Wound Care


By definition, a wound is a physical injury that results in an opening or break of the skin.


There are several types of wounds, including surgical, traumatic and chronic wounds. Traumatic wounds may be caused by mechanical, traumatic or thermal injury, including contusions, abrasions, punctures, fractures, burns and frostbite. The surgical wound is usually clean and easiest to heal. By definition, chronic wounds may be more difficult to heal, and include pressure sores and diabetic ulcers.

Generally, wounds can be further classified into 2 categories: partial and full thickness. Partial thickness wounds present with damage to the epidermal and dermal tissues, including flame burns, scalds and blisters, usually being painful to the touch. Full thickness wounds present with damage to epidermal, dermal, or subcutaneous tissues, including flame burns, boiling liquids and chemical burns, usually without pain being evident.

The most common type of wound is a traumatic wound. Traumatic wounds are categorized into several types: (1) abrasion - exists when the surface of the skin or a mucous membrane is scraped away, (2) contusion - an injury where the surface of the skin is not broken, but underlying or internal tissues are damaged, usually resulting from a sharp blow to the body and frequently producing a discoloration or bruising of the skin surface, (3) incision - a traumatic wound made with a sharp instrument that produces a clean cut, such as a scalpel, (4) tunneled wound - presents with a passageway under the surface of the skin that is generally open at the skin level, with most of the tunneling not seen, (5) laceration - the skin is irregularly torn and a penetration wound results from events like a stab or gunshot, (6) bites - abrasions and/or contusions caused by the entrance and crushing of teeth, usually in animals, humans or insects, (7) cuts - classified as traumatic wounds where there is only a minor break in the integrity of the skin, (8) thermal wounds - include heat injuries such burns, sunburns and electric injuries.

Burns are thermal wounds that are further classified into degrees, from first to third degree. First-degree burns are superficial, partial thickness wounds with damage only to the epidermis. The outstanding feature of first-degree burns is redness, with sunburns being one of the most common. Second-degree burns are usually deeper that first-degree burns, and are partial-thickness wounds with destruction of the epidermis and some of the dermis. Second-degree burns are usually waxy white, dry but elastic and are painful to the touch. Third degree burns are full-thickness wounds with destruction to the epidermis, dermis and some subcutaneous tissue. They appear blanched white, dry, leathery and have an inelastic eschar. Third degree burns are very serious wounds and may require skin grafting. Other thermal wounds include cold injuries such as frostbite, chemical wounds (resulting from exposure to strong acid or alkaline substances which release thermal energy upon skin contact) and radiation wounds result from exposure to radiation, either accidental or in cancer therapy.

Surgical wounds result from the trauma induced by surgery. Surgical wounds include: (1) post-surgical incisions, including dental extraction, (2) suture site wounds, (3) donor site wounds such as in blood donation, (4) IV site wounds, (5) skin graft wounds, (6) periostomy skin wounds, and (7) peritracheotomy wounds.

The most difficult wounds to treat are the chronic, non-healing wounds. These include:

  1. Diabetic Wounds -- present themselves as ulcers and are manifestations of the diabetic disease process. Diabetic wounds are further classified as:
    • Neurotropic Ulcers – with the most common being foot ulcers found in diabetics, compromising motor and sensory function in the foot. They result from micro/macro vessel damage, neuropathy and changes in foot configuration.
    • Ischemic Ulcers – these ulcers resulting from a deficiency of blood in a body part as a result of constriction or obstruction of a blood vessel.

  2. Arterial Ulcers – resulting from the presence of occlusive disease, predominantly arteriosclerosis. Circulation to the lower limbs may be compromised. Arterial ulcers present with a pale wound base, well-defined wound edges, minimal exudate and are generally painful. These types of wounds are common in diabetics and individuals with CVD.

  3. Venous Ulcers – resulting from prolonged venous hypertension. Venous ulcers usually present with a red wound base, presence of yellow fibrin, ill-defined, irregular wound edges and have moderate to heavy exudate. Peripheral tissue edema is usually present with little or no pain. Approximately 6-7 million people have chronic venous insufficiency, which causes lower extremity ulcers. (1)

  4. Pressure Ulcers – these are superficial or deep and serous lesions resulting from shear, friction or excessive pressure for prolonged periods of time, affecting over 2.9 million people annually. (2)
      Stage 1 – nonblanchable erythema of intact skin; darker skinned individuals may develop skin discoloration, warmth, edema or hardness. Stage 2 – partial thickness skin loss involving the epidermis, dermis, or both. The ulcer is presented as an abrasion, blister or as a shallow wound. Stage 3 – full thickness skin loss involving damage and necrosis to the subcutaneous tissue that may extend down to, but not through, the underlying fascia. The ulcer presents itself as a deep crater, with or without undermining of adjacent tissues. Stage 4 – full thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures. Tunneling may be associated with stage 4 pressure wounds.
Repair of the Wound:

The process of repair and regeneration following injury represents one of the most fundamental defense mechanisms of an organism against the environment. Wound healing in individuals generally occurs over a reasonable length of time. However, there are reasons that wounds may not heal appropriately, such as in impaired immunity, diseases such as diabetes and CVD, immobility, poor nutrition and the like. Intervention is necessary in these individuals. Even with minor injuries such as cuts, wounds in impaired individuals may readily develop into very traumatic injuries requiring medication, hospitalization and even surgery. In general, if a wound does not heal within a month, medical intervention is necessary.

