 24hrs of acute GI patients their gut is not able to tolerate these diets as it is in an impaired state and not able to breakdown complex fats and proteins. Microenteral nutrition is a safe and simple solution to begin enteral feeding within as little as 2hrs of patient arriving. Once vomiting has been stabilized, offering a small volume of microenteral nutrition often by tube feed or syringe, trickle feeds the gi tract and directly nourishes the Enterocytes to stop Atrophy and begin recovery. Starting at 0.5ml per kg every 2hrs and increasing by 50% every 4 -8hrs nourishes the wall of the small intestine, helping rebuild the barrier and strengthen the enterocytes to tolerate more complex proteins and sugars. This small amount of specially formulated nutrients enables the clinician to treat the organ and not just the symptoms and the earlier enteral nutrition is begun, the faster the patient recovers. Oralade is the first ready to use microenteral nutrition product developed for animals, to provide exactly the nutrients enterocytes require to stop atrophy and begin recovery.
Containing zero fat and only 1% protein it requires no digestion and is instantly absorbed. The isotonic balance of fluids, electolytes, glucose and simple amino acids provides the nutrition needed to feed the GI tract. Upon patient showing tolerance for higher calorie enteral diets, Oralade makes a perfect complement to any prescription diet as it has no contraindications and is also hypoallergenic. Rather than blending diets in water, adding Oralade increases absorption, provides rehydration and increases palatability.
Oral Rehydration Therapy
Oral rehydration therapy provides a balanced increased level of fluids and electrolytes (including, sodium, potassium and chloride) and water. High palatability encourages fluid intake and simple glucose provides needed energy.
Feeding patients early and proactively with a combination of fluids, electrolytes, functional amnio acids and simple sugars supports enterocyte recovery
Critical care nutrition and oral rehydration support from DAY 1
Why Vets Choose
Oralade Gi Support
- Tried and Tested Recipe
- 8 out of 10 dogs prefer Oralade over leading electrolyte brand
- Up to 70% more fluid intake with Oralade compared with plain water
GI Support References
1. Sævik B Skancke E, Trangerud C (2012) A longitudinal study on diarrhoea and vomiting in young dogs of four large breeds Acta Vet Scand. 54(1): 8.
2. Hubbard K, Skelly BJ, McKelvie J, Wood JLN. Risk of vomiting and diarrhoea in dogs. Veterinary Record 2007;161:755-757
3. Vieler E et al (1995). Electron microscopic demonstration of viruses in feces of dogs with diarrhea, Tierarztl Prax 23: 66-69.
4. Schulz B S, Strauch C, Mueller R S, Eichhorn W and Hartmann K (2008). Comparison of the prevalence of enteric viruses in healthy dogs and those
with acute haemorrhagic diarrhoea by electron microscopy, The Journal of Small Animal Practice 49: 84-88.
5. PAL trial, Netherlands 2009. Data on file.
6. Evaluation of an oral electrolyte solution for treatment of mild to moderate dehydration in dogs with hemorrhagic diarrhea Erica L. Reineke, VMD,
Karie Walton, VMD; Cynthia M. Otto, DVM, PhD, DACVECC (J Am Vet Med Assoc 2013;243:851–857)
7. Outcome of study measuring the percentage of hospitalised dogs spontaneously drinking Oralade in preference to water.Katherine Howie VN
VTS(ECC) Katherine Howie VN VTS(ECC)
RF Support References
1. O’Neill, DG, Church, DB, McGreevy, PD. Prevalence of disorders recorded in cats attending primary-care veterinary practices in England. Vet J 2014; 202: 286–291.
2. Lulich, JP, Osborne, CA, O’Brien, TD. Feline renal failure: questions, answers, questions. Compen Contin Educ Pract Vet 1992; 14: 127–152.
3. O’Neill, DG, Church, DB, McGreevy, PD. Longevity and mortality of cats attending primary care veterinary practices in England. J Feline Med Surg 2015; 17: 125–133.
4. Bartlett, PC, Van Buren, JW, Bartlett, AD. Case-control study of risk factors associated with feline and canine chronic kidney disease. Vet Med Int 2010; 2010: 957570.
5. Greene, JP, Lefebvre, SL, Wang, M. Risk factors associated with the development of chronic kidney disease in cats evaluated at primary care veterinary hospitals. J Am Vet Med Assoc 2014; 244: 320–327.
6. Hughes, KL, Slater, MR, Geller, S. Diet and lifestyle variables as risk factors for chronic renal failure in pet cats. Prev Vet Med 2002; 55: 1–15.
7. Jepson, RE, Brodbelt, D, Vallance, C. Evaluation of predictors of the development of azotemia in cats. J Vet Intern Med 2009; 23: 806–813.
8. Sparks, AH, Caney, S, Chalboub, S, et al. ISFM Consensus Guidelines on the Diagnosis and Management of Feline Chronic Kidney Disease. Journal of Feline Medicine and Surgery (2016) 18, 219–239.
9. Reference for palatability trails.
10. Quimby, JM, Updates on Management of Feline CKD. Proceedings of Companion animal Nutrition Symposium. October 21-22, 2019, Prague, Czech Republic, pp12-15.
11. Laflamme, D. Controversies Regarding Nutrition and Renal Health in Cats. Proceedings of Companion animal Nutrition Symposium. October 21-22, 2019, Prague, Czech Republic, pp16-19.
12. Bijsmans ES, Jepson RE, Syme HM, Elliott J, Niessen SJM. Psychometric validation of a general health quality of life tool for cats used to compare healthy cats and cats with chronic kidney disease. J Vet Intern Med. 2016;30(1):183-191. 10.1111/jvim.13656.
13. Kidder, AC, Chew, D. Treatment options for hyperphosphatemia in feline CKD: what’s out there? J Feline Med Surg 2009; 11: 913–924.
14. Lau, W. L., Savoj, J., Nakata, M. B. & Vaziri, N. D. Altered microbiome in chronic kidney disease: systemic effects of gut-derived uremic toxins. Clin. Sci. 132, 509–522 (2018).
15. Tang, W. H. et al. Gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway contributes to both development of renal insufficiency and mortality risk in chronic kidney disease. Circ. Res. 116, 448–455 (2015).
16. Vaziri, N. D. et al. Disintegration of colonic epithelial tight junction in uremia: a likely cause of CKD-associated inflammation. Nephrol. Dial. Transplant. 27, 2686–2693 (2012).
17. Wong, J. et al. Expansion of urease- and uricase-containing, indole- and pcresol-forming and contraction of short-chain fatty acid-producing intestinal microbiota in ESRD. Am. J. Nephrol. 39, 230–237 (2014).
18. Chen, Y. Y. et al. Microbiome-metabolome reveals the contribution of gutkidney axis on kidney disease. J. Transl. Med. 17, 5 (2019).