Nutrition And Wound Healing

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Nutrition And Wound Healing

Postby patoco » Fri Jul 07, 2006 10:24 pm

Nutrition And Wound Healing

Lymphedema People


Nutrition And Wound Healing

By James Collier BSc (Hons) - Consultant in Nutrition and Moderator of

The importance of good nutrition in the healing of wounds and the promotion of health is widely accepted, but remains of low priority in health care and insufficient numbers of patients receive nutritional assessment. Practitioners need to become more knowledgeable about the role of nutrition in the promotion of wound healing.

Whereas good nutrition facilitates healing, malnutrition delays, inhibits and complicates the process (Williams and Leaper 2000). Nutritional support is fundamental to patient care and needs vary on an individual patient basis.

Before we examine the importance of nutritional assessment, we need to look at the nutrients which have key roles in the healing process:

Protein depletion can affect the rate and quality of wound healing (Gray and Cooper 2001). There is an increase in demand for protein in the presence of a wound, a requirement further increased in the event of sepsis or stress. Protein is required as part of the inflammatory process, in the immune response and in the development of granulation tissue. The main protein synthesised during the healing process is collagen, and the strength of the collagen determines wound strength.

Even short periods of low protein intake can result in significantly delayed wound healing. Protein inadequacy has also been shown to affect remodelling of the wound. In extreme cases of hypoalbuminaemia (i.e. low levels of the serum protein albumin) from long periods of insufficient protein intake, oedema may develop.

The amino acid arginine becomes essential during severe stress. It is abundant in the structure of collagen, and increases its tensile strength. Arginine metabolism is also related to the production of nitric oxide, which is bactericidal, and also aids wound healing through microvascular and haemodynamic changes.

As part of the healing process the body enters a hypermetabolic phase, where there is an increase in demand for carbohydrate. Cellular activity is fuelled by adenosine triphosphate (ATP) which is derived from glucose, providing the energy for the inflammatory response to occur. In the case of insufficient carbohydrate, the body breaks down protein to provide glucose for cellular activity (Gray and Cooper 2001). Therefore, in order to correct hypoalbuminaemia, carbohydrate is required as well as protein.

Fats have a key role in cell membrane structure and function. Certain fatty acids are essential, as they cannot be synthesised in sufficient amounts, so must be provided by diet. The role of essential fatty acids in wound healing is unclear, but as they are involved in the synthesis of new cells, depletion would certainly delay wound healing. It is debatable as to whether omega-3 polyunsaturated fatty acids (PUFAs) are more beneficial than omega-6 PUFAs. Omega-3s are anti-inflammatory, which aids wound healing, but may inhibit clotting which is disadvantageous (Williams and Leaper 2000).

B-Complex vitamins are co-factors or co-enzymes in a number of metabolic functions involved in wound healing, particularly in the energy release from carbohydrates.

Vitamin C has an important role in collagen synthesis, in the formation of bonds between strands of collagen fibre, helping to provide extra strength and stability. There is loads of evidence showing increased requirements for vitamin C during injury, stress and sepsis, but there is no evidence that mega dosing improves clinical outcomes (Gray and Cooper 2001).

Vitamin K is involved in the formation of thrombin, and deficiency in the presence of wounds could lead to a haematoma. Vitamin A is also involved in the cross-linking of collagen and the proliferation of epithelial cells.

Zinc is required for protein synthesis and is also a co-factor in enzymatic reactions. There is an increased demand for zinc during cell proliferation and protein secretion. Zinc also has an inhibitory effect on bacterial growth, and is involved in the immune response. Early studies suggest zinc supplementation, over and above that of the hospital diet, speed wound healing. Recent studies have shown no benefit, unless the patient has low serum zinc status (Gray and Cooper 2001).

Iron is a co-factor in collagen synthesis, and deficiency in iron delays wound healing. Copper is also involved in collagen synthesis.

The issue of supplementation in aiding wound healing is debatable. It is doubtless that a sufficient intake of all nutrients is needed, and that requirements may be raised during the healing process. This is often also the time when the patient, feeling unwell, has a poor appetite and dietary intake. There is some argument for supplementation with vitamin C and zinc in wound healing, but the evidence seems to point to being only when the patient is deficient in intake or has a low serum status. It is therefore necessary to check status of these two micronutrients along with other biochemical parameters in appropriate patients.

The ideal way to meet requirements of the above nutrients is by consuming adequate intake of normal foods (Perkins 2000). A normal hospital diet provides foods from all four food groups, but is often insufficient in quantity for patients with increased requirements. These patients may require supplementation with sip feeds, which are also fortified with an array of micronutrients. If a patient is consuming adequate amounts of food and sip feed supplements, it is doubtful that he/she will require specific vitamin or mineral supplements. In patients who have particularly stubborn wounds, a multi-vitamin and multi-mineral supplement may be administered.