Immediately after injury, the wound fills with blood and a clot forms. The clot contains a threadlike protein called fibrin, which binds the edges of the wound together and stops any bleeding. If tissues are damaged, a cascade of cellular events is initiated to prepare the injured area for the deposition of collagen, which ultimately will replace damaged mesenchymal tissues. Wound healing occurs in several stages.

1. Inflammation: A wound initiates a natural inflammatory response with heat, redness, pain, swelling and impaired function of the involved body tissues. Vasoconstriction occurs within seconds and lasts only a few minutes. This response is followed by vasodilation with a concomitant increase in vascular permeability. Next, pronounced leakage of serum proteins occurs into the wound for approximately 10-20minutes. The final stage of inflammation spans a period of several hours and is characterized by vascular stasis, local hemorrhage and infiltration of tissues with leukocytes. Vasoactive substances are released from cells in the local environment, most notably histamine. Histamine-induced vasodilation is brief, and seldom lasts more than one hour. Other unknown factors may be involved, including kinins and serotonin.

Polymorphonuclear leukocytes (neutrophils) emigrate to the wound site and are the predominant cellular species present. The neutrophils actively phagocytize and digest bacteria, debris and foreign materials, along with playing a key role in controlling infection at the wound site. After cellular emigration terminates, however, the neutrophils degenerate and die within a few days. As neutrophils die, their remains are digested as well and become the early stages of pus or wound exudate.

By approximately the fourth day after the initial wound, the neutrophils are replaced by macrophages which are largely responsible for debridement of the wound. These macrophages actively phagocytize bacteria and other particulate matter. More than 30 hydrolytic enzymes have been identified in macrophage lysosomes. (3) Of note is aspirin, cortisone and antihistamines all exert their anti-inflammatory effects by stabilizing lysosomal membranes, which may adversely affect macrophage digestive ability, decreasing their ability to debride the wound. Vitamin A has been shown to reverse the lysosomal stability produced by drugs including glucocorticoids. (4) During the inflammatory phase the patient will develop leukocytosis, a mildly elevated temperature, and general malaise. Wound management during this phase of healing should include monitoring the wound for erythema or swelling and redness outside the edges of the wound, possibly indicating infection.

2. Proliferative Phase: The second stage of wound healing begins three to four days after wounding, and lasts approximately 21 days. During this stage, the wound starts to get smaller and new tissue begins to grow.

3. Remodeling Phase: This final stage of healing begins about day 21 and can continue for as long as one to two years post-injury. Collagen that has been deposited in the wound is remodeled, making the healed wound stronger and more like the adjacent tissue. New collagen continues to be deposited, and this compresses the blood vessels in the healing wound, so that the scar eventually becomes a thin, flat, white line. The scar is a vascular collagen tissue that does not sweat, grow hair, or tan in the sunlight. Maximum scar strength is achieved in about three months.

Wound contraction is the final step of the remodeling phase. Wound contraction is the mechanism by which the edges of a wound are drawn together by the interaction of cells with the collagenous matrix. Wound contraction may be affected agents that interfere with the cell cytoskeleton, such as colchicine, which may decrease the rate and extent of contraction. (5)

Some factors that may negatively influence wound healing include:

    Age – aging may alter many phases of wound healing including: vascular changes, reduced liver function and synthesis of clotting factors, slowed inflammatory response, reduced immune function, changes in collagen. Obesity - adipose tissue lacks adequate blood supply to resist bacterial infection or deliver nutrients and cellular elements for healing. Malnutrition – may impair all phases of wound healing due to vitamin and mineral deficiencies. (6) Decreased oxygenation of wound site - low arterial oxygen tension alters synthesis of collagen and formation of epithelial cells. (7) Smoking – creates hypoxic environment due to vasoconstrictive properties. Diabetes – this condition may impair perfusion through capillary destruction, may cause hemoglobin to have a greater affinity for oxygen so it fails to release oxygen to tissues, and may alter the ability of leukocytes to perform phagocytosis. (8) Diabetic neuropathy further impairs healing by interrupting the neurologic control such as pain sensation and vasodilatory functions. Studies have shown that diabetic laboratory animals have decreased collagen synthesis, and decreased rate of cell growth or accumulation in the wound site. (9) Insulin deficiency has been linked with defects in the inflammatory and proliferate phases of wound healing. (10) Radiation – creates poorly oxygenated tissues at wound site. (11) Wound stress - vomiting, abdominal distention and respiratory effort may stress suture lines in applicable patients and disrupt the wound layer. Pharmaceutical medications – some medications may decrease the rate and extent of wound healing. Anti-inflammatory steroids may decrease the tensile strength of closed wounds (12) slow the rate of epithelialization, (13) and neovascularization (14) and severely inhibit wound contraction. (15) Also, estrogen and progestogens have been reported to have a negative effect on some phases of wound healing, with a decrease in granuloma formation and decrease in angiogenesis. (16)


Nurse Practitioner,The 24(10):66,69-70,73,74.

    Simple traumatic lacerations are one of the most common reasons for visits to the emergency department.

Geriatrics 53(5):88-90,92-94.

    Common causes of wounds in older persons are pressure and friction.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

Serious complications may occur to neglected wounds and, at times, even the best cared for wounds. If you notice any of these signs when examining your wounds, you should see a doctor immediately:

    Redness, excessive swelling, or tenderness in the wound area Throbbing pain or tenderness in the wound area Red streaks in the skin around the wound or progressing away from the wound Pus or watery discharge collected beneath the skin or draining from the wound Tender lumps or swelling in your armpit, groin or neck Foul odor from the wound Generalized chills or fever

Treatment Options


Some non-pharmacological interventions that may encourage the healing of a wound include:

    Limiting wound size – the smaller the wound, the faster the rate of healing. Encourage blood supple – proper blood supply is critical for the wound to receive nutrient and oxygen. Micro-organism containment – make sure the wound is properly cleaned. Adequate nutrition – proper nutritional status is a major factor in rate and extent of wound healing. Reduce physical and mental stresses - both physical and mental stress can depress immunity, thereby decreasing the ability of a wound to heal appropriately.

