ESPEN Guidelines on Enteral Nutrition: Geriatrics.

Nutritional intake is often compromised in elderly, multimorbid patients. Enteral nutrition (EN) by means of oral nutritional supplements (ONS) and tube feeding (TF) offers the possibility to increase or to insure nutrient intake in case of insufficient oral food intake. The present guideline is intended to give evidence-based recommendations for the use of ONS and TF in geriatric patients. It was developed by an interdisciplinary expert group in accordance with officially accepted standards and is based on all relevant publications since 1985. The guideline was discussed and accepted in a consensus conference. EN by means of ONS is recommended for geriatric patients at nutritional risk, in case of multimorbidity and frailty, and following orthopaedic-surgical procedures. In elderly people at risk of undernutrition ONS improve nutritional status and reduce mortality. After orthopaedic-surgery ONS reduce unfavourable outcome. TF is clearly indicated in patients with neurologic dysphagia. In contrast, TF is not indicated in final disease states, including final dementia, and in order to facilitate patient care. Altogether, it is strongly recommended not to wait until severe undernutrition has developed, but to start EN therapy early, as soon as a nutritional risk becomes apparent.

TPN-induced catch-up of growth in a 22-y-old male with radiation enteritis.

Nutritional rehabilitation of malnourished children with growth arrest is generally associated with a catch-up of growth but the occurrence of this compensatory phenomenon in adulthood is not well recognized. We investigated a case of maturation and growth acceleration secondary to nutritional intervention in a 22-y-old patient. After treatment for a rhabdomyosarcoma of the bladder at age 7 y, the patient developed severe malabsorption secondary to radiation enteritis and short bowel syndrome. As a result of profound malnutrition, growth and maturation were severely impaired. Initiation of home total parenteral nutrition at age 22 y led to an increase in height, substantial weight gain, advancement of bone age, and sexual maturation evidenced by appearance of secondary sex characteristics and normalization of hormone concentrations. The development of signs of puberty and a growth spurt appearing at this late age clearly show the potential for maturation and growth once malnutrition is corrected.

Percutaneous endoscopic gastrostomy and jejunostomy for long-term feeding in patients with cancer of the head and neck.

Enteral feeding is often required in patients with cancer of the head and neck. Percutaneous endoscopic gastrostomies (PEGs) and jejunostomies (PEJs) can facilitate enteral feeding in patients who require this treatment. The endoscopic technique allows for the placement of feeding gastrostomies and jejunostomies without a surgical procedure and eliminates the need for nasal tubes for long-term enteral feeding. Forty-two patients with head and neck tumors were referred for placement of PEGs because of severe dysphagia induced by tumors, surgery, radiation, or chemotherapy. The procedure was performed in the gastroenterology suite. Patients were sedated with intravenous meperidine and diazepam, and local anesthetic with lidocaine was applied to the area of incision. Average procedure time was approximately 20 minutes. The procedure was successful in 39 patients in whom tubes were placed ranging in diameter from 15F to 22F. PEGs were placed in 36 patients with intact stomachs and PEJs in three patients with previous gastrectomies. The remaining three procedures were unsuccessful because of technical reasons. There were three localized skin infections, and all responded to antibiotic therapy. Neither peritonitis nor any other immediate complication occurred. In 16 nonhospitalized patients, the procedure was performed on an outpatient basis. After a mean followup of 4.5 +/- 6 months of enteral feeding in the home, there was only one case of aspiration and subsequent pneumonia, and this case responded to antibiotics. No other long-term complications were noted. Thus feeding gastrostomies and jejunostomies can be placed safely and easily in patients with cancers of the head and neck by endoscopic methods without abdominal surgery. These tubes can be used for enteral feeding and eliminate the need for nasogastric tubes. They are better tolerated, are of a wider diameter, and have a reduced risk for migration, clogging, and aspiration-related complications.

Consequences of phosphate imbalance.

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.