Due to increased requirements, and the fact that many patients have a poor appetite and dietary intake, where oral sip feeds cannot help, artificial nutritional support may be initiated in the form of naso-gastric or gastrostomy feeding. Often patients are fed overnight by tube and encouraged to eat during the day, with the aim to wean them off tube feeding as nutritional status improves.

Nutritional Assessment
If a patients nutritional status is compromised, and they are unlikely to meet their requirements recovery will be delayed. Therefore nutritional assessment is vital to provide a baseline to work from. A good nutritional assessment involves the multidisciplinary approach including medical, nursing and dietetic staff. A number of assessment techniques may be employed including biochemical tests, weight, body mass index, anthropometry and dietary assessments. Nutritional Screening is an invaluable method of basic assessment done at nursing level. This is where a number of questions are asked concerning the patient's nutritional status to come up with a risk score, in order to identify possible risk of undernutrition. From this appropriate action can be initiated, which may include more detailed nutritional assessment.

It is obvious that nutrition plays a crucial role in wound healing, but there is little evidence that supplementing a patient's diet with specific nutrients in isolation improves clinical outcome. Further research is needed to identify the levels of supplements that will be of benefit to malnourished patients (Gray and Cooper 2001). Recommendations to patients with wounds should be to consume a healthy balanced diet, with sufficient quantities of energy and protein foods. All patients with wounds should have appropriate nutritional assessment through the multidisciplinary team.

Gray D, Cooper P. Nutrition and Wound healing: what is the link? Journal of Wound Care 2001 10(3) p86-89
Perkins L. Nutritional Balance in Wound Healing. Clinical Nutrition Update 2000 5(1), p8-10
Williams L, Leaper D. Nutrition and Wound Healing. Clinical Nutrition Update 2000 5(1), p3-5 ... ealing.asp


Wound Healing and Nutrition - a review

Kirk Hamilton

A review of the role of protein, vitamin A, zinc, vitamins C and E and iron in wound healing. Evidence of significant malnutrition has been found in alcoholics, the poor, the elderly and the chronically ill.

Protein malnutrition has been found in up to 25% of all hospitalized patients while 50% of general surgery patients experience moderate to severe protein malnutrition. Inadequate nutrition slows wound healing, decreases immunocompetence, increases susceptibility to infection, causes longer hospital stays and increases mortality and morbidity. To support wound healing, the USRDA goes up to 2 to 4 g/kg per day as opposed to 0.8 g/kg per day in healthy subjects. Protein deficiency is considered mild when serum albumin measures 3.5-3.9 g/dl, moderate at 2.5-3.5 g/dl, severe at less than 2.5 g/dl.

Vitamin A deficiency usually occurs without symptoms and is difficult to detect outside a hospital setting. Vitamin A deficiency is common when measured in hospitalized patients. Individuals who are severely injured or burned can become vitamin A deficient, which impedes wound healing. Vitamin A plays an important role in each stage of wound healing. It enhances the early inflammatory phase. In vitamin A deficiency there is a reduction in fibronectin on the wound surface with a subsequent decrease in cell chemotaxis, adhesion and tissue repair. Postoperative vitamin A supplementations for 7 days can increase collagen synthesis, the bursting strength of the scar and lymphocyte activation.

A large supplemental dose of vitamin A can reverse the postoperative suppression of immune response and improve healing retarded by stress, diabetes and radiation. Infrequent high doses of vitamin A are generally safe when given for vitamin A deficiency. Vitamin A can exhibit an anti-steroid activity. Wounds retarded by anti-inflammatory steroids are stimulated by retinoids far more than normal wounds. To avoid anti-steroid activity, vitamin A can be applied topically to the wound or with sponge implants. Topical vitamin A increases the epithelialization of wounds and improves the cosmetic appearance of scars. Dietary sources include liver, dairy products, egg yolk, yellow and dark green leafy vegetables and deep yellow or orange fruit.

Zinc is one of the oldest agents that can help promote wound healing. Zinc was used topically as calamine lotion as far back as 1500 B.C. by the Egyptians. There are approximately 200 zinc-requiring enzymes in the body, such as DNA polymerase which is needed for cell proliferation during healing. Superoxide dismutase is required to remove superoxide radicals produced by leukocytes during debridement. Marginal zinc deficiency is quite common in the USA. The poor, inner city dwellers, and pregnant or breast-feeding women, are also at risk of zinc deficiency. Plasma zinc concentrations of less than 70 g/dl is considered deficient. The soil is poor in zinc in 32 states of the USA. Vegetarians are at risk for zinc deficiency since cereal grains are low in zinc and more is removed during the milling process. In zinc deficiency there is delayed closure of wounds and ulcers. The collagen produced has reduced tensile strength.