The pharmacological approach to wound healing may include:

    Topical antibacterial agents, including cleansers, creams, ointments. Growth factors. Analgesics. Enzymatic debriders. Collagen. Wound dressings (primary or secondary) - a primary dressing is placed in direct contact with the wound and may provide absorptive capacity and prevent desiccation, infection and adhesion of the secondary dressing to the wound. A secondary dressing is placed over a primary dressing to provide further protection, absorptive capacity, compression, and occlusion if need. The selection of materials for primary or secondary dressings is governed by the particular application. Some commonly used dressings include alginates, absorbent dressings, composite, foam, contact layers, compression, non-adherent dressings, occlusive or semi-occlusive dressings, hydrophilic or hydrophobic dressings, hydrocolloid and hydrogel dressings among others. Hyperbaric oxygen.

Nutritional Supplementation

Protein: In the United States, the Recommended Daily Allowance (USRDA) for protein intake for healthy individuals is 0.8 grams per kilogram of body weight per day. To support wound healing, the USRDA protein requirement is substantially higher at 2 to 4 gm/kg/day. (17) Furthermore, approximately 25% of hospitalized patients exhibit signs of malnutrition while 50% of general surgery patients reportedly have moderate-to-severe protein malnutrition. (18)

In protein-deficient patients, the inflammatory stage of wound healing is significantly prolonged. (19) This allows macrophages and granulocytes to secrete proteolytic enzymes into a wound area for an extended period of time which can result in an additional 30 to 50 percent of the protein surrounding a wound site being destroyed. (20) Increased inflammation also reduces the proliferation of fibroblasts which causes a reduction in proteoglycan and collagen synthesis that would normally replace the destroyed protein. Revascularization and wound remodeling are also impaired. Actually, any process in wound healing that requires protein synthesis will be compromised in the absence of adequate protein nutriture.

Protein supplementation before a surgical procedure is more effective than supplementation after surgery. As little as one week of preoperative protein supplementation has been shown to improve wound healing. (21) Unfortunately, patients frequently decrease food intake prior to surgery because of decreased mobility, reduced appetite related to the current illness, or for diagnostic tests. Therefore, it is important to educate patients about the importance of an optimal diet prior to surgery and/or during the wound healing process. Appropriate protein recommendations include fish, lean meats, eggs, vegetable protein such as soy, or the use of a dipeptide ion exchange resin whey powder.


Zinc has a long history as an agent used to promote wound healing. It was used topically as calamine lotion as far back as 1500 BC by the Egyptians. There are over 200 zinc requiring enzymes in the body. Zinc is important in wound healing because it is a required constituent of many proteins and plays a central role in regulating cellular division and differentiation. (22) In cases of zinc deficiency, it is known that zinc supplementation accelerates the healing process. (23) Conversely, zinc deficiency is known to delay the wound healing process. (24)

Stress from events such as surgery, burns, or other accidental injury, causes serum zinc levels to decline. (25) , (26) , (27) The results of a randomized, double-blind study revealed that the topical application of a zinc oxide-containing compress helped heal leg ulcers. Zinc oxide-treated patients reported an 83% success rate compared to a 42% success rate in individuals treated with an identical compress without zinc oxide. (28)

In general, topical zinc is widely recognized as an effective treatment for wound healing whereas oral zinc supplementation only seems to be beneficial in patients who are zinc deficient. (29)


L-glutamine is a conditionally essential amino acid whose requirements increase dramatically during critical illness. Catabolic states causes glutamine metabolism to increase dramatically, causing its tissue and plasma pools become depleted. In fact, glutamine’s uptake during stress exceeds that of any other amino acid. It is involved in nitrogen exchange, the regulation of neucleotide and protein synthesis, and it is an important substrate for rapidly dividing cells, including those of the gastrointestinal tract, pancreas, pulmonary alveoli, and white blood cells. Because it is an effective nitrogen donor and a precursor for nucleotide and protein synthesis, glutamine is extremely important when wounded tissues are rebuilding. (30)

In one test, 28 patients undergoing elective abdominal surgery were randomly divided into two groups. The control group received a standard 1.5 gm of amino acid daily in their TPN formulation. The TPN formulation for the test group contained 1.2 gm of the standard amino acid mix and an additional 300 mg of glutamine. Patients receiving the glutamine supplementation obtained improved nitrogen balance and improved lymphocyte recovery on day 6 in addition to other benefits. Postoperative hospital stay was also 6.2 days shorter in the glutamine-supplemented group. (31)

In an animal experiment, 2 groups of rats were given a diet containing either 3% glutamine or 3% glycine for 8 days after undergoing abdominal radiation. After irradiation, the survival rate was 100% in animals receiving glutamine compared with 45% in animals receiving glycine. Glutamine ingestion also reduced bloody diarrhea and the incidence of bowel perforation. Rats receiving glutamine supplementation experienced marked increases in villous height, villous number, and the number of mitoses per crypt. These results indicate that oral glutamine supplementation after abdominal radiation enhanced gut glutamine metabolism, improved mucosal morphology, and reduced the morbidity and mortality associated with this abdominal radiation model. (32)

In general, glutamine supplementation will substantially speed up the healing process for individuals undergoing surgery, radiation, or who have been exposed to burns or other sorts of trauma.

Vitamin C

Vitamin C plays several critical roles in wound healing. It is necessary for the synthesis of collagen and elastin, which is essential in the repair of injured tissue. Wound healing is impaired when vitamin C levels are not adequate. For example, in a dental study, the healing rate of gingival tissue was compared in patients receiving 250 mg of vitamin C twice daily, 500 mg of vitamin C twice daily, and placebo controls. Wound healing was 40% faster in patients taking 250 mg of vitamin C twice daily, and healing was 50% faster in patients who took 500 mg of vitamin C twice daily. (33)

Vitamin C causes an increased migration of leukocytes to the site of a wound, thereby increasing resistance to infection. Once at the wound site, neutrophils need adequate amounts of vitamin C in order to produce superoxide free radicals to kill bacteria. (34) Severe trauma such as burns, fractures, or major surgery cause a substantial decrease in plasma vitamin C levels. At the same time, the stresses associated with injury and wound healing increases the body’s need for vitamin C.

A summary of vitamin C’s effects include increasing the strength of new collagen formation and the rate of healing, enhancing the immune system and fighting infections, in addition to its well known anti-oxidant, free radical scavenging effects.

Vitamin A

Vitamin A is an important immune system nutrient. Studies report that vitamin A deficiency is common in hospitalized patients, and individuals who are severely wounded or burned can become vitamin A deficient, which impedes wound healing. (35)

Vitamin A plays a significant role in each stage of wound healing. It enhances the early inflammatory phase, causing increased numbers of monocytes and macrophages to migrate to the wound site. It also promotes phagocytic activity and facilitates wound debridement. On the other hand, in vitamin A deficiency, phagocytic activity decreases resulting in an increased accumulation of pus and debris. During the proliferation stage vitamin A stimulates fibroblast differentiation and collagen deposition which increases the tensile strength of the wound. (36)


Iron is an essential nutrient for new cellular growth and wound healing. The enzyme ribonucleotide reductase, which requires iron as a cofactor, is necessary for DNA synthesis. Since cells cannot divide without prior DNA synthesis, iron deficiency can retard the proliferation of cells involved in wound debridement and healing. (37)

The enzyme facilitates the hydroxylation of proline is iron-dependent. Without adequate hydroxylation of proline, collagen that is produced is weaker than normal, which compromises the wound healing process. (38)

It is important for health professionals to recognize that iron deficiency anemia is a relatively common problem in menstruating women, and that anemic patients of any age will exhibit delayed wound healing.

Vitamin E

Vitamin E supplementation has been shown to enhance immune function and increase resistance to infection. It also helps prevent excessive free radical destruction to wounded tissue, thus reducing secondary damage and improving the healing process. (39)

When vitamin E is applied topically to wounds it may inhibit collagen synthesis. For example, in a study with laboratory animals, back incisions had a significantly lower tensile strength after 7 days of treatment. However, topical administration of vitamin E did produce a marked reduction in scar formation and in the apparent size of the area of injury. This suggests that topical vitamin E may provide some cosmetic benefits, but if the strength of a wound closure is important, topical vitamin E should be avoided. (40)


Arginine is an amino acid that promotes healing. After a surgical procedure, rats receiving diets supplemented with arginine do better than control rats on arginine-free diets. Rats administered arginine are more capable of surviving a bacterial challenge, exhibit improved immune function, higher protein levels and a faster rate of healing. (41)

Arginine also increases T-cell-mediated activity, which enhances immune function. Finally, arginine is an important constituent of wound proteins, and supplementation with arginine has been shown to significantly increase the amount of collagen deposited into a wound site during the healing process. (42)

Herbal Supplementation


Used since ancient times as a healing agent, calendula is mentioned in herbal books that date back to 1373. Extracts of calendula flowers are popular in Europe where they are employed in various first aid creams and cosmetics. Calendula is a very popular homeopathic remedy also, used topically for skin problems including diaper rash and other conditions in children and infants. (43) Calendula is listed in the German Commission E Monograhs for use as a mouthwash for the oral and pharyngeal mucosa as well as topically for the skin. (44)

Calendula extracts have been used topically to promote wound healing, with several studies reporting a measurable effect. In a laboratory study, an ointment containing a 5% fractionated extract of calendula flowers markedly stimulated the physiological regeneration and epithelialization of wound tissue, reported to be due to more intensive metabolism of glycoproteins, nucleoproteins and collagen proteins during the regenerative period in the tissues. (45) Another later study reported immune activation by calendula extracts using in vitro granulocyte tests and in vivo carbon clearance tests, both laboratory determinants of immune activation. (46) Calendula extracts have also been reported to be anti-inflammatory, which also aids in wound repair and healing. (47) , (48) The anti-inflammatory effect has been reported to be due to the triterpenoids (specifically faradiol) found in calendula. (49)

Tea Tree Oil

An oil from the leaves has been used medicinally for centuries and was first reported to the western world by the crew of Captain James Cook's expeditions in the 1700s. The plant gained widespread notoriety because of claims of its ability to treat various problems including skin ailments, cuts, and burns.