Zinc deficiency also affects the immune system by causing a reduction in lymphocytes, natural killer cells, and the size of the thymus. There is an increased susceptibility to recurring infection and poor wound healing. Topical zinc oxide inhibits bacterial growth for extended periods, especially of gram-positive bacteria. Smell, taste and vision may also be affected by zinc deficiency. Only those with low plasma zinc levels respond positively to oral zinc administration.

Postsurgical patients have a low tolerance for food intake and dietary zinc. Zinc can be given by intravenous drip to improve clinical wound healing. Intravenous nutritional therapy of surgical patients can improve healing if it contains trace elements. The benefit is even better if given before surgery. There is an apparent decrease in serum zinc during wound healing. Topical administration of zinc chloride as a spray or ointment reduces the size of the wound, shortens healing time and produces less dehiscence. Zinc oxide is effective in enhancing wound healing while zinc sulphate is not.

Vitamin C is required for the hydroxylation of proline and, subsequently, for the synthesis of strong collagen. Poor wound healing is one of the symptoms of scurvy. A deficiency of vitamin C can lead to the breakdown of already healed wounds. Plasma vitamin C levels decrease during fracture, burns, or major surgeries. The USRDA of 60 to 100 mg increases to 500-1500 mg per day in burn victims. Stress associated with injury and wound healing results in an increased need for vitamin C.

Wound healing is directly accompanied by the oxidation of ascorbic acid. Levels of vitamin C rise in healing tissue and return to normal after it is healed. Dietary supplements from 100-300 mg to 1 gm per day can return plasma levels to normal in postoperative patients. Vitamin C in combination with pantothenic acid has been shown to increase skin strength and fibroblastic content of scar tissue. A deficiency of both, causes prolonged wound healing. After treatment for 24 hours with vitamin C, human skin fibroblasts in culture showed a 2- to 3-fold increase in type I collagen synthesis. Megadoses of vitamin C, even when given to patients with normal vitamin C levels, can accelerate collagen formation above the degeneration rate of damaged collagen. Vitamin C is useful in leg ulcers. Vitamin C shortly after thermal injury can significantly reduce tissue necrosis.

Vitamin E is a lipid-soluble antioxidant which accumulates in the cell membranes where it protects polyunsaturated fatty acids from oxidation by free radicals. The USRDA is 15 IU per day. Vitamin E has an anti-inflammatory action due to its ability to inhibit phospholipase-A2 activity and, therefore, the production of prostaglandins. Vitamin E also has a lysosomal-stabilizing ability, which is probably related to its ability to stabilize membranes in general. Vitamin E can also inhibit collagen synthesis. Tendons allowed to heal in the presence of vitamin E had a significantly lower peak strength after an 8 week period than those healed in the absence of vitamin E. Back incisions showed a significant decrease in tensile strength from retarded collagen synthesis in rats treated for 7 days with vitamin E. When the incisions did heal, there was a marked decrease in scar formation and the apparent size of the zone of injury. Topical administration for cosmetic purposes may be beneficial, although some patients have developed rashes from this.

Vitamin E enhances the immune response in a dose-dependent fashion. Vitamin E has normalized the breaking strength of wounds in patients receiving pre-operative irradiation, probably because of its antioxidant capabilities. Vitamin E in combination with other drugs is recommended for the treatment of burns. Improved wound healing was also observed in patients with a history of deep vein thrombosis.

The enzyme that produces deoxyribonucleotides for DNA synthesis, ribonucleotide reductase, requires iron as a cofactor. Cells cannot divide without prior DNA synthesis, so a lack of iron would impair the proliferation of all cells involved in wound debridement and healing. Serum iron levels less than 30 mg/100 ml are deficient. Normal values are 70 to 130 mg/100 ml. Iron is also involved in the hydroxylation of proline. Proline hydroxylase requires iron. Without hydroxylation of proline, collagen triple helix formation is unstable and results in collagen weakness. Therefore, wound healing during iron deficiency is weaker. Some critically ill patients may require therapeutic doses of nutrients that are approximately 10 times the recommended daily allowance.

The above abstract first appeared in Journal of the Australasian College of Nutritional & Environmental Medicine, Vol. 14, No. 2, November 1995, page 15.

[Last updated Wednesday, 28 September 2005]

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