Tea tree oil has historically been used in many conditions including the treatment of acne, aphthous stomatitis, tinea pedis, boils, burns, carbuncles, corns, gingivitis, herpes, empyema, impetigo, infections of the nail bed, insect bites, lice, mouth ulcers, pharyngitis, psoriasis, root canal treatment, ringworm, sinus infections, skin and vaginal infections, thrush, and tonsillitis - a literal panacea for topical infectious conditions. Also, as early as 1930, the antiseptic properties of the plant were recognized by the Australian dental profession. (50)

The therapeutic use of tea tree oil is largely based on its antiseptic and antifungal properties. This claim is supported by its efficacy against a wide range of organisms including Candida albicans, Propionibacterium acnes, Pseudomonas aeruginosa, Staphylococcus aureus, Staphylococcus epidermis, Streptococcus pyrogenes, Trichomonas vaginalis, and Trichomonas mentagrophytes. (51) , (52) The ability of tea tree oil to disrupt the permeability barrier of cell membrane structures and the accompanying loss of chemiosmotic control is the most likely source of its lethal action at minimum inhibitory levels. (53) Reports suggest that P. aeruginosa is less sensitive than other bacteria listed and may develop tolerance to the oil. (54)

Of recent interest is a study that determined the susceptibility of methicillin-resistant Staphylococcus aureus (MRSA) to tea tree oil in-vitro. (55) MRSA is a common pathogen recognized in hard to treat nosocomial (hospital acquired) infections. In the study all 60 MRSA tested against tea tree oil by the disc diffusion method and modified broth microdilution were susceptible, with MICs and MBCs of 0.25% and 0.5% respectively. Also tested were mupirocin-susceptible and mupirocin-resistant MRSA, and there was no difference in tea tree oil susceptibility between the two. The universal susceptibility to tea tree oil of all MRSA isolated tested, including those who were mupirocin-resistant, represents a significant result which may find application in the control of MRSA. A recent report also supports the use of tea tree oil in the hospital and community setting to help prevent spread of multi-resistant bacteria such as MRSA, glycopeptide-resistant enterococci, aminoglycoside-resistant klebsiellae, Pseudomonas aeruginosa and Stenotrophomonas maltophilia. (56)

Data indicates that some essential oils are active against Candida sp., suggesting that they may be useful in the topical treatment of superficial candida infections. (57) Recent tests on three intra-vaginal tea tree oil products showed these products to have MICs and minimum fungicidal concentrations comparable to those of non-formulated tea tree oil, indicating that the tea tree oil contained in these products has retained its anti-candidal activity. (58)

Tea tree oil was reported effective in tinea pedis. (59) One hundred and four patients completed a randomized, double-blind trial to evaluate the efficacy of 10% w/w tea tree oil cream compared with 1% tolnaftate and placebo creams in the treatment of this infection. Results of this study reported that tea tree oil cream (10% w/w) appeared to reduce the symptomatology of tinea pedis as effectively as tolnaftate 1%, but is no more effective than placebo in achieving a mycological cure.

Aloe Vera

Aloe vera leaf gel has been heralded for centuries as a topical wound healing agent, including traumatic wounds (from mechanical, traumatic or thermal injury, including contusions, abrasions, punctures, fractures, sunburn, burns and frost bite), and chronic wounds (including pressure sores and diabetic ulcers). (60) In one study, it was observed that aloe increased the collagen content of the granulation tissue as well as cross-linking as seen by increased aldehyde content and decreased acid solubility. (61) The type I/type III collagen ratio of treated groups were lower than that of the untreated controls, indicating enhanced levels of type III collagen. Interestingly, wounds treated either by topical application or oral administration of aloe in rats were found to result in similar effects.

The influence of aloe on the glycosaminoglycan (GAG) components of the matrix in a healing wound has also been reported as a mechanism in wound healing. The early stage of wound healing is characterized by the laying down of a provisional matrix, which is then followed by the formation of granulation tissue and synthesis of collagen and elastin. The provisional matrix or the ground substance consists of GAGs and proteoglycans (PGs), which are protein GAG conjugates. A recent study reported the influence of Aloe vera on the content of GAG and its types in the granulation tissue of healing wounds. (62) The amount of ground substance synthesized was found to be higher in the wounds treated with aloe vera gel, with the levels of the reported glycohydrolases (hyaluronic acid and dermatan sulphate) being elevated, indicating increased turnover of the matrix. Both topical and oral treatments with aloe vera were found to have a positive influence on the synthesis of GAGs and thereby beneficially modulate wound healing. Aloe also contains vitamins and minerals (including vitamin C, E and zinc) which have been reported beneficial in wound healing. (63) , (64)

Aloe vera has been reported for years to be effective in treating various types of burns. (65) , (66) A recent study supported these findings, where aloe vera gel was reported to increase microcirculation to the burn area, causing vasodilation and increased post-capillary venular permeability. (67) There has been a report of aloe hindering the wound healing process, causing a thickness of granulation tissue with a decreased amount of hair follicles as compared to 1% silver sulfadiazine cream. (68)

Aloe vera gel also aids in wound healing topically due its anti-inflammatory activity. (69) Aloe constituents with anti-inflammatory activity include: (1) mannose-6-phosphate, (70) , (71) (2) the glycoproteins aloctin A and alprogen, (72) , (73) (3) a C-glucosyl chromone, (74) (4) the anthraquinones, (75) (5) and gibberellin. (76)

Gotu Kola

Gotu kola is reported to have a positive effect on tissues, specifically skin, connective tissue, lymph and mucous membranes. (77) , (78) , (79) It does not contain any caffeine and is not related in any way to kola nut. Gotu kola has been used primarily for venous insufficiency, soft tissue inflammation and infection and for post surgical wound healing. (80) , (81) Asiaticosides are reported to exert a preferential stimulation of collagen synthesis, in addition to stimulating glycosaminoglycan synthesis. (82) Also, 1gotu kola’s affects the connective tissue by strengthening weakened veins. (83) Gotu kola may assist in the maintenance of connective tissue. In the treatment of scleroderma, gotu kola may also assist in stabilizing connective tissue growth, reducing its formation. (84) It reportedly stimulates the formation of hyaluronidase and chondroitin sulfate, as well as exerting a balancing effect on the connective tissue. (85) It is believed to have an effect on keratinization, which aids in thickening skin in areas of infection. (86) Gotu kola is used topically and internally for skin conditions including psoriasis and eczema. (87)


Apis mellifica

Typical Dosage: 6X or 6C, 30X or 30CPuncture wounds that are swollen and hot with stinging pains; Better from cold applications

Calendula officinalis(topical)

Typical Dosage: N/ATopically for minor skin irritations from cuts and scrapes

Hepar sulphuris calcareum

Typical Dosage: 6X or 6C, 30X or 30CRed, swollen, painful wounds

Hypericum perforatum

Typical Dosage: 6X or 6C, 30X or 30CNerve pain from cuts and scrapes

Ledum palustre

Typical Dosage: 6X or 6C, 30X or 30CPuncture wounds associated with redness, swelling, and throbbing pain


  1. The United States Census Bureau: Statistical Abstract of the U.S. 1994.
  2. Weissmann G. The role of lysosomes in inflammation and disease. Ann Rev Med. 1967;18:97.
  3. Weissmann G. The role of lysosomes in inflammation and disease. Ann Rev Med. 1967;18:97.
  4. View Abstract: Ayello EA, et al. Nutritional aspects of wound healing. Home Healthc Nurse. Nov1999;17(11):719-29.
  5. Yannas IV. What criteria should be used for designing artificial skin repalcement and how well do the current graft materials meet these criteria? J Trauma. 1984;24(Suppl):535-538.
  6. View Abstract: Young ME. Malnutriton and wound healing. Heart Lung. 1988;17:60-67.
  7. Chvapil M, et al. The influence of various oxygen tensions upon proline hydroxylation and the metabolism of collagenous and non-collagenous proteins in skin slices. Hoppe Seyler Z Phsiol Chem. Berlin. 1968;349:211-217.
  8. LoGerfo FW, et al. Vascular and microvascular disease of the foot in diabetes: Implications for foot care. N Eng J Med. 1984;311:1615-1619.
  9. View Abstract: Arguilla ER, et al. Wound healing: a model for the study of diabetic microangiopathy. Diabetes. 1976;25(Suppl 2):811.
  10. Goodson WH, et al. Studies of wound healing in experimental diabetes mellitus. J Surg Res. 1977;22:221.
  11. View Abstract: Erlichman RJ, et al. Common complications of wound healing. Surg Clin NA. 1991;71(6):1323-1337.
  12. Ehrlich HP, et al. The effect of cortisone and anabolic steroids on the tensile strength of healing wounds. Ann Surg. 1969;170:203.
  13. Baker BL, et al. Interference with wound healing by the local action of adrenocortical steroids. Endocrin. 1950;46:544.
  14. Howes EL, et al. Retardation of wound healing by cortisone. Surgery. 1950;28:177.
  15. Stephens F, et al. The effect of delayed administration of corticosteroids on wound contractions. Ann Surg. 1971;173:214.
  16. Nyman S, et al. Impaired wound healing in progesterone-treated rabbits. Acta Chir Scand. 1973;139(5):415-419.
  17. View Abstract: Doweiko JP, Nompleggi D. The role of albumin in human physiology and pathophysiology: part III, albumin and disease states. J Parenter Enteral Nutr. 1991;15:476.
  18. View Abstract: Mazzotta MY. Nutrition and Wound Healing. J Am Podiatric Med Ass. Sep1994;84(9): 456-462.
  19. View Abstract: Gallucci RM, Simeonova PP, Matheson JM, et al. Impaired cutaneous wound healing in interleukin-6-deficient and immunosuppressed mice. FASEB J. Dec2000;14(15):2525-31.
  20. View Abstract: Erlichman RJ, et al. Common complications of wound healing. Surg Clin NA. 1991;71(6):1323-1337.
  21. View Abstract: Windsor J, et al. Wound healing response in surgical patients: recent food intake is more important than nutritional status. Br J Surg. 1988;75:135.
  22. View Abstract: Fabris N, Mocchegiani E. Zinc, human diseases and aging. Milano. Aging. Apr1995;7(2):77-93.
  23. View Abstract: Okada A, et al. Zinc in clinical surgery: a research review. Japanese Journal of Surgery. 1990;20:635.
  24. View Abstract: Andrews M, Gallagher-Allred C. The role of zinc in wound healing. Adv Wound Care. Apr1999;12(3):137-8.
  25. View Abstract: Boosalis MG, et al. Increased urinary zinc excretion after thermal injury. J Lab Clin Med. Dec1991;118(6):538-45.
  26. View Abstract: Antila H, et al. Serum iron, zinc, copper, selenium, and bromide concentrations after coronary bypass operation. JPEN J Parenter Enteral Nutr. Jan1990;14(1):85-9.
  27. View Abstract: Mountokalakis T, et al. Differential effect of surgical injury and thermal burn on zinc metabolism in man. Klin Wochenschr. Jul1980;58(13):695-7.
  28. View Abstract: Stromberg HE, Agren MS. Topical zinc oxide treatment improves arterial and venous leg ulcers. Br J Dermatol. Oct1984;111(4):461-8.
  29. View Abstract: Agren MS. Studies on zinc in wound healing. Stockh. Acta Derm Venereol Suppl. 1990;154:1-36.
  30. View Abstract: Balzola FA, Boggio-Bertinet D. The metabolic role of glutamine. Minerva Gastroenterol Dietol. Mar1996;42(1):17-26.
  31. View Abstract: Morlion BJ, et al. Total parenteral nutrition with glutamine dipeptide after major abdominal surgery: a randomized, double-blind, controlled study. Ann Surg. Feb1998;227(2):302-8.
  32. View Abstract: Klimberg VS, et al. Oral glutamine accelerates healing of the small intestine and improves outcome after whole abdominal radiation. Arch Surg. Aug1990;125(8):1040-5.
  33. View Abstract: Ringsdorf WM Jr, Cheraskin E. Vitamin C and human wound healing. Oral Surgery. 1982;53(3):231-236.
  34. Orgill D, Demling RH. Current concepts and approaches to wound healing. Critical Care Medicine. 1988;16:899.
  35. View Abstract: Hunt TK. Vitamin A and wound healing. J Am Acad Dermatol. 1986;15:517.
  36. View Abstract: Demetriou AA, et al. Vitamin A and retinoic acid induced fibroblast differentiation in vitro. Surgery. 1985;98:931.
  37. Ward CG. Influence of iron on infection. Am J Surg. 1986;42:166.
  38. View Abstract: Mazzotta MY. Nutrition and Wound Healing. J Am Podiatric Med Ass. Sep1994;84(9): 456-462.
  39. Goldstein R, et al. Effect of vitamin E and allopurinol on lipid peroxide and glutathione level in acute skin grafts. J Inves Dermatol. 1990;95:470.
  40. View Abstract: Greenwald DP. Zone II flexor tendon repair: Effects of vitamins A, E and B-carotene. J Surg Res. 1990;49:98.
  41. View Abstract: Nirgiotis JG, et al. The Effects of an Arginine-Free Enteral Diet on Wound Healing and Immune Function in the Postsurgical Rat. Journal of Pediatric Surgery. Aug1991;26(8):936-941.
  42. View Abstract: Barbul A, et al. Arginine enhances wound healing and lymphocyte immune responses in humans. Surgery. Aug1990;108(2):331-336.
  43. View Abstract: Kaplan B. Homoeopathy: 3. Everyday uses for all the family. Prof Care Mother Child. Oct1994;4(7):212-3.
  44. View Abstract: Schmidgall J, et al. Evidence for bioadhesive effects of polysaccharides and polysaccharide-containing herbs in an ex vivo bioadhesion assay on buccal membranes. Planta Med. Feb2000;66(1):48-53.
  45. View Abstract: Klouchek-Popova E, et al. Influence of the physiological regeneration and epithelialization using fractions isolated from Calendula officinalis. Acta Physiol Pharmacol Bulg. 1982;8(4):63-7.
  46. View Abstract: Wagner H, et al. [Immunostimulating action of polysaccharides (heteroglycans) from higher plants]. Arzneimittelforschung. 1985;35(7):1069-75.
  47. View Abstract: Akihisa T, et al. Triterpene alcohols from the flowers of compositae and their anti-inflammatory effects. Phytochemistry. Dec1996;43(6):1255-60.
  48. Bezakova L, et al. Inhibitory activity of isorhamnetin glycosides from Calendula officinalis L. on the activity of lipoxygenase. Pharmazie. Feb1996;51(2):126-7.
  49. View Abstract: Della Loggia R, et al. The role of triterpenoids in the topical anti-inflammatory activity of Calendula officinalis flowers. Planta Med. Dec1994;60(6):516-20.
  50. Penfold AR, Morrison FR. Some notes on the Essential oil of M. alternifolia. Aust J Dent. Mar1930;417-4181930.
  51. View Abstract: Mann CM, et al. The outer membrane of pseudomonas aeruginosa NCTC 6749 contributes to its tolerance to the essential oil of melaleuca alternifolia. Lett Appl Microbiol. Apr2000;30(4):294-7.
  52. Carson CF, et al. Efficacy and safety of tea tree oil as a topical antimicrobial agent. J Hosp Infect. Nov1998;40(3):175-8.
  53. View Abstract: Cox SD, et al. The mode of antimicrobial action of the essential oil of Melaleuca alternifolia (tea tree oil). J Appl Microbiol. Jan2000;88(1):170-5.
  54. View Abstract: Mann CM, et al. The outer membrane of pseudomonas aeruginosa NCTC 6749 contributes to its tolerance to the essential oil of melaleuca alternifolia. Lett Appl Microbiol. Apr2000;30(4):294-7.
  55. View Abstract: Carson CF, et al. Susceptibility of methicillin-resistant Staphylococcus aureus to the essential oil of Melaleuca alternifolia. J Antimicrob Chemother. Mar1995;35(3):421-4.
  56. View Abstract: May J, et al. Time-kill studies of tea tree oils on clinical isolates. J Antimicrob Chemother. May2000;45(5):639-643.
  57. View Abstract: Nenoff P, et al. Antifungal activity of the essential oil of Melaleuca alternifolia (tea tree oil) against pathogenic fungi in vitro. Skin Pharmacol. 1996;9(6):388-94.
  58. View Abstract: Hammer KA, et al. In-vitro activity of essential oils, in particular Melaleuca alternifolia (tea tree) oil and tea tree oil products, against Candida spp. J Antimicrob Chemother. Nov1998;42(5):591-5.
  59. View Abstract: Tong MM, et al. Tea tree oil in the treatment of tinea pedis. Australas J Dermatol. 1992;33(3):145-9.
  60. Salcido R. Complementary and alternative medicine in wound healing. Adv Wound Care. Nov1999;12(9):438.
  61. View Abstract: Chithra P, et al. Influence of Aloe vera on collagen characteristics in healing dermal wounds in rats. Mol Cell Biochem. Apr1998;181(1-2):71-6.
  62. View Abstract: Chithra P, et al. Influence of Aloe vera on the glycosaminoglycans in the matrix of healing dermal wounds in rats. J Ethnopharmacol. Jan1998;59(3):179-86.
  63. View Abstract: Andrews M, et al. The role of zinc in wound healing. Adv Wound Care. Apr1999;12(3):137-8.
  64. View Abstract: Wipke-Tevis DD, et al. Nutrition, tissue oxygenation, and healing of venous leg ulcers. J Vasc Nurs. Sep1998;16(3):48-56.
  65. View Abstract: Visuthikosol V, et al. Effect of aloe vera gel to healing of burn wound a clinical and histologic study. J Med Assoc Thai. Aug1995;78(8):403-9.
  66. View Abstract: Rodriquez-Bigas M, et al. Comparative evaluation of aloe vera in the management of burn wounds in guinea pigs. Plast Reconstr Surg. Mar1988;81(3):386-9.
  67. View Abstract: Somboonwong J, et al. Therapeutic effects of Aloe vera on cutaneous microcirculation and wound healing in second degree burn model in rats. J Med Assoc Thai. Apr2000;83(4):417-25.
  68. View Abstract: Kaufman T, et al. Aloe vera gel hindered wound healing of experimental second-degree burns: a quantitative controlled study. J Burn Care Rehabil. Mar1988;9(2):156-9.
  69. View Abstract: Reynolds T, et al. Aloe vera leaf gel: a review update. J Ethnopharmacol. Dec1999;68(1-3):3-37.
  70. View Abstract: Davis RH, et al. Anti-inflammatory and wound healing activity of a growth substance in Aloe vera. J Am Podiatr Med Assoc. Feb1994;84(2):77-81.
  71. View Abstract: Vazquez B, et al. Antiinflammatory activity of extracts from Aloe vera gel. J Ethnopharmacol. Dec1996;55(1):69-75.
  72. View Abstract: Saito H, et al. Pharmacological studies on a plant lectin aloctin A. II. Inhibitory effect of aloctin A on experimental models of inflammation in rats. Jpn J Pharmacol. Feb1982;32(1):139-42.
  73. View Abstract: Ro JY, et al. Inhibitory mechanism of aloe single component (alprogen) on mediator release in guinea pig lung mast cells activated with specific antigen-antibody reactions. J Pharmacol Exp Ther. Jan2000;292(1):114-21.
  74. View Abstract: Hutter JA, et al. Antiinflammatory C-glucosyl chromone from Aloe barbadensis. J Nat Prod. May1996;59(5):541-3.
  75. View Abstract: Davis RH, et al. Anti-inflammatory activity of Aloe vera against a spectrum of irritants. J Am Podiatr Med Assoc. Jun1989;79(6):263-76.
  76. View Abstract: Davis RH, et al. Aloe vera and gibberellin. Anti-inflammatory activity in diabetes. J Am Podiatr Med Assoc. Jan1989;79(1):24-6.
  77. View Abstract: Suguna L, et al. Effects of Centella asiatica Extract on Dermal Wound Healing in Rats. Indian J Exp Biol. 1996;34(12):1208-11.
  78. View Abstract: Hausen BM. Centella asiatica (Indian Pennywort), an Effective Therapeutic But a Weak Sensitizer. Contact Dermatitis. 1993;29(4):175-79.
  79. View Abstract: Tenni R, et al. Effect of the Triterpenoid Fraction of Centella asiatica on Macromolecules of the Connective Matrix in Human Skin Fibroblast Cultures. Ital J Biochem. 1988;37(2):69-77.
  80. View Abstract: Maquart FX, et al. Stimulation of Collagen Synthesis in Fibroblast Cultures by a Triterpene Extracted from Centella asiatica. Connect Tissue Res. 1990;24(2):107-20.
  81. View Abstract: Cesarone MR, et al. The Microcirculatory Activity of Centella asiatica in Venous Insufficiency. A Double-blind Study. Minerva Cardioangiol. 1994;42(6):299-304.
  82. View Abstract: Marquart FX, et al. Triterpenes from Centella asiatica stimulate extracellular matrix accumulation in rat experimental wounds. Eur J Dermatol. Jun1999;9(4):289-96.
  83. Allegra C. Comparative Capillaroscopic Study of Certain Bioflavonoids and Total Triterpenic Fractions of Centella asiatica in Venous Insufficiency. Clin Ter. 1984;99:507-13.
  84. View Abstract: Tenni R, et al. Effect of the Triterpenoid Fraction of Centella asiatica on Macromolecules of the Connective Matrix in Human Skin Fibroblast Cultures. Ital J Biochem. 1988;37(2):69-77.
  85. View Abstract: Shukla A, et al. In vitro and in vivo wound healing activity of asiaticoside isolated from Centella asiatica. J Ethnopharmacol. Apr1999;65(1):1-11.
  86. View Abstract: Poizot A, et al. Modification of the Kinetics of Healing after Iterative Exeresis in the Rat. Action of a Triterpenoid and Its Derivatives on the Duration of Healing. C R Acad Sci Hebd Seances Acad Sci D. 1978;286(10):789-92.
  87. Natarajan S, et al. Effect of topical Hydrocotyle Asiatica in psoriasis. Indian J Dermatol. Jul1973;18(4):82-